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+2024 ESC Guidelines forthemanagement of elevated blood pressure andhypertension Developed bythetask force onthemanagement ofelevated blood pressure and hypertension oftheEuropean Society ofCardiology (ESC) and endorsed bythe European Society ofEndocrinology (ESE) andtheEuropean Stroke Organisation (ESO) Authors/Task Force Members: John William McEvoy  *†,(Chairperson) (Ireland), Cian P.McCarthy ‡,(Task Force Co-ordinator) (United States ofAmerica), Rosa Maria Bruno ‡,(Task Force Co-ordinator) (France), Sofie Brouwers (Belgium), Michelle D.Canavan  (Ireland), Claudio Ceconi  (Italy), Ruxandra Maria Christodorescu  (Romania), Stella S.Daskalopoulou  (Canada), Charles J.Ferro 1(United Kingdom), EvaGerdts  (Norway), Henner Hanssen (Switzerland), Julie Harris (United Kingdom), Lucas Lauder (Switzerland/Germany), Richard J.McManus  (United Kingdom), Gerard J.Molloy (Ireland), Kazem Rahimi  (United Kingdom), Vera Regitz-Zagrosek (Germany), Gian Paolo Rossi 2(Italy), ElseCharlotte Sandset 3(Norway), Bart Scheenaerts (Belgium), JanA.Staessen  (Belgium), Izabella Uchmanowicz  (Poland), Maurizio Volterrani  (Italy), Rhian M.Touyz  *†,(Chairperson) (Canada), andESC Scientific Document Group *Corresponding authors: John William McEvoy, Department ofCardiology, University ofGalway School ofMedicine, Galway, Ireland, and National Institute for Prevention and Cardiovascular Health, Galway, Ireland. Tel: +353 91 544310, E-mail: johnwilliam.mcevoy@universityofgalway.ie; and Rhian M. Touyz, Department ofMedicine, McGill University, Montreal, Canada, Department ofFamily Medicine, McGill University, Montreal, Canada, and the Research Institute ofthe McGill University Health Centre, McGill University, Montreal, Canada. Tel: +1514 934 1934 ext 71608, E-mail: Rhian.touyz@mcgill.ca †The two Chairpersons contributed equally tothe document and are joint corresponding authors. ‡The two Task Force Co-ordinators contributed equally tothe document. Author/Task Force Member affiliations arelisted inauthor information. 1Representing the European Renal Association (ERA),2Representing the European Society ofEndocrinology (ESE),3Representing the European Stroke Organisation (ESO),4Representing the European Geriatric Medicine Society (EuGMS). ESC Clinical Practice Guidelines (CPG) Committee: listed intheAppendix. ESC subspecialty communities having participated inthedevelopment ofthisdocument: Associations: Association ofCardiovascular Nursing &Allied Professions (ACNAP), European Association ofPreventive Cardiology (EAPC), European Association ofPercutaneous Cardiovascular Interventions (EAPCI), Heart Failure Association (HFA). Councils: Council for Cardiology Practice, Council onHypertension, Council onStroke. Working Groups: Aorta and Peripheral Vascular Diseases, Cardiovascular Pharmacotherapy, E-Cardiology. Patient Forum Disclaimer. The ESC Guidelines represent the views ofthe ESC and were produced after careful consideration ofthe scientific and medical knowledge and the evidence available atthe time oftheir publication. The ESC isnot responsible inthe event ofany contradiction, discrepancy and/or ambiguity between the ESC Guidelines and any other official recommendations orguide- lines issued bythe relevant public health authorities, inparticular inrelation togood use ofhealthcare ortherapeutic strategies. Health professionals are encouraged totake the ESC Guidelines fully into account when exercising their clinical judgment, aswell asinthe determination and the implementation ofpreventive, diagnostic ortherapeutic medical strategies; however, the ESC Guidelines donot override, inany way whatsoever, the individual responsibility ofhealth professionals tomake appropriate and accurate decisions inconsideration ofeach patient’s health condition and inconsultation with that patient and, where appropriate and/or necessary, the patient’s caregiver. Nor dothe ESC Guidelines exempt health professionals from taking into full and careful consideration the relevant official updated recommendations orguidelines issued bythe competent public health authorities, inorder tomanage each patient’s case inlight ofthe scientifically accepted data pursuant totheir respective ethical and professional obligations. Itisalso the health professional’s responsibility toverify the applicable rules and regulations relating todrugs and medical devices atthe time ofprescription. The ESC warns readers that the technical language may bemisinterpreted and declines any responsibility inthis respect. Permissions. The content ofthese European Society ofCardiology (ESC) Guidelines has been published forpersonal and educational use only. No commercial use isauthorized. No part of the ESC Guidelines may betranslated orreproduced inany form without written permission from the ESC. Permissions can beobtained upon submission ofawritten request toOxford University Press, the publisher oftheEuropean Heart Journal and the party authorized tohandle such permissions onbehalf ofthe ESC (journals.permissions@oup.com). ©The European Society ofCardiology 2024. Allrights reserved. For permissions, please email: journals.permissions@oup.comEuropean Heart Journal (2024) 00, 1–107 https://doi.org/10.1093/eurheartj/ehae178 ESC GUIDELINES
+Document Reviewers: Ana Abreu, (CPG Review Co-ordinator) (Portugal), Michael Hecht Olsen, (CPG Review Co-ordinator) (Denmark), Marco Ambrosetti (Italy), Emmanuel Androulakis (United Kingdom), LiaEviBang (Denmark), Jesper Nørgaard Bech (Denmark), Michael A.Borger (Germany), Pierre Boutouyrie (France), LuísBronze (Portugal), Sergio Buccheri (Sweden), Regina Dalmau (Spain), Maria Carmen DePablo Zarzosa (Spain), Christian Delles (United Kingdom), Maria Manuela Fiuza (Portugal), Rahima Gabulova (Azerbaijan), Bjørn Olav Haugen (Norway), Christian Heiss (United Kingdom), Borja Ibanez (Spain), Stefan James (Sweden), Vikas Kapil (United Kingdom), Meral Kayikçioglu (Turkey), Lars Køber (Denmark), Konstantinos C.Koskinas (Switzerland), Emanuela Teresa Locati (Italy), Sharon MacDonald (United Kingdom), Anastasia S.Mihailidou (Australia), Borislava Mihaylova (United Kingdom), Richard Mindham (United Kingdom), Martin Bodtker Mortensen (Denmark), Sandor Nardai (Hungary), LisNeubeck (United Kingdom), Jens Cosedis Nielsen (Denmark), Peter M.Nilsson (Sweden), Agnes A.Pasquet (Belgium), Mónica Mendes Pedro (Portugal), EvaPrescott (Denmark), Amina Rakisheva (Kazakhstan), Ernst Rietzschel (Belgium), Bianca Rocca (Italy), Xavier Rossello (Spain), Jean-Paul Schmid (Switzerland), Eduard Shantsila (United Kingdom), Isabella Sudano (Switzerland), Ana Teresa Timóteo (Portugal), Georgios Tsivgoulis3(Greece), Andrea Ungar4 (Italy), Ilonca Vaartjes (Netherlands), Frank Visseren (Netherlands), Heinz Voeller (Germany), Christiaan Vrints (Belgium), Adam Witkowski (Poland), Maria-Christina Zennaro2(France), andKatja Zeppenfeld (Netherlands) Allexperts involved inthedevelopment ofthese guidelines have submitted declarations ofinterest, which arereported inasupplementary document totheguidelines. Seethe European Heart Journal online or www.escardio.org/Guidelines forsupplementary documents, aswell asevidence tables. Click here toaccess thecorresponding ESC CardioMed chapters. ------------------------------------------------------------------------------------------------------------------------------------------------------------Keywords Guidelines •Blood pressure •Hypertension •Hypertension-mediated organ damage •Blood pressure measurement •Ambulatory blood pressure monitoring •Home blood pressure monitoring •Antihypertensive medication • Hypertension treatment •Hypertension targets •Secondary hypertension •Cardiovascular disease risk estimation • Cardiovascular disease prevention •Resistant hypertension •Hypertension screening Table ofcontents 1.Preamble ...................................................................................................................... 7 2.Introduction ............................................................................................................... 8 2.1. What isnew ..................................................................................................... 9 3.Pathophysiology ofelevated blood pressure and hypertension ....... 17 4.Clinical consequences ofelevated blood pressure and hypertension ........................................................................................................ 17 5.Measuring blood pressure ................................................................................. 18 5.1. Introduction and pertinent definitions ................................................ 18 5.2. Practical recommendations for measuring blood pressure ....... 19 5.2.1. Clinical validation ofequipment for measuring blood pressure ............................................................................................................... 19 5.2.2. Office blood pressure measurement .......................................... 19 5.2.3. Home blood pressure measurement .......................................... 20 5.2.4. Ambulatory blood pressure measurement .............................. 22 5.2.5. Comparison ofhome and ambulatory blood pressure monitoring ........................................................................................................... 23 5.3. What isthe best method for measuring blood pressure to diagnose hypertension? ...................................................................................... 235.3.1. Blood pressure measurement for hypertension screening 23 5.3.2. Blood pressure measurement fordiagnosing hypertension 23 5.4. What isthe best method formeasuring blood pressure for long-term management ofhypertension? .................................................. 23 5.4.1. Home monitoring ................................................................................ 23 5.4.2. Ambulatory monitoring .................................................................... 23 5.5. Measuring blood pressure inselected groups ................................. 24 5.5.1. Pregnancy ................................................................................................ 24 5.5.2. Atrial fibrillation .................................................................................... 24 5.5.3. Orthostatic hypotension .................................................................. 24 5.6. Novel methods ofmeasuring blood pressure ................................. 24 6.Definition and classification ofelevated blood pressure and hypertension, and cardiovascular disease risk assessment ....................... 25 6.1. Definition and classification ofelevated blood pressure and hypertension ........................................................................................................... 25 6.2. Principles ofarisk-based approach for managing blood pressure and preventing cardiovascular disease ...................................... 25 6.2.1. Role ofcardiovascular disease risk assessment ...................... 25 6.3. Predicting cardiovascular disease risk .................................................. 26 6.3.1. 10-year cardiovascular disease risk-prediction models ....... 272 ESC Guidelines
+6.4. Refining cardiovascular disease risk estimation beyond risk models ....................................................................................................................... 28 6.4.1. Sex-specific non-traditional cardiovascular disease risk modifiers .............................................................................................................. 28 6.4.2. Non-traditional cardiovascular disease risk modifiers shared bymen and women ......................................................................... 29 6.4.3. Additional risk decision tests .......................................................... 30 6.5. Summary ofthe cardiovascular disease risk stratification approach for allocating blood pressure treatment ................................ 30 7.Diagnosing hypertension and investigating underlying causes ........... 32 7.1. Screening forhypertension ...................................................................... 32 7.2. Confirming the diagnosis ofhypertension ........................................ 32 7.3. Communicating the diagnosis ................................................................. 33 7.4. Baseline assessment and diagnostic approach ................................. 33 7.4.1. Medical history, medication history, and physical examination ........................................................................................................ 33 7.4.2. Drug adherence and persistence with treatment ................. 34 7.4.3. Routine and optional tests ............................................................... 34 7.4.3.1. The kidneys .................................................................................... 36 7.4.3.2. The heart ........................................................................................ 36 7.4.3.3. The arteries ................................................................................... 37 7.4.4. Genetic testing ...................................................................................... 37 7.5. Resistant hypertension: definition and diagnosis ............................ 37 7.6. Secondary hypertension: when toscreen/further investigations 39 7.6.1. General considerations ..................................................................... 39 7.6.2. Primary aldosteronism ...................................................................... 39 7.6.3. Renovascular hypertension ............................................................. 40 7.6.4. Obstructive sleep apnoea syndrome .......................................... 40 7.6.5. Phaeochromocytoma/paraganglioma .......................................... 43 8.Preventing and treating elevated blood pressure and hypertension 43 8.1. Prevention strategies inearly life........................................................... 43 8.2. Non-pharmacological interventions ..................................................... 43 8.2.1. Dietary sodium and potassium intake ........................................ 43 8.2.1.1. Sodium ............................................................................................. 43 8.2.1.2. Potassium ........................................................................................ 44 8.2.2. Physical activity and exercise .......................................................... 45 8.2.3. Weight reduction and diet .............................................................. 46 8.2.4. Alcohol, coffee, and soft drinks ..................................................... 46 8.2.5. Smoking .................................................................................................... 46 8.3. Pharmacological interventions ................................................................ 47 8.3.1. Treatment strategy toreduce adverse cardiovascular disease outcomes ............................................................................................. 47 8.3.2. Drug classes with evidence onclinical outcomes inthe target population .............................................................................................. 47 8.3.3. New therapies with blood pressure-lowering properties that await supportive evidence from cardiovascular outcomes trials prior toguideline endorsement and routine use in hypertension ...................................................................................................... 48 8.3.4. Drug combinations and up-titrating strategies ....................... 48 8.3.5. Apractical algorithm forintensive, effective, and tolerable blood pressure lowering with drug therapy, including considerations around single-pill combinations .................................. 48 8.3.6. Timing ofblood pressure-lowering drug treatment ............ 51 8.4. Selecting patients for pharmacological blood pressure- lowering treatment .............................................................................................. 518.5. Intensity ofblood pressure-lowering therapy and ideal treatment targets .................................................................................................. 53 8.5.1. Expected degree ofblood pressure reduction with approved drugs ................................................................................................. 53 8.5.2. The ideal target ofblood pressure-lowering treatment ..... 53 8.5.3. Personalizing treatment strategies ............................................... 54 8.5.4. Duration and monitoring ofdrug therapy ................................ 55 8.6. Device-based blood pressure lowering .............................................. 55 8.6.1. Catheter-based renal denervation ............................................... 55 8.6.2. Other devices ........................................................................................ 57 8.7. Unintended and potentially harmful consequences ofblood pressure lowering and implications for treatment targets ................. 57 8.7.1. Adverse effects ofblood pressure-lowering medications .57 8.7.1.1. Symptomatic adverse effects ................................................. 57 8.7.1.2. Renal effects .................................................................................. 57 8.7.1.3. Erectile dysfunction .................................................................... 57 8.7.2. Pillburden and non-adherence ...................................................... 57 8.7.3. Potentially harmful consequences ofblood pressure lowering for frail older people ................................................................... 57 8.7.4. Clinical inertia inblood pressure lowering ............................... 57 9.Managing specific patient groups orcircumstances ............................... 58 9.1. Young adulthood (18–40 years) ............................................................ 58 9.1.1. Definition and epidemiology ........................................................... 58 9.1.2. Secondary hypertension inyoung adulthood .......................... 58 9.1.3. Measurement and management ofblood pressure in young adults ....................................................................................................... 58 9.2. Pregnancy ......................................................................................................... 58 9.2.1. Definition and epidemiology ........................................................... 58 9.2.2. Classifying hypertension inpregnancy ........................................ 58 9.2.3. Measuring blood pressure inpregnancy .................................... 59 9.2.4. Investigating hypertension inpregnancy .................................... 59 9.2.5. Preventing hypertension and pre-eclampsia ............................ 59 9.2.6. Treatment initiation and blood pressure targets ................... 59 9.2.7. Managing mild hypertension inpregnancy (office blood pressure 140–159/90–109 mmHg) .......................................................... 59 9.2.8. Managing severe hypertension inpregnancy (>160/110 mmHg) .................................................................................................................. 60 9.2.9. Managing blood pressure post-partum ...................................... 60 9.2.10. Risk ofrecurrence ofhypertensive disorders ina subsequent pregnancy ................................................................................... 60 9.3. Very old age (≥85 years), frailty, multimorbidity, and polypharmacy .......................................................................................................... 60 9.3.1. Definition offrailty .............................................................................. 60 9.3.2. Randomized controlled trials ofblood pressure lowering infrail older patients ....................................................................................... 61 9.3.3. Starting blood pressure-lowering treatment invery oldor frail patients ........................................................................................................ 62 9.3.4. Maintaining blood pressure lowering invery old orfrail patients ................................................................................................................. 62 9.4. Isolated systolic and diastolic hypertension ...................................... 62 9.4.1. Definition ofisolated systolic hypertension ............................. 62 9.4.2. Isolated systolic hypertension, risk factors, and ageing ....... 62 9.4.3. Isolated systolic hypertension inyoung adults ........................ 63 9.4.4. Isolated diastolic hypertension ....................................................... 63 9.5. Orthostatic hypotension with supine hypertension ..................... 63ESC Guidelines 3
+9.6. Diabetes ........................................................................................................... 64 9.6.1. Diabetes and elevated blood pressure/hypertension .......... 64 9.6.2. J-shaped curve ofblood pressure and risk of cardiovascular disease inpatients with diabetes ................................ 64 9.6.3. Managing blood pressure indiabetes .......................................... 64 9.7. Chronic kidney disease .............................................................................. 64 9.7.1. Relationship between hypertension and chronic kidney disease ................................................................................................................... 64 9.7.2. Blood pressure lowering inchronic kidney disease .............. 65 9.7.3. Managing blood pressure inchronic kidney disease ............. 65 9.7.4. Blood pressure targets inchronic kidney disease ................. 65 9.8. Cardiac disease .............................................................................................. 65 9.8.1. Blood pressure thresholds and targets inpatients with cardiac disease ................................................................................................... 65 9.8.2. Coronary artery disease with particular reference tothe blood pressure J-curve .................................................................................. 66 9.8.3. Valvular heart disease ........................................................................ 66 9.8.4. Heart failure ........................................................................................... 66 9.8.5. Heart rhythm disease (including AF) ........................................... 67 9.9. Chronic cerebrovascular disease and/or cognitive impairment ............................................................................ 67 9.9.1. Role ofhypertension inchronic cerebrovascular disease ..67 9.9.2. Treatment inpatients with history ofprior stroke or transient ischaemic attack ............................................................................ 67 9.9.3. Treatment inpatients with chronic cerebrovascular disease and cognitive impairment ............................................................. 67 9.10. Aortopathy ................................................................................................... 68 9.10.1. Coarctation ofthe aorta ................................................................ 68 9.10.2. Bicuspid aortic valve-related aortopathy ................................ 68 9.10.3. Preventing aortic dilation and dissection inhigh-risk patients ................................................................................................................. 68 9.11. Different ethnic groups ........................................................................... 68 9.12. Nocturnal hypertension .......................................................................... 68 9.12.1. Definition .............................................................................................. 68 9.12.2. Epidemiology ....................................................................................... 69 9.12.3. Night-time blood pressure asacardiovascular disease risk factor ............................................................................................................ 69 9.12.4. Treatment ofnocturnal hypertension ..................................... 69 9.13. Resistant hypertension ............................................................................ 69 9.13.1. Definition ofresistant hypertension ......................................... 69 9.13.2. Non-pharmacological interventions .......................................... 69 9.13.3. Pharmacological interventions ..................................................... 69 9.13.4. Devices for blood pressure lowering ....................................... 70 9.14. Management ofspecific causes ofsecondary hypertension ...71 9.14.1. General considerations ................................................................... 71 9.14.2. Primary aldosteronism .................................................................... 71 9.14.3. Renovascular hypertension ........................................................... 71 9.14.4. Phaeochromocytoma/paraganglioma ....................................... 72 9.14.5. Obstructive sleep apnoea syndrome ........................................ 72 9.14.6. Drug-induced hypertension .......................................................... 72 9.14.6.1. Anticancer drug-induced hypertension ........................... 72 9.14.7. Other forms ofsecondary hypertension ................................ 72 10. Acute and short-term lowering ofblood pressure ............................. 72 10.1. Acute blood pressure management inhypertensive emergencies ............................................................................................................. 7210.1.1. Definition and characteristics ofhypertensive emergencies ........................................................................................................ 72 10.1.2. Acute management ofhypertensive emergencies .............. 73 10.1.3. Prognosis and follow-up ................................................................ 73 10.2. Acute blood pressure management inacute intracerebral haemorrhage ........................................................................................................... 73 10.3. Acute blood pressure management inacute ischaemic stroke 73 10.4. Acute blood pressure management inpre-eclampsia and severe hypertension inpregnancy ................................................................. 74 10.4.1. Pre-eclampsia ...................................................................................... 74 10.4.2. Severe acute hypertension inpregnancy ................................ 74 10.5. Peri-operative acute management ofelevated blood pressure 74 10.5.1. Blood pressure-lowering drugs inthe peri-operative phase ..................................................................................................................... 74 11. Patient-centred care inhypertension ........................................................ 75 11.1. Definition ...................................................................................................... 75 11.2. Communicating consequences oftreatment ................................ 75 11.3. Self-measuring and monitoring ............................................................ 76 11.4. Facilitating medication adherence and persistence ..................... 76 11.5. Multidisciplinary management .............................................................. 76 12. Key messages ....................................................................................................... 77 13. Gaps inthe evidence ........................................................................................ 78 14. ‘What todo’ and ‘what not todo’ messages from the guidelines 78 15. Evidence tables .................................................................................................... 82 16. Data availability statement .............................................................................. 82 17. Author information ........................................................................................... 82 18. Appendix ................................................................................................................ 82 19. References ............................................................................................................. 83 Tables ofRecommendations Recommendation Table 1—Recommendations for measuring blood pressure (see Evidence Tables 1–8) ..................................................... 24 Recommendation Table 2—Recommendations for categorizing blood pressure (see Evidence Table 9)............................................................ 25 Recommendation Table 3—Recommendations for assessing cardiovascular disease risk among individuals with elevated blood pressure (office systolic blood pressure 120–139 mmHg ordiastolic blood pressure 70–89 mmHg) (see Evidence Tables 10and 11) ......... 28 Recommendation Table 4—Recommendations for refining cardiovascular disease risk (see Evidence Tables 12–14) ......................... 30 Recommendation Table 5—Recommendations forblood pressure screening (see Evidence Table 15) ..................................................................... 32 Recommendation Table 6—Recommendations for confirming hypertension diagnosis ............................................................................................. 32 Recommendation Table 7—Recommendations forassessing adherence and persistence with treatment (see Evidence Table 16) .... 34 Recommendation Table 8—Recommendations forassessing renal hypertension-mediated organ damage ............................................................. 36 Recommendation Table 9—Recommendations for assessing cardiac hypertension-mediated organ damage ............................................. 36 Recommendation Table 10—Recommendations for assessing vascular hypertension-mediated organ damage (see Evidence Table 17) ........................................................................................................................ 37 Recommendation Table 11—Recommendations forgenetic testing inhypertension management ............................................................................... 374 ESC Guidelines
+Recommendation Table 12—Recommendations for resistant hypertension work-up (see Evidence Table 18) ........................................... 39 Recommendation Table 13—Recommendations forscreening for secondary hypertension (see Evidence Tables 19and 20) ...................... 43 Recommendation Table 14—Recommendations forscreening for hypertension inchildren and adolescents (see Evidence Table 21) ..... 43 Recommendation Table 15—Recommendations for non-pharmacological treatment ofblood pressure and cardiovascular risk reduction (see Evidence Tables 22–26) ....................................................... 47 Recommendation Table 16—Recommendations for pharmacological treatment ofhypertension (see Evidence Tables 27, 28, and 29) .................................................................................................................... 51 Recommendation Table 17—Recommendations for initiating blood pressure-lowering treatment (see Evidence Tables 30–32) ...... 52 Recommendation Table 18—Recommendations for blood pressure targets with treatment (see Evidence Table 34) ....................... 55 Recommendation Table 19—Recommendations for follow-up in patients with treated hypertension (see Evidence Table 33) ................. 55 Recommendation Table 20—Recommendations for device-based treatment ofhypertension (see Evidence Table 35) .................................. 56 Recommendation Table 21—Recommendations for managing hypertension inyoung adults (see Evidence Tables 36and 37) ............ 58 Recommendation Table 22—Recommendations for managing hypertension inpregnancy (see Evidence Tables 38–40) ........................ 60 Recommendation Table 23—Recommendations for managing hypertension inpatients who are very old orfrail (see Evidence Table 41) ........................................................................................................................ 62 Recommendation Table 24—Recommendations for managing hypertension inpatients with orthostatic hypotension ............................ 64 Recommendation Table 25—Recommendations for managing hypertension inpatients with diabetes ............................................................. 64 Recommendation Table 26—Recommendations for managing hypertension inpatients with chronic kidney disease ................................ 65 Recommendation Table 27—Recommendations for managing hypertension inpatients with cardiac disease ............................................... 67 Recommendation Table 28—Recommendations for managing hypertension inpatients with chronic cerebrovascular disease and cognitive impairment ................................................................................................ 68 Recommendation Table 29—Recommendations for managing hypertension indifferent ethnic groups ........................................................... 68 Recommendation Table 30—Recommendations for treating resistant hypertension (see Evidence Tables 42and 43) ......................... 70 Recommendation Table 31—Recommendations for managing hypertension inpatients with renovascular hypertension (see Evidence Tables 44and 45) ................................................................................... 71 Recommendation Table 32—Recommendations for acutely managing blood pressure inpatients with intracerebral haemorrhage oracute ischaemic stroke ...................................................................................... 73 Recommendation Table 33—Recommendations for acutely managing blood pressure inpatients with severe hypertension in pregnancy and pre-eclampsia (see Evidence Table 46) ............................. 74 Recommendation Table 34—Recommendations for communicating consequences oftreatment (see Evidence Table 47) ........................................................................................................................ 76 Recommendation Table 35—Recommendations forself-measuring and monitoring blood pressure (see Evidence Table 48) ........................ 76 Recommendation Table 36—Recommendations for multi/ interdisciplinary blood pressure management (see Evidence Table 49) ........................................................................................................................ 76Listoftables Table 1Classes ofrecommendations .................................................................. 7 Table 2Levels ofevidence ........................................................................................ 8 Table 3New recommendations ............................................................................ 9 Table 4Revised recommendations .................................................................... 12 Table 5Comparison ofoffice, home, and ambulatory blood pressure measurement thresholds for elevated blood pressure and hypertension ................................................................................................................ 22 Table 6Comparison ofambulatory and home blood pressure monitoring ..................................................................................................................... 23 Table 7Key illness representations and treatment beliefs: how these apply tocommunicating ahypertension diagnosis tothe patient (note that gender influences these representations) ................................. 34 Table 8Routine tests recommended inthe initial work-up ofa patient with elevated blood pressure orhypertension ............................. 35 Table 9Optional tests that may beused asclinically indicated intheinitial work-up ofapatient with elevated blood pressure orhypertension to assess hypertension-mediated organ damage orestablished cardiovascular disease ........................................................................................................... 36 Table 10Current definition ofresistant hypertension ............................. 39 Table 11Conditions found tocause pseudo-resistance orresistance toblood pressure-lowering treatment ............................................................. 39 Table 12Drugs and conditions that affect aldosterone, renin, and aldosterone-to-renin ratio ..................................................................................... 40 Table 13Optional tests that should beused toscreen forsecondary hypertension inthe presence ofsuggestive signs, symptoms, or medical history ............................................................................................................ 41 Table 14Initiation ofblood pressure-lowering treatment based on confirmed blood pressure category and cardiovascular disease risk ..52 Table 15What todoand what not todo..................................................... 78 Listoffigures Figure 1Pathophysiology ofelevated blood pressure and hypertension ................................................................................................................ 17 Figure 2Persistently elevated blood pressure and hypertension lead to hypertension-mediated organ damage and cardiovascular disease ........... 18 Figure 3Summary ofoffice blood pressure measurement ..................... 20 Figure 4Summary ofhome blood pressure measurement ..................... 21 Figure 5Summary ofambulatory blood pressure measurement ......... 22 Figure 6Blood pressure categories ................................................................... 26 Figure 7Sufficiently high cardiovascular risk conditions that warrant blood pressure-lowering treatment among adults with elevated blood pressure ............................................................................................................ 27 Figure 8Cardiovascular disease risk modifiers toconsider for up-classification ofrisk ............................................................................................. 29 Figure 9Summary ofcardiovascular disease risk-stratification approach forblood pressure treatment inadults with elevated blood pressure ............................................................................................................ 31 Figure 10Protocol for confirming hypertension diagnosis ...................... 33 Figure 11Definitions, assessments, and potential interventions for the three phases ofadherence toBP-lowering medications .................. 35 Figure 12Tests and criteria for defining hypertension-mediated organ damage and considerations for their use inclinical practice ..... 38 Figure 13Summary ofprimary aldosteronism asacommon form of secondary hypertension .......................................................................................... 41 Figure 14Summary ofrenovascular disease asacommon form of secondary hypertension .......................................................................................... 42ESC Guidelines 5
+Figure 15Summary ofobstructive sleep apnoea asacommon form ofsecondary hypertension .................................................................................... 42 Figure 16Physical activity according todifferent types ofexercise and reduction ofblood pressure and overall cardiovascular disease risk .................................................................................................................................... 44 Figure 17Effects ofmain lifestyle factors onblood pressure and cardiovascular risk reduction ................................................................................ 45 Figure 18Practical algorithm for pharmacological blood pressure lowering ......................................................................................................................... 49 Figure 19Central Illustration ................................................................................ 50 Figure 20Systolic blood pressure categories and treatment target range ................................................................................................................................ 54 Figure 21Frailty assessment inthe management ofblood pressure ..61 Figure 22Management ofresistant hypertension ....................................... 70 Figure 23Patient-centred care ............................................................................ 75 Figure 24The five dimensions ofadherence (WHO, 2003) applied tohypertension .......................................................................................................... 77 Abbreviations andacronyms ABI Ankle–brachial index ABPM Ambulatory blood pressure monitoring ACCORD Action toControl Cardiovascular Risk inDiabetes ACE Angiotensin-converting enzyme ACR Albumin:creatinine ratio AF Atrial fibrillation AHI Apnoea–hypopnoea index ALARA Aslow asreasonably achievable ALLHAT Antihypertensive and Lipid-Lowering Treatment toPrevent Heart Attack AOBP Automated office blood pressure (measurement) ARB Angiotensin receptor blocker ARNi Angiotensin receptor-neprilysin inhibitor ARR Aldosterone-to-renin ratio ASCVD Atherosclerotic cardiovascular disease BMI Body mass index BP Blood pressure BSA Body surface area CAC Coronary artery calcium CAD Coronary artery disease CCB Calcium channel blocker CHAP Chronic Hypertension and Pregnancy CI Confidence interval CKD Chronic kidney disease CKD-EPI Chronic Kidney Disease Epidemiology Collaboration COVID-19 Coronavirus disease 2019 CPAP Continuous positive airway pressure CPG Clinical Practice Guidelines CT Computed tomography CVD Cardiovascular disease DASH Dietary Approaches toStop Hypertension DBP Diastolic blood pressure DECIDE-Salt Diet, ExerCIse and carDiovascular hEalth–Salt EACTS European Association forCardio-Thoracic Surgery ECG Electrocardiogram eGFR Estimated glomerular filtration rate EPIC European Prospective Investigation into Cancer and NutritionESC European Society ofCardiology ESH European Society ofHypertension ESPRIT Effects ofintensive Systolic blood Pressure lowering treatment inreducing RIsk ofvascular evenTs FMD-RVH Fibromuscular dysplasia-induced renovascular hypertension GFR Glomerular filtration rate GLP-1 Glucagon-like peptide-1 GP General practitioner HbA1c Glycated haemoglobin HBPM Home blood pressure monitoring HDL High-density lipoprotein HFpEF Heart failure with preserved ejection fraction HF(m)rEF Heart failure with (mildly) reduced ejection fraction HIV Human immunodeficiency virus HMOD Hypertension-mediated organ damage i.m. Intramuscular i.v. Intravenous KDIGO Kidney Disease: Improving Global Outcomes LA Left atrial LDL Low-density lipoprotein LV Left ventricular LVH Left ventricular hypertrophy MRA Mineralocorticoid receptor antagonist MRI Magnetic resonance imaging NNT Number needed totreat NT-proBNP N-terminal pro-brain natriuretic peptide OSAS Obstructive sleep apnoea syndrome PPGL Phaeochromocytoma/paraganglioma PREOP-ACEI Prospective Randomized Evaluation of Preoperative Angiotensin-Converting Enzyme Inhibition PREMs Patient-Reported Experience Measures PROMS Patient-Reported Outcome Measures PTRA Percutaneous transluminal renal angioplasty PWV Pulse wave velocity RAAS Renin-angiotensin-aldosterone system RADIANCE-HTN AStudy ofthe Recor Medical Paradise System in Clinical Hypertension RAS Renin–angiotensin system RCT Randomized controlled trial RVH Renovascular hypertension RWT Relative wall thickness SBP Systolic blood pressure SCORE2 Systematic COronary Risk Evaluation 2 SCORE2-OP Systematic COronary Risk Evaluation 2–Older Persons SGLT2 Sodium–glucose co-transporter 2 SNP Single-nucleotide polymorphism SNS Sympathetic nervous system SPC Single-pill combination SPRINT Systolic Blood Pressure Intervention Trial SSaSS Salt Substitute and Stroke Study STEP Strategy ofBlood Pressure Intervention inElderly Hypertensive Patients STEP-1 Semaglutide Treatment Effect inPeople with Obesity6 ESC Guidelines
+TIA Transient ischaemic attack TRIUMPH Treating Resistant Hypertension Using Lifestyle Modification toPromote Health TSH Thyroid-stimulating hormone WHO World Health Organization WML White matter lesion 1.Preamble Guidelines evaluate and summarize available evidence with the aim ofas- sisting health professionals inproposing the best diagnostic ortherapeut- icapproach foranindividual patient with agiven condition. Guidelines are intended for use byhealth professionals and the European Society of Cardiology (ESC) makes itsguidelines freely available. ESC Guidelines donot override the individual responsibility ofhealth professionals tomake appropriate and accurate decisions inconsider- ation ofeach patient’s health condition and inconsultation with that pa- tient orthe patient’s caregiver where appropriate and/or necessary. Itis also the health professional’s responsibility toverify the rules and reg- ulations applicable ineach country todrugs and devices atthe time of prescription and torespect the ethical rules oftheir profession. ESC Guidelines represent theofficial position oftheESC onagiven topic and are regularly updated when warranted bynew evidence. ESC Policies and Procedures for formulating and issuing ESC Guidelines can be found onthe ESC website (https:/ /www.escardio.org/Guidelines/Clinical- Practice-Guidelines/Guidelines-development/Writing-ESC-Guidelines). This guideline version updates and replaces the previous version from 2018.The Members ofthis task force were selected bythe ESC toinclude professionals involved inthe medical care ofpatients with this path- ology, aswell aspatient representatives and methodologists. The se- lection procedure included anopen call for authors and aimed to include members from across the whole ofthe ESC region and from relevant ESC Subspecialty Communities. Consideration was gi- ven todiversity and inclusion, notably with respect togender and country oforigin. The task force performed acritical review and evaluation ofthe published literature ondiagnostic and therapeutic approaches including assessment ofthe risk-benefit ratio. The strength ofevery recommendation and the level ofevidence supporting them were weighed and scored according topredefined scales asoutlined in Tables 1and2below. Patient-Reported Outcome Measures (PROMs) and Patient-Reported Experience Measures (PREMs) were also evaluated asthe basis for recommendations and/or discussion inthese guidelines. The task force followed ESC voting procedures and allapproved recom- mendations were subject toavote and achieved atleast 75% agreement among voting members. Members ofthe task force with declared inter- ests onspecific topics were asked toabstain from voting onrelated recommendations. The experts ofthe writing and reviewing panels provided declaration ofinterest forms forallrelationships that might beperceived asreal or potential sources ofconflicts ofinterest. Their declarations ofinterest were reviewed according tothe ESC declaration ofinterest rules, which can befound on the ESC website (http:/ /www.escardio.org/ guidelines) and have been compiled inareport published inasupple- mentary document with the guidelines. Funding for the development ofESC Guidelines isderived entirely from the ESC with noinvolvement ofthe healthcare industry. Table 1Classes ofrecommendations ©ESC 2024Classes of recommendations Class I Evidence and/or general agreement that a given treatment or procedure is beneficial, useful, effective.  Conflicting evidence and/or a divergence of opinion about the usefulness/  efficacy of the given treatment or procedure.  Is recommended o r is indicatedWording to use Definition Class III Evidence or general agreement that the given treatment or procedure is not useful/effective, and in some cases may be harmful. Is not recommended     Class IIb Usefulness/efficacy is less well established by evidence/opinion.May be considered    Class IIa Weight of evidence/opinion is in favour of usefulness/efficacy. Should be consideredClass II  ©ESC 2024ESC Guidelines 7
+The ESC Clinical Practice Guidelines (CPG) Committee supervises and co-ordinates the preparation ofnew guidelines and isresponsible for the approval process. Inaddition to review by the CPG Committee, ESC Guidelines undergo multiple rounds ofdouble-blind peer review byexternal experts, including members from across the whole ofthe ESC region, allNational Cardiac Societies ofthe ESC and from relevant ESC Subspecialty Communities. After appropriate revisions, the guidelines are signed offbyallthe experts inthe task force. The finalized document issigned off bythe CPG Committee for publication intheEuropean Heart Journal. ESC Guidelines are based onanalyses ofpublished evidence, chiefly onclinical trials and meta-analyses oftrials, but potentially including other types ofstudies. Evidence tables summarizing key information from relevant studies are generated early inthe guideline development process tofacilitate the formulation ofrecommendations, toenhance comprehension ofrecommendations after publication, and reinforce transparency inthe guidelines development process. The tables are published intheir own section ofESC Guidelines and reference specific recommendation tables. Off-label use ofmedication may bepresented inthese guidelines ifa sufficient level ofevidence shows that itcan beconsidered medically ap- propriate foragiven condition. However, the final decisions concerning anindividual patient must bemade bythe responsible health profes- sional giving special consideration to: •The specific situation ofthe patient. Unless otherwise provided for bynational regulations, off-label use ofmedication should belimited tosituations where itisinthe patient’s interest with regard tothe quality, safety, and efficacy ofcare, and only after the patient has been informed and has provided consent; •Country-specific health regulations, indications by governmental drug regulatory agencies, and the ethical rules towhich health profes- sionals are subject, where applicable.2.Introduction This 2024 document updates the 2018 ESC/European Society of Hypertension (ESH) Guidelines onthe management ofarterial hyper- tension.1While the current document builds on prior guidelines, it also incorporates important updates and new recommendations based oncurrent evidence. For example: (1) The title has changed from ‘Guidelines onthe management ofar- terial hypertension’ to‘Guidelines onthe management ofelevated blood pressure and hypertension’. This isbased onevidence that the risk for cardiovascular disease (CVD) attributable toblood pressure (BP) isonacontinuous exposure scale, not abinary scale ofnormotension vs.hypertension.2,3Updated evidence also in- creasingly demonstrates the benefit on CVD outcomes of BP-lowering medications among persons with high CVD risk and BPlevels that are elevated but that donot meet traditional thresh- olds used todefine hypertension. The term ‘arterial’ isremoved from the title ofthe 2024 Guidelines, asarterial hypertension can also occur inthe pulmonary arteries, which isnot afocus here. (2) The 2024 Guidelines continue todefine hypertension asoffice sys- tolic BPof≥140 mmHg ordiastolic BPof≥90 mmHg. However, a new BPcategory called ‘Elevated BP’ isintroduced. Elevated BPis defined asanoffice systolic BPof120–139 mmHg ordiastolic BP of70–89 mmHg. (3) Amajor, evidence-based change inthe 2024 Guidelines isthe rec- ommendation topursue atarget systolic BPof120–129 mmHg among adults receiving BP-lowering medications. There are several important caveats tothis recommendation, including: (i)the re- quirement that treatment tothis BP target iswell tolerated by the patient, (ii)the fact that more lenient BPtargets can beconsid- ered inpersons with symptomatic orthostatic hypotension, those aged 85years orover, orthose with moderate-to-severe frailtyTable 2Levels ofevidence Level of evidence A Level of evidence B Level of evidence CData derived from multiple randomized clinical trials or meta-analyses. Data derived from a single randomized clinical trial or large non-randomized studies. Consensus of opinion of the experts and/or small studies, retrospective studies, registries. ©ESC 2024 ©ESC 20248 ESC Guidelines
+or limited life expectancy, and (iii) astrong emphasis on out-of-office BP measurement toconfirm the systolic BP target of120–129 mmHg isachieved. For those selected individual cases where atarget systolic BPof120–129 mmHg isnot pursued, either due tointolerance orthe existence ofconditions that favour a more lenient BPtarget, we recommend targeting aBPthat isas low asreasonably achievable. Personalized clinical decision-making and shared decisions with the patient are also emphasized. (4) Another important change inthe 2024 Guidelines compared with earlier versions isthe increased focus onevidence related tofatal and non-fatal CVD outcomes rather than surrogate outcomes such asBPlowering alone. Except for lifestyle interventions and low-risk non-pharmacological interventions aimed atimplementation orcare delivery, the current guidelines require that, foraClass Irecommen- dation tobemade foradrug orprocedural intervention, theevidence must show benefit onCVD outcomes and not only BPlowering. (5) The task force comprised ofabalanced representation ofmales and females. (6) The present guidelines consider sex and gender asanintegral com- ponent throughout the document, rather than inaseparate section atthe end. Inthis document, sex isthe biological condition ofbeing female ormale from conception, based ongenes, and gender isthe socio-cultural dimension ofbeing awoman oraman inagiven soci- ety, based ongender roles, gender norms, gender identity, and gen- der relations valid inthe respective society atagiven timepoint.4,5(7) The 2024 Guidelines are written tomake them more ‘user friendly’. Input from general practitioners (GPs) was obtained inthis regard, and one task force member isaGP. Given the ageing population in Europe, there was also afocus ontailoring treatment with respect to frailty and into older age, which isaddressed inmultiple sections. Moreover, patient input and their lived experiences are considered throughout. We also now include evidence tables in the Supplementary section toprovide improved transparency regarding our recommendations. Asappropriate, readers who wish toseek add- itional details and information are referred tothe Supplementary data online and tothe  ESC CardioMed.6 (8) The task force recognized that amajor challenge inguideline usage ispoor implementation. This likely contributes tosuboptimal con- trol ofhypertension.7–9Toaddress this, adedicated section onim- plementation isincluded inthe Supplementary data online. Moreover, through anew initiative, we include information from national societies following asurvey onguideline implementation completed during the national society peer review ofthe guidelines document. Itishoped this information may help inform national so- cieties about potential barriers toimplementation. 2.1.What isnew These 2024 Guidelines contain anumber ofnew and revised recom- mendations, which are summarized inTables 3and4,respectively. Table 3New recommendations Recommendations ClassaLevelb 5.Measuring blood pressure Itisrecommended tomeasure BPusing avalidated and calibrated device, toenforce the correct measurement technique, and toapply a consistent approach toBPmeasurement for each patient.I B Out-of-office BPmeasurement isrecommended fordiagnostic purposes, particularly because itcan detect both white-coat hypertension and masked hypertension. Where out-of-office measurements arenot logistically and/or economically feasible, then itisrecommended that the diagnosis beconfirmed with arepeat office BPmeasurement using the correct standardized measurement technique.I B Most automated oscillometric monitors have not been validated forBPmeasurement inAF; BPmeasurement should beconsidered using a manual auscultatory method inthese circumstances, where possible.IIa C Anassessment fororthostatic hypotension (≥20 systolic BPand/or ≥10 diastolic BPmmHg drop at1and/or 3min after standing) should be considered atleast atthe initial diagnosis ofelevated BPorhypertension and thereafter ifsuggestive symptoms arise. This should be performed after the patient isfirst lying orsitting for 5min.IIa C 6.Definition andclassification ofelevated blood pressure andhypertension, andcardiovascular disease riskassessment Itisrecommended touse arisk-based approach inthe treatment ofelevated BP, and individuals with moderate orsevere CKD, established CVD, HMOD, diabetes mellitus, orfamilial hypercholesterolaemia are considered atincreased risk for CVD events.I B Itisrecommended that, irrespective ofage, individuals with elevated BPand aSCORE2 orSCORE2-OP CVD risk of≥10% beconsidered at increased risk for CVD for the purposes ofrisk-based management oftheir elevated BP.I B SCORE2-Diabetes should beconsidered toestimate CVD risk among type 2diabetes mellitus patients with elevated BP, particularly ifthey are<60 years ofage.IIa B History ofpregnancy complications (gestational diabetes, gestational hypertension, pre-term delivery, pre-eclampsia, one ormore stillbirths, and recurrent miscarriage) are sex-specific risk modifiers that should beconsidered toup-classify individuals with elevated BPand borderline increased 10-year CVD risk (5% to<10% risk).IIa B High-risk ethnicity (e.g. South Asian), family history ofpremature onset atherosclerotic CVD, socio-economic deprivation, auto-immune inflammatory disorders, HIV, and severe mental illness are risk modifiers shared byboth sexes that should beconsidered toup-classify individuals with elevated BPand borderline increased 10-year CVD risk (5% to<10% risk).IIa B After assessing 10-year predicted CVD risk and non-traditional CVD risk modifiers, ifarisk-based BP-lowering treatment decision remains uncertain forindividuals with elevated BP,measuring CAC score, carotid orfemoral plaque using ultrasound, high-sensitivity cardiac troponin orB-type natriuretic peptide biomarkers, orarterial stiffness using pulse wave velocity, may beconsidered toimprove risk stratification among patients with borderline increased 10-year CVD risk (5% to<10% risk) after shared decision-making and considering costs.IIb B ContinuedESC Guidelines 9
+7.Diagnosing hypertension andinvestigating underlying causes Opportunistic screening for elevated BPand hypertension should beconsidered: •Atleast every 3years for adults aged <40 years. •Atleast annually for adults aged ≥40 years.IIa C Inindividuals with elevated BPwho donot currently meet risk thresholds forBP-lowering treatment, arepeat BPmeasurement and risk assessment within 1year should beconsidered.IIa C Other forms ofscreening for hypertension (i.e. systematic screening, self-screening, and non-physician screening) may beconsidered, depending ontheir feasibility indifferent countries and healthcare systems.IIb B Inindividuals with increased CVD risk where their screening office BPis120–139/70–89 mmHg, itisrecommended tomeasure BPout of office, using ABPM and/or HBPM or,ifnot logistically feasible, make repeated office BPmeasurements onmore than one visit.I B Objective evaluation ofadherence (either directly observed treatment ordetecting prescribed drugs inblood orurine samples) should be considered inthe clinical work-up ofpatients with apparent resistant hypertension, ifresources allow.IIa B Ifmoderate-to-severe CKD isdiagnosed, itisrecommended torepeat measurements ofserum creatinine, eGFR, and urine ACR at least annually.I C Coronary artery calcium scoring may beconsidered inpatients with elevated BPorhypertension when itislikely tochange patient management. IIb B Patients with resistant hypertension should beconsidered for referral toclinical centres with expertise inhypertension management for further testing.IIa B Itisrecommended that patients with hypertension presenting with suggestive signs, symptoms, ormedical history ofsecondary hypertension are appropriately screened for secondary hypertension.I B Screening for primary aldosteronism byrenin and aldosterone measurements should beconsidered inalladults with confirmed hypertension (BP≥140/90 mmHg).IIa B 8.Preventing andtreating elevated blood pressure Opportunistic screening with office BPmeasurements tomonitor development ofBPduring late childhood and adolescence, especially ifone orboth parents have hypertension, should beconsidered tobetter predict development ofadult hypertension and associated CVD risk.IIa B Itisrecommended torestrict free sugar consumption, inparticular sugar-sweetened beverages, toamaximum of10% ofenergy intake. Itisalso recommended todiscourage consumption ofsugar-sweetened beverages, such assoft drinks and fruit juices, starting atyoung age.I B Inpatients with hypertension without moderate-to-advanced CKD and with high daily sodium intake, anincrease ofpotassium intake by 0.5–1.0 g/day—for example through sodium substitution with potassium-enriched salt (comprising 75% sodium chloride and 25% potassium chloride) orthrough diets rich infruits and vegetables—should beconsidered.IIa A Inpatients with CKD ortaking potassium-sparing medication, such assome diuretics, ACE inhibitors, ARBs, orspironolactone, monitoring serum levels ofpotassium should beconsidered ifdietary potassium isbeing increased.IIa C Itisrecommended totake medications atthe most convenient time ofday for the patient, toestablish ahabitual pattern ofmedication taking toimprove adherence.I B Inadults with elevated BPand low/medium CVD risk (<10% over 10years), BPlowering with lifestyle measures isrecommended and can reduce the risk ofCVD.I B Inadults with elevated BPand sufficiently high CVD risk, after 3months oflifestyle intervention, BPlowering with pharmacological treatment isrecommended for those with confirmed BP≥130/80 mmHg toreduce CVD risk.I A Itisrecommended that inhypertensive patients with confirmed BP≥140/90 mmHg, irrespective ofCVD risk, lifestyle measures and pharmacological BP-lowering treatment isinitiated promptly toreduce CVD risk.I A Itisrecommended tomaintain BP-lowering drug treatment lifelong, even beyond the age of85years, ifwell tolerated. I A Because the benefit inreducing CVD outcomes isuncertain inthese settings, and noting that close monitoring oftreatment tolerance is advised, BP-lowering treatment should only beconsidered from ≥140/90 mmHg (office) among persons meeting the following criteria: •pre-treatment symptomatic orthostatic hypotension; •age≥85 years; •clinically significant moderate-to-severe frailty; •and/or limited predicted lifespan (<3 years).IIa B Incases where BP-lowering treatment ispoorly tolerated and achieving atarget systolic of120–129 mmHg isnot possible, itis recommended totarget asystolic BPlevel that is‘aslow asreasonably achievable’ (ALARA principle).I A Once BPiscontrolled and stable under BP-lowering therapy, atleast ayearly follow-up for BPand other CVD risk factors should beconsidered.IIa C Continued10 ESC Guidelines
+9.Managing specific patient groups orcircumstances Young adults Comprehensive screening forthe main causes ofsecondary hypertension isrecommended inadults diagnosed with hypertension before the age of40years, except for obese young adults where itisrecommended tostart with anobstructive sleep apnoea evaluation.I B Since SCORE2 has not been validated for individuals <40 years, screening for HMOD may beconsidered insuch young individuals with elevated BPwithout other increased CVD risk conditions toidentify additional individuals for possible medical treatment.IIb B Hypertension inpregnancy Inconsultation with anobstetrician, low- tomoderate-intensity exercise isrecommended inallpregnant women without contraindications toreduce the risk ofgestational hypertension and pre-eclampsia.I B HBPM and ABPM should beconsidered toexclude white-coat and masked hypertension, which are more common inpregnancy. IIa C Older andfrail patients Itisrecommended that treatment ofelevated BPand hypertension among older patients aged <85 years who are not moderately to severely frail follows the same guidelines asfor younger people, provided BP-lowering treatment iswell tolerated.I A When initiating BP-lowering treatment for patients aged ≥85 years, and/or with moderate-to-severe frailty (atany age), long-acting dihydropyridine CCBs orRAS inhibitors should beconsidered, followed, ifnecessary, byalow-dose diuretic iftolerated, but preferably not abeta-blocker (unless compelling indications exist) oranalpha-blocker.IIa B Asthe safety and efficacy ofBPtreatment isless certain inindividuals with moderate orsevere frailty, clinicians should consider screening older adults forfrailty using validated clinical tests; frail patients’ health priorities and ashared-decision approach should beconsidered when deciding onBPtreatments and targets.IIa C IfBPdrops with progressing frailty, deprescription ofBP-lowering medications (and other drugs that can reduce BP, such assedatives and prostate-specific alpha-blockers) may beconsidered.IIb C Hypertension andorthostatic hypotension Before starting orintensifying BP-lowering medication, itisrecommended totest fororthostatic hypotension, byfirst having the patient sit orliefor 5min and then measuring BP1and/or 3min after standing.I B Itisrecommended topursue non-pharmacological approaches asthe first-line treatment oforthostatic hypotension among persons with supine hypertension. For such patients, itisalso recommended toswitch BP-lowering medications that worsen orthostatic hypotension to analternative BP-lowering therapy and not tosimply de-intensify therapy.I A Chronic kidney disease Inhypertensive patients with CKD and eGFR >20 mL/min/1.73 m2,SGLT2 inhibitors are recommended toimprove outcomes inthe context oftheir modest BP-lowering properties.I A Other conditions BP-lowering drug treatment isrecommended forpeople with pre-diabetes orobesity when confirmed office BPis≥140/90 mmHg orwhen office BPis130–139/80–89 mmHg and the patient isatpredicted 10-year risk ofCVD ≥10% orwith high-risk conditions, despite a maximum of3months oflifestyle therapy.I A Inpatients with ahistory ofaortic valve stenosis and/or regurgitation who require BP-lowering treatment, RAS blockers should be considered aspart ofthat treatment.IIa C Inpatients with ahistory ofmoderate-to-severe mitral valve regurgitation who require BP-lowering treatment, RAS blockers should be considered aspart ofthat treatment.IIa C Renovascular hypertension Renal artery angioplasty without stenting should beconsidered forpatients with hypertension and haemodynamically significant renal artery stenosis due tofibromuscular dysplasia.IIa C Renal artery angioplasty and stenting may beconsidered inpatients with haemodynamically significant, atherosclerotic, renal artery stenosis (stenosis of70%–99%, or50%–69% with post-stenotic dilatation and/or significant trans-stenotic pressure gradient) with: •Recurrent heart failure, unstable angina, orsudden-onset flash pulmonary oedema despite maximally tolerated medical therapy; •Resistant hypertension; •Hypertension with unexplained unilaterally small kidney orCKD; •Bilateral renal artery stenosis orunilateral renal artery stenosis inasolitary viable kidney.IIb C Renal artery angioplasty isnot recommended inpatients without confirmed haemodynamically significant renal artery stenosis. III A 10.Acute andshort-term lowering ofblood pressure Inpatients with intracerebral haemorrhage presenting with systolic BP≥220 mmHg, acute reduction insystolic BP>70 mmHg from initial levels within 1hofcommencing treatment isnot recommended.III B ContinuedESC Guidelines 11
+11.Patient-centred care inhypertension Aninformed discussion about CVD risk and treatment benefits tailored tothe needs ofapatient isrecommended aspart ofhypertension management.I C Motivational interviewing should beconsidered forpatients with hypertension athospitals and community health centres toassist patients incontrolling their BPand toenhance treatment adherence.IIa B Physician–patient web communications are aneffective tool that should beconsidered inprimary care, including reporting onhome BP readings.IIa C Home BPmeasurement for managing hypertension byusing self-monitored BPisrecommended toachieve better BPcontrol. I B Self-measurement, when properly performed, isrecommended due topositive effects onthe acceptance ofadiagnosis ofhypertension, patient empowerment, and adherence totreatment.I C Enhanced self-monitoring ofBPusing adevice paired with aconnected smartphone application may beconsidered, though evidence todate suggests that this may benomore effective than standard self-monitoring.IIb B Multidisciplinary approaches inthe management ofpatients with elevated BPand hypertension, including appropriate and safe task-shifting away from physicians are recommended toimprove BPcontrol.I A ©ESC 2024 ABPM, ambulatory blood pressure monitoring; ACE, angiotensin-converting enzyme; ACR, albumin-to-creatinine ratio (urine); AF, atrial fibrillation; ALARA, aslow asreasonably achievable; ARB, angiotensin receptor blocker; BP, blood pressure; CAC, coronary artery calcium; CCB, calcium channel blocker; CKD, chronic kidney disease; CVD, cardiovascular disease; eGFR, estimated glomerular filtration rate; HBPM, home blood pressure monitoring; HFpEF, heart failure with preserved ejection fraction; HIV, human immunodeficiency virus; HMOD, hypertension-mediated organ damage; MRA, mineralocorticoid receptor antagonist; RAS, renin–angiotensin system; SCORE2, Systematic COronary Risk Evaluation 2;SCORE2-OP, Systematic COronary Risk Evaluation 2–Older Persons; SGLT2, sodium–glucose co-transporter 2. aClass ofrecommendation. bLevel ofevidence. Table 4Revised recommendations Recommendations in2018 version ClassaLevelbRecommendations in2024 version ClassaLevelb 6.Definition andclassification ofelevated blood pressure andhypertension Itisrecommended that BPbeclassified asoptimal, normal, high–normal, orgrades 1–3 hypertension, according tooffice BP.I CItisrecommended that BPbecategorized as non-elevated BP, elevated BP, and hypertension toaid treatment decisions.I B CV risk assessment with the SCORE system is recommended for hypertensive patients who are not already athigh orvery high risk due toestablished CVD, renal disease, ordiabetes, amarkedly elevated single risk factor (e.g. cholesterol), orhypertensive LVH. I BSCORE2 isrecommended forassessing 10-year risk of fatal and non-fatal CVD among individuals aged 40–69 years with elevated BPwho are not already considered atincreased risk due tomoderate orsevere CKD, established CVD, HMOD, diabetes mellitus, orfamilial hypercholesterolaemia.I B SCORE2-OP isrecommended for assessing the 10-year risk offatal and non-fatal CVD among individuals aged ≥70 years with elevated BPwho are not already considered atincreased risk due to moderate orsevere CKD, established CVD, HMOD, diabetes mellitus, orfamilial hypercholesterolaemia.I B 7.Diagnosing hypertension andinvestigating underlying causes Itisrecommended that the diagnosis ofhypertension should bebased on: •Repeated office BPmeasurements onmore than one visit, except when hypertension issevere (e.g. grade 3 and especially inhigh-risk patients). Ateach visit, three BPmeasurements should berecorded, 1–2 min apart, and additional measurements should beperformed if the first two readings differ by>10 mmHg. The patient’s BPisthe average ofthe last two BPreadings. Or •Out-of-office BPmeasurement with ABPM and/or HBPM, provided that these measurements are logistically and economically feasible.I CWhere screening office BPis140–159/90–99 mmHg, itis recommended that the diagnosis ofhypertension should bebased onout-of-office BPmeasurement with ABPM and/or HBPM. Ifthese measurements are not logistically oreconomically feasible, then diagnosis can bemade on repeated office BPmeasurements onmore than one visit.I B Where screening office BPis≥160/100 mmHg: •Itisrecommended that BP160–179/100–109 mmHg beconfirmed assoon aspossible (e.g. within 1 month) preferably byeither home orambulatory BP measurements. •Itisrecommended when BP≥180/110 mmHg that hypertensive emergency beexcluded.I C Continued12 ESC Guidelines
+Echocardiography isrecommended inhypertensive patients when there are ECG abnormalities orsigns or symptoms ofLVdysfunction.I BEchocardiography isrecommended inpatients with hypertension and ECG abnormalities, orsigns or symptoms ofcardiac disease.I B Echocardiography may beconsidered when the detection ofLVH may influence treatment decisions. IIb BEchocardiography may beconsidered inpatients with elevated BP, particularly when itislikely tochange patient management.IIb B Ultrasound examination ofthe carotid arteries may be considered for the detection ofasymptomatic atherosclerotic plaques orcarotid stenosis inpatients with documented vascular disease elsewhere.IIb BUltrasound examination ofthe carotid orfemoral arteries for detecting plaque may beconsidered in patients with elevated BPorhypertension when itis likely tochange patient management.IIb B Measurement ofPWV may beconsidered for measuring arterial stiffness. IIb BMeasurement ofPWV may beconsidered inpatients with elevated BPorhypertension when itislikely to change patient management.IIb B 8.Preventing andtreating elevated blood pressure Regular aerobic exercise (e.g. atleast 30min of moderate dynamic exercise on5–7 days/week) is recommended. I AModerate intensity aerobic exercise of≥150 min/week (≥30 min, 5–7 days/week) oralternatively 75min of vigorous intensity aerobic exercise per week over 3 days are recommended and should becomplemented with low- ormoderate-intensity dynamic orisometric resistance training (2–3 times/week) toreduce BPand CVD risk.I A Body-weight control isindicated toavoid obesity (BMI >30 kg/m2orwaist circumference >102 cminmen and >88 cm inwomen), asisaiming athealthy BMI (about 20–25 kg/m2)and waist circumference values (<94 cmin men and<80 cminwomen) toreduce BPand CV risk.I AItisrecommended toaim forastable and healthy BMI (20–25 kg/m2)and waist circumference values (<94 cm inmen and<80 cminwomen) toreduce BPand CVD risk.I A Increased consumption ofvegetables, fresh fruits, fish, nuts, and unsaturated fatty acids (olive oil); low consumption ofred meat; and consumption oflow-fat dairy products are recommended.I AAdopting ahealthy and balanced diet, such asthe Mediterranean orDASH diets, isrecommended tohelp reduce BPand CVD risk.I A Itisrecommended torestrict alcohol consumption to: •Less than 14units/week for men. •Less than 8units/week for women. I AMen and women are recommended todrink less alcohol than the upper limit, which isabout 100 g/week ofpure alcohol. How this translates into number of drinks depends onportion size (the standards ofwhich differ per country), but most drinks contain 8–14 gof alcohol per drink. Preferably, itisrecommended to avoid alcohol toachieve the best health outcomes.I B Among allanti-hypertensive drugs, ACE inhibitors, ARBs, beta-blockers, CCBs, and diuretics (thiazides and thiazide-like drugs, such aschlorthalidone and indapamide) have demonstrated effective reduction of BPand CV events inRCTs, and thus are indicated asthe basis ofanti-hypertensive treatment strategies.I AAmong allBP-lowering drugs, ACE inhibitors, ARBs, dihydropyridine CCBs, and diuretics (thiazides and thiazide-like drugs such aschlorthalidone and indapamide) have demonstrated the most effective reduction ofBPand CVD events, and are therefore recommended asfirst-line treatments tolower BP.I A Itisrecommended that ifBPisnot controlled with a three-drug combination, treatment should be increased bythe addition ofspironolactone or,ifnot tolerated, other diuretics such asamiloride orhigher doses ofother diuretics, abeta-blocker, oran alpha-blocker.I BIfBPisnot controlled with athree-drug combination and inwhom spironolactone isnot effective or tolerated, treatment with eplerenone instead of spironolactone, orthe addition ofabeta-blocker ifnot already indicated and, next, acentrally acting BP-lowering medication, analpha-blocker, hydralazine, orapotassium-sparing diuretic should beconsidered.IIa B 8.Preventing andtreating elevated blood pressure (blood pressure targets) Itisrecommended that the first objective oftreatment should betolower BPto<140/90 mmHg inallpatients and, provided that the treatment iswell tolerated, treated BPvalues should betargeted to130/80 mmHg orlower inmost patients.I AToreduce CVD risk, itisrecommended that treated systolic BPvalues inmost adults betargeted to120– 129 mmHg, provided the treatment iswell tolerated. I A ContinuedESC Guidelines 13
+Adiastolic BPtarget of<80 mmHg should be considered forallhypertensive patients, independent of the level ofrisk and comorbidities. IIa BIncases where on-treatment systolic BPisatorbelow target (120–129 mmHg) but diastolic BPisnot attarget (≥80 mmHg), intensifying BP-lowering treatment to achieve anon-treatment diastolic BPof70–79 mmHg may beconsidered toreduce CVD risk.IIb C Inolder patients (aged ≥65 years) receiving BP-lowering drugs: •Itisrecommended that systolic BPshould be targeted toaBPrange of130–139 mmHg. I ABecause the CVD benefit ofanon-treatment systolic BP target of120–129 mmHg may not generalize tothe following specific settings, personalized and more lenient systolic BPtargets (e.g.<140 mmHg): should be considered among patients meeting thefollowing criteria: •pre-treatment, symptomatic, orthostatic hypotension; •and/or age≥85 years.IIa C Because the CVD benefit ofanon-treatment systolic BP target of120–129 mmHg may not generalize tothe following specific settings, personalized and more lenient BPtargets (e.g.<140/90 mmHg) may beconsidered among patients meeting the following criteria: •clinically significant, moderate tosevere frailty atany age; •and/or limited predicted lifespan (<3 years).IIb C 8.Preventing andtreating elevated blood pressure (renal denervation) Use ofdevice-based therapies isnot recommended for the routine treatment ofhypertension, unless inthe context ofclinical studies and RCTs, until further evidence regarding their safety and efficacy becomes available. III BToreduce BP, and ifperformed atamedium-to-high volume centre, catheter-based renal denervation may beconsidered for resistant hypertension patients who have BPthat isuncontrolled despite athree BP-lowering drug combination (including athiazide or thiazide-like diuretic), and who express apreference to undergo renal denervation after ashared risk-benefit discussion and multidisciplinary assessment.IIb B Toreduce BP, and ifperformed atamedium-to-high volume centre, catheter-based renal denervation may beconsidered for patients with both increased CVD risk and uncontrolled hypertension onfewer than three drugs, ifthey express apreference toundergo renal denervation after ashared risk-benefit discussion and multidisciplinary assessment.IIb A Due toalack ofadequately powered outcomes trials demonstrating itssafety and CVD benefits, renal denervation isnot recommended asafirst-line BP-lowering intervention for hypertension.III C Renal denervation isnot recommended for treating hypertension inpatients with moderately toseverely impaired renal function (eGFR <40 mL/min/1.73 m2)or secondary causes ofhypertension, until further evidence becomes available.III C 9.1.Managing specific patient groups orcircumstances Hypertension inpregnancy Inwomen with gestational hypertension, pre-existing hypertension superimposed bygestational hypertension, orwith hypertension and subclinical organ damage orsymptoms, initiation ofdrug treatment isrecommended when systolic BPis ≥140 mmHg ordiastolic BP≥90 mmHg.I CInwomen with gestational hypertension, starting drug treatment isrecommended for those with confirmed systolic BP≥140 mmHg ordiastolic BP≥90 mmHg.I B Continued14 ESC Guidelines
+Inallother cases, initiation ofdrug treatment is recommended when systolic BPis≥150 mmHg or diastolic BPis≥95 mmHg. I CInpregnant women with chronic hypertension, starting drug treatment isrecommended for those with confirmed office systolic BP≥140 mmHg ordiastolic BP≥90 mmHg.I B Inwomen with chronic and gestational hypertension, it isrecommended tolower BPbelow 140/90 mmHg but not below 80mmHg for diastolic BP.I C Systolic BP≥170 mmHg ordiastolic BP≥110 mmHg in apregnant woman isanemergency, and admission to hospital isrecommended.I CSystolic BP≥160 mmHg ordiastolic BP≥110 mmHg in pregnancy can indicate anemergency, and immediate hospitalization should beconsidered.IIa C Diabetes Antihypertensive drug treatment isrecommended for people with diabetes when office BPis≥140/90 mmHg. I AInmost adults with elevated BPand diabetes, after a maximum of3months oflifestyle intervention, BP lowering with pharmacological treatment is recommended for those with confirmed office BP ≥130/80 mmHg toreduce CVD risk.I A Inpeople with diabetes receiving BP-lowering drugs itisrecommended: •Totarget SBP to130 mmHg and<130 mmHg if tolerated, but not<120 mmHg. •Inolder people (aged ≥65 years aged), totarget toan SBP range of130–139 mmHg.I AInpersons with diabetes who are receiving BP-lowering drugs, itisrecommended totarget systolic BPto120– 129 mmHg, iftolerated. I A Chronic kidney disease Inpatients with diabetic ornon-diabetic CKD, itis recommended that anoffice BP≥140/90 mmHg be treated with lifestyle advice and BP-lowering medication.I AInpatients with diabetic ornon-diabetic moderate-to-severe CKD and confirmed BP≥130/80 mmHg, lifestyle optimization and BP-lowering medication are recommended toreduce CVD risk, provided such treatment iswell tolerated.I A Inpatients with diabetic ornon-diabetic CKD: Inadults with moderate-to-severe CKD who are receiving BP-lowering drugs and who have eGFR >30 mL/min/1.73 m2,itisrecommended totarget systolic BPto120–129 mmHg, iftolerated. Individualized BP targets are recommended for those with lower eGFR orrenal transplantation.I A•Itisrecommended tolower systolic BPtoarange of 130–139 mmHg.I A •Individualized treatment should beconsidered according toitstolerability and impact onrenal function and electrolytes.IIa C RAS blockers are more effective atreducing albuminuria than other antihypertensive agents, and are recommended aspart ofthe treatment strategy in hypertensive patients inthe presence of microalbuminuria orproteinuria.I AACE inhibitors orARBs are more effective atreducing albuminuria than other BP-lowering agents and should beconsidered aspart ofthe treatment strategy for patients with hypertension and microalbuminuria or proteinuria.IIa B Heart failure Inpatients with HFrEF, itisrecommended that BP-lowering treatment comprises anACE inhibitor or ARB, abeta-blocker and diuretic and/or MRA if required.I AInpatients with symptomatic HFrEF/HFmrEF, the following treatments with BP-lowering effects are recommended toimprove outcomes: ACE inhibitors (or ARBs ifACE inhibitors are not tolerated) orARNi, beta-blocker, MRA, and SGLT2 inhibitors.I A Inpatients with HFpEF, because nospecific drug has proven itssuperiority, allmajor agents can beused. I CInhypertensive patients with symptomatic HFpEF, SGLT2 inhibitors are recommended toimprove outcomes inthe context oftheir modest BP-lowering properties.I A Inpatients with symptomatic HFpEF who have BP above target, ARBs and/or MRAs may beconsidered to reduce heart failure hospitalizations and reduce BP.IIb B ContinuedESC Guidelines 15
+Stroke Inallhypertensive patients with ischaemic stroke or TIA, anSBP target range of120–130 mmHg should be considered.IIa BInpatients with confirmed BP≥130/80 mmHg with a history ofTIA orstroke asystolic BPtarget of120–129 mmHg isrecommended toreduce CVD outcomes, provided treatment istolerated.I A Different ethnic groups Inblack patients, initial antihypertensive treatment should include adiuretic oraCCB, either in combination orwith aRAS blocker.I BInblack patients from Sub-Saharan Africa who require BP-lowering treatment, combination therapy including aCCB combined with either athiazide diuretic ora RAS blocker should beconsidered.IIa B Resistant hypertension Recommended treatment ofresistant hypertension is: •Reinforcement oflifestyle measures, especially sodium restriction. •Addition oflow-dose spironolactone toexisting treatment. •Or the addition offurther diuretic therapy if intolerant tospironolactone, with either eplerenone, amiloride, ahigher dose thiazide/thiazide-like diuretic, oraloop diuretic. •Or the addition ofbisoprolol ordoxazosin.I BInpatients with resistant hypertension and uncontrolled BPdespite use offirst-line BP-lowering therapies, the addition ofspironolactone toexisting treatment should beconsidered.IIa B Inpatients with resistant hypertension inwhom spironolactone isnot effective ortolerated, treatment with eplerenone instead ofspironolactone, orthe addition ofabeta-blocker ifnot already indicated, and, next, acentrally acting BP-lowering medication, an alpha-blocker, orhydralazine, orapotassium-sparing diuretic should beconsidered.IIa B Toreduce BP, and ifperformed atamedium-to-high volume centre, catheter-based renal denervation may beconsidered for resistant hypertension patients who have BPthat isuncontrolled despite athree BP-lowering drug combination, and who express a preference toundergo renal denervation after ashared risk-benefit discussion and multidisciplinary assessment.IIb B 10.Acute andshort-term management ofblood pressure Inpatients with acute intracerebral haemorrhage: Inpatients with intracerebral haemorrhage, immediate BPlowering (within 6hofsymptom onset) should be considered toasystolic target 140–160 mmHg to prevent haematoma expansion and improve functional outcome.IIa A•Immediate BPlowering isnot recommended for patients with systolic BP<220 mmHg.III A •Inpatients with systolic BP≥220 mmHg, careful acute BPlowering with i.v.therapy to<180 mmHg should beconsidered.IIa B Inhypertensive patients with anacute cerebrovascular event, anti-hypertensive treatment isrecommended:For patients with ischaemic stroke orTIA and an indication for blood pressure lowering, itis recommended that BPlowering therapy be commenced before hospital discharge.I B•Immediately for TIA. I A •After several days inischaemic stroke. I A Insevere hypertension, drug treatment with i.v. labetalol, oral methyldopa, ornifedipine is recommended.I CInsevere hypertension inpregnancy, drug treatment with i.v.labetalol, oral methyldopa, ororal nifedipine is recommended. Intravenous hydralazine isasecond-line option.I C ©ESC 2024 ABPM, ambulatory blood pressure monitoring; ACE, angiotensin-converting enzyme; ACR, albumin-to-creatinine ratio (urine); ARB, angiotensin receptor blocker; ARNi, angiotensin receptor–neprilysin inhibitor; BMI, body mass index; BP, blood pressure; CCB, calcium channel blocker; CKD, chronic kidney disease; CV, cardiovascular; CVD, cardiovascular disease; DASH, Dietary Approaches toStop Hypertension; eGFR, estimated glomerular filtration rate; HBPM, home blood pressure monitoring; HFpEF, heart failure with preserved ejection fraction; HF(m)rEF, heart failure with (mildly) reduced ejection fraction; HFrEF, heart failure with reduced ejection fraction; HMOD, hypertension-mediated organ damage; i.v., intravenous; LVH, left ventricular hypertrophy; MRA, mineralocorticoid receptor antagonist; RAS, renin–angiotensin system; RCT, randomized controlled trial; SBP, systolic blood pressure; SCORE2, Systematic COronary Risk Evaluation 2;SCORE2-OP, Systematic COronary Risk Evaluation 2–Older Persons; SGLT2, sodium–glucose co-transporter 2;TIA, transient ischaemic attack. aClass ofrecommendation. bLevel ofevidence.16 ESC Guidelines
+3.Pathophysiology ofelevated blood pressure andhypertension Persistently high BPinsystemic arteries isthe hallmark ofhypertension, which isthe most important modifiable risk factor for all-cause and CVD morbidity and mortality globally.2Most patients with hypertension have essential orprimary hypertension, where the exact cause remains unknown, while anestimated 10% have secondary hypertension, with anidentifiable cause (notably some studies indicate that the prevalence ofsecondary hypertension may besubstantially higher, with modern systematic screening).10 The pathophysiology ofhypertension involves complex interactions between environmental and behavioural factors, genes, hormonal net- works, and multiple organ systems (renal, cardiovascular, and central nervous system11)(Figure 1). Inaddition, vascular and immunemechanisms are involved.12Dysregulation ofthese processes leads to hypertension, which ifuncontrolled, can lead tohypertension-mediated organ damage (HMOD) and adverse CVD outcomes. Details onthe pathophysiological processes, molecular mechanisms, and environmental and psychosocial elements that underlie hypertension are provided inthe Supplementary text (Supplementary data online). 4.Clinical consequences of elevated blood pressure andhypertension Longstanding hypertension causes organ damage and ultimately leads tocardiovascular, cerebrovascular, and clinical renal disease, which are allmajor contributors tothe global burden ofchronic disease Physical activity Sedentary behaviour Sleep quality/quantity Dietary patterns Sodium and potassium intake Obesity Alcohol consumption Drugs or substances that increase BP Geopolitical status Noise pollution Air pollution ClimateSalt sensitivity Pressure- natriuresis RAAS Renal ischaemia RAAS Endothelin system Sex hormones Endothelial dysfunction Small artery remodelling Large artery stiffness         Biological sex BP-associated SNPs Monogenic forms of hypertension Epigenetic and foetal programming Stress Low socio-economic status Social deprivation Healthcare access Gender identity, roles and norms Gender-based violence DiscriminationBehavioural factors Genetic factors Socio-economic and psychosocial factors Environmental factors Hormonal mechanismsRenal mechanisms Neural m echanisms Vascular mechanisms Autonomic nervous system (SNS/PNS) Baroreceptor re/f_lex Figure 1Pathophysiology ofelevated blood pressure and hypertension. BP, blood pressure; PNS, parasympathetic nervous system; RAAS, renin-angiotensin-aldosterone system; SNP, single-nucleotide polymorphism; SNS, sympathetic nervous system. Complex interplay between genes, environmental, and behavioural factors, organs, physiological systems, and neurohumoral processes contribute toBPregulation. Dysfunction ofthese processes leads tohypertension. The contribution ofthese factors toelevated BPand hypertension may differ among males and females.ESC Guidelines 17
+(Figure 2).2,13–22Organs adversely affected byelevated BPand hyper- tension include the heart, brain, kidneys, eyes, and vessels (macrocir- culation and microcirculation inorgans with low resistance, such as the brain or kidney23),which undergo structural and functional changes. Although factors besides BPcan contribute tothese changes (i.e. dyslipidaemia, hyperglycaemia), we use the term ‘hypertension- mediated organ damage’ toindicate the presence ofsubclinical complications ofhypertension that indicate high risk for subsequent clinical events. HMOD may have different profiles inmen and women; forinstance, left ventricular hypertrophy (LVH) and left atrial dilatation are more frequent inwomen.24–28 Evidence ofHMOD usually indicates long-standing elevated BPand/ orhypertension and confers incremental prognostic information re- garding CVD risk inallBP categories.29–31Unless treated, HMOD can progress from asymptomatic tosymptomatic, ultimately resulting inovert CVD events.31 The pathophysiological mechanisms underlying HMOD inthe heart, brain, kidneys, vessels, and eyes are detailed inthe Supplementary text (Supplementary data online). The clinical consequences ofHMOD, es- pecially cerebrovascular disease (stroke and cognitive decline), kidney disease (acute and chronic), and heart disease [heart failure, atrial fibril- lation (AF), ischaemic heart disease, and valvular disease] are also dis- cussed inthe Supplementary text (Supplementary data online). In addition, the Supplement highlights the impact ofdifferent measures ofBPonCVD risk, including systolic BP, diastolic BP, pulse pressure, and BPvariability.22,32–365.Measuring blood pressure 5.1.Introduction andpertinent definitions This section reviews practical aspects ofBPmeasurement, including technique and clinical validation ofdevices. Italso reviews the evi- dence for the most appropriate BP measurement methods when screening populations for hypertension, diagnosing hypertension, and managing patients receiving BP-lowering interventions. The cur- rent guidelines promote use ofout-of-office measurement for diagnosis and ongoing management ofhypertension, reflecting in- creasing evidence for the stronger relationship ofhome and ambula- tory monitoring with outcomes, the ability todetect white-coat and masked hypertension, new BP treatment targets aslow as 120–129 mmHg systolic (Table 5),and evidence supporting enabling patient involvement and shared decision-making. Definitions: Systolic BP: arterial BP during systole (maximum arterial pulsatile pressure). This ismeasured using anauscultatory device at the onset ofthe first Korotkoff sound. Oscillometric devices esti- mate systole using analgorithm that imputes from mean arterial pressure.37 Diastolic BP: arterial BPduring diastole (minimum arterial pulsatile pressure). This ismeasured using anauscultatory device atthe time of complete disappearance ofthe Korotkoff sounds (fifth sound). Ifthere isno disappearance ofsounds (no fifth sound) then the fourth See footnote for information on sex-differences White matter lesions Silent microinfarctsMicrobleedsBrain atrophy Cognitive impairmentVascular dementiaIschaemic strokeCerebral haemorrhageBrain Microvascular remodellingHypertensive retinopathyEye AtherosclerosisVascular calcificationArterial stiffnessLarge and medium arteries Endothelial dysfunction    VasoreactivityVascular remodellingFibrosis and inflammation   Peripheral vascularresistance MicrocirculationLVH LA and LV dilatation AF Obstructive and non-obstructive CAD  Myocardial Infarction   Diastolic and/or systolic   heart failureHeart Kidney Glomerular arteriolar hypertensionGlomerulosclerosisAlbuminuria/Proteinuria  GFRFigure 2Persistently elevated blood pressure and hypertension lead tohypertension-mediated organ damage and cardiovascular disease. AF, atrial fibrillation; CAD, coronary artery disease; GFR, glomerular filtration rate; LA, left atrial; LV, left ventricular; LVH, left ventricular hypertrophy. See the supplementary data online fordetailed information onsex differences.18 ESC Guidelines
+Korotkoff sound (muffling) isused to estimate diastolic BP. Oscillometric devices estimate diastole using an algorithm that imputes from mean arterial pressure.37 Inter-arm difference: systolic BPdifference of>10 mmHg when BPismeasured sequentially ineach arm.38 Postural/orthostatic hypotension: decrement of≥20 mmHg insystolic BPand/or ≥10 mmHg indiastolic BPwhen BPismeasured inthe standing position at1and/or 3min after standing following a 5-min period inthe sitting orlying position. White-coat hypertension: BP that isabove the threshold for diagnosing hypertension inthe office but below the threshold inhome/ ambulatory settings, e.g.≥140/90 mmHg inoffice but<135/85 mmHg athome/ambulatory daytime (or 24-h BP<130/80 mmHg). Masked hypertension: BP that isbelow the hypertension diagnostic threshold inthe office but above the hypertension diagnostic threshold inhome/ambulatory settings, e.g.<140/90 mmHg inclinic but ≥135/85 mmHg at home/ambulatory daytime (or 24-h BP ≥130/80 mmHg). Office BP: also known asclinic BP. The two terms are interchange- able. This guidelines document uses ‘office BP’ preferentially. Ofnote, office BPcan bemeasured manually orusing anautomated device. In addition, automated office BP(AOBP) can beconducted inasetting at- tended byahealthcare professional orinanunattended fashion. Finally, not alloffice BPmeasurements are equal, with some facilities using a standardized method (which isrecommended and outlined below) and others unfortunately using suboptimal approaches tooffice BP measurement. Home BPmeasurement (HBPM): anout-of-office approach tomeasuring BPwhen the patient measures their own BPathome using avalidated monitor (usually anupper-arm oscillometric cuff device). Ambulatory BPmeasurement (ABPM): anout-of-office BP measurement that uses afully automated oscillometric device, usually for a24-h period, and measures BPatsetintervals. 5.2.Practical recommendations for measuring blood pressure 5.2.1. Clinical validation ofequipment formeasuring blood pressure Aprerequisite ofBP measurement isthat itmust beundertaken using adevice that has been clinically validated and confirmed to beaccurate. Of the commercially available oscillometric BPmeas- urement devices, asfew as6% have been adequately tested.39–41 National and international organizations provide lists ofvalidated monitors (e.g. www.stridebp.org, www.validatebp.org). Since the 2018 ESC/ESH Guidelines onthe management ofarter- ialhypertension, three arbiters ofdevice accuracy (the Association for the Advancement ofMedical Instrumentation, the ESH, and the International Organization for Standardization) have published a universal standard for validating devices for measuring BP.42This standard will likely become widely adopted. Validation standards and methodology need tobedeveloped and implemented for novel BPmeasurement devices that are non-occlusive and ‘cuffless’.43,44 5.2.2. Office blood pressure measurement AllBPmeasurements can beinfluenced bycircumstances ofmeasure- ment, including position, ambient temperature, the technique ofmeas- urement, accuracy ofequipment, and physical condition of thepatient.45For BPmeasurements inthe office, werecommend following astandardized method (Figure 3). Patient preparation: BPshould bemeasured with the patient seated comfortably after 5min ofrest. Patients should avoid exercising and stimulants (caffeine, tobacco) for atleast 30min before measure- ment. The patient’s bladder should beemptied ifneeded.46Patients should beseated with their legs unfolded and their back supported at the time ofmeasurement. The arm should besupported (toavoid iso- metric exercise-induced increases inBP). Clothing atthe location ofthe cuff placement should beremoved; rolling upofshirt sleeves should be avoided asthis can result inatourniquet effect. BPmeasurement technique: auscultatory or oscillometric techniques can beused tomeasure BPnon-invasively. The manual aus- cultatory approach isthe traditional method ofmeasuring systolic and diastolic BPatthe brachial artery site using astethoscope. Incontrast, oscillometric devices compute mean arterial BP using the oscillation amplitude with cuff deflation (or inflation) and then estimate systolic and diastolic BP. Oscillometric devices can besemi-automated (taking one reading per activation) orfully automated (obtaining multiple read- ings before averaging them). Oscillometric devices are not typically va- lidated foruse inAF, and the manual auscultatory method ispreferred inthese circumstances when feasible.47–49 BPcuffselection andpositioning: anappropriately sized cuff should beused, asanunder-sized orover-sized cuff will artificially elevate orreduce BP, respectively.50The bladder length should be 75%–100% and the width 35%–50% ofthe arm circumference. The arm circumference can bemeasured atthe mid-point ofthe olecranon and the acromion but many cuffs include sizing indicators. The cuff should bepositioned onthe patient’s upper arm atthe level ofthe heart with the lower edge ofthe cuff afew centimetres above the antecubital fossa. The stethoscope should not beplaced under the cuff. Inthose with significant obesity where acorrectly fitting upper arm cuff isnot available, measurement atthe lower arm orwrist can beconsidered asanalternative.51 BPmeasurement bymanual auscultation: three BP mea- surements should betaken, each 1–2 min apart, and additional mea- surements only ifthe readings differ by>10 mmHg (e.g. this may occur with arrhythmias orwhite-coat effects). The BPrecorded should bethe average ofthe last two BPreadings. BPmeasurement using AOBP measurement: asnoted above, AOBP using oscillometric devices may beobtained with (at- tended) orwithout (unattended) clinicians orstaff present. Clear evi- dence regarding superiority ofunattended vs. attended AOBP in managing BPtoreduce rates ofCVD islacking; however, because BP readings may differ for unattended vs.attended measurements,52we advise that aconsistent approach beused depending onlocal resource and preference. AOBP monitors typically make three orsixreadings at 1-min intervals and provide anaverage. AOBP correlates more closely with mean ABPM than with the manual auscultatory technique and may reduce measurement error and white-coat effects.53 Inter-arm BPdifference: attheinitial visit, BPshould bemeasured inboth arms todetect aninter-arm difference. Though devices allowing simultaneous measurement inboth arms exist, sequential arm measure- ment isconsidered sufficiently reliable.54,55Measurement inthe contra- lateral arm should beundertaken once the three measurements inthe index arm have been taken, and ifadifference isdetected, further meas- urement inthe original arm isindicated toensure the difference iscon- sistent. Ifsystolic BPdiffers by>10 mmHg between arms, subsequent measurements are obtained using the arm with the higher BP value. Significant inter-arm BP differences may reflect arterial stenosis orESC Guidelines 19
+coarctation oftheaorta, which may require investigation. Also, ofnote, in some patients one arm ispreferred tothe other forroutine BPmeasure- ment (e.g. toavoid measurement ofBPinanarm with anarteriovenous fistula oranarm where axillary lymph node dissection has occurred). Postural/orthostatic hypotension: patients should be as- sessed for orthostatic hypotension atthe initial visit and ifconcerning symptoms arise. After 5min ofrest inthe sitting orlying position, BP should bemeasured at1min and/or 3min after standing, with athresh- old fororthostatic hypotension of≥20/10 mmHg (systolic BP/diastolic BP) drop. Measurement after lying may bemore sensitive fordetectingorthostatic hypotension and may better predict falls but may beless feasible than measurement after sitting inclinical practice.56 Pulse assessment: heart rate should berecorded atthe initial visit and arrhythmia excluded. 5.2.3. Home blood pressure measurement HBPM isanout-of-office approach tomeasuring BPwhen the patient measures their own BPathome using avalidated monitor (usually an upper-arm oscillometric cuff device).57,58Aconsistent approach to >10 mmHg 1  2  3 4 5  6  7 8Office blood pressure measurement Measure after 5 min seated comfortably in a  quiet environmentUse a validated device  with an appropriate cuff  size based on arm circumferencePlace the BP cuff at the level  of the heart with the patient's  back and arm supported Assess for orthostatic  hypotension at Ist visit and  thereafter by symptomsMeasure BP three times  (1–2 min apart) and  average the last 2 readings Record heart rate and exclude arrhythmia  by pulse palpationMeasure BP in both  arms at the Ist visit to  detect between arm  differencesObtain further measurements if the  readings differ by  >10 mmHg 90 62Figure 3Summary ofoffice blood pressure measurement. BP, blood pressure.20 ESC Guidelines
+HBPM should beused (Figure 4).Patients should becounselled tofol- low the same preparation steps asused inclinics, which are outlined inSection 5.2.2. Two measurements should betaken ateach measure- ment session, performed 1–2 min apart. Measurements should be made twice aday (morning and evening) atthe same time for amin- imum of3days and upto7days.59Atthe end ofthe measurement per- iod, allreadings are averaged. Ifthe average after 3days isclose tothe treatment threshold, then measurement should continue forthe full7 days. Patients should beinformed tokeep arecord oftheir home BPvalues and toask their healthcare provider that the device accuracy beintermittently checked. Devices older than 4years may beinaccur- ate and, ifinaccurate, should bereplaced.60 Anaverage HBPM of≥135/85 mmHg (equivalent toanoffice BPof ≥140/90 mmHg) should beused todiagnose hypertension and anaver- age systolic BP of120–134 mmHg ordiastolic BP of70–84 mmHg should beused todiagnose elevated BP. Ofnote, weuse the same low- erBPthreshold (120/70 mmHg) for both office and HBPM indefining elevated BP.61 3Home-based blood pressure measurement 1 Use a validated BP  device 2 Measure BP in a quiet room  after 5 min of rest with arm  and back supported Obtain two readings on each occasion, 1–2 min apart 4 Obtain readings twice a day  (morninga and evening) for  at least 3 and ideally 7 days average HBPM ≥135/85 mmHgHypertension: 5 Record and average all  readings and present  results to clinician Figure 4Summary ofhome blood pressure measurement. BP, blood pressure; HBPM, home blood pressure measurement.aMorning HBPM readings should beobtained before breakfast and before intake ofmedication but not immediately after awakening.ESC Guidelines 21
+5.2.4. Ambulatory blood pressure measurement ABPM (summarized inFigure 5)isanout-of-office BPmeasurement that uses afully automated device, usually for a24-h period. The devices measure BP by the oscillometric method and are pro- grammed to measure BP atset intervals. Readings are usually obtained at15–30 min intervals during the day (typically 7a.m. to 11 p.m.) and 30–60 min intervals atnight (typically 11 p.m. to 7a.m.). The software usually provides average BP measurements for daytime, night-time, and 24h.Aminimum of70% useable BP recordings isrequired for avalid measurement session, typicallynumbering ≥27 measurements over 24h.Preferably, seven noctur- nal readings should also beobtained.62However, emerging data in- dicate that ≥8/≥4 wake/sleep readings may beadequate ifmore cannot be obtained.63Prior tousing mean ABPM values (either 24h,daytime, ornight-time) the raw BPvalues ateach measurement should bereviewed for possible outlier orerroneous values. Adiary should record activities (e.g. meals and exercise) and sleep time to assist interpretation. The diagnostic thresholds for elevated BPand hypertension using ABPM, and comparison with office BP and HBPM, are provided inTable 5.61,64 1  2  3 4Ambulatory blood pressure measurement Use a validated BP  deviceDevice usually records BP at  15–30 min intervals during the  day and 30 –60 min at nightA minimum of 70% usable BP recordings is required A diary of the patient's activities,  intake of medications and sleep  time should be completed ABPM ≥130/80 mmHg over 24 h or ≥135/85 mmHg for the daytime average or ≥120/70 mmHg for the night-time averageHypertension: Figure 5Summary ofambulatory blood pressure measurement. ABPM, ambulatory blood pressure measurement; BP, blood pressure. Table 5Comparison ofoffice, home, and ambulatory blood pressure measurement thresholds forelevated blood pressure andhypertension Office BP (mmHg)aHome BP (mmHg)Daytime ABPM (mmHg)24hABPM (mmHg)Night-time ABPM (mmHg) Reference Non-elevated BP <120/70 <120/70 <120/70 <115/65 <110/60 Elevated BP 120/70–<140/90 120/70–<135/85 120/70–<135/85 115/65–<130/80 110/60–<120/70 Hypertension ≥140/90 ≥135/85 ≥135/85 ≥130/80 ≥120/70 ©ESC 2024 ABPM, ambulatory blood pressure monitoring; BP, blood pressure. aThe BPthresholds provided assume that astandardized approach tooffice BPmeasurement isperformed (Figure 3).However, evidence indicates that office BPmeasurement inroutine clinical settings isoften not done using astandardized approach and, inthis case, the routine office BPvalue may be5–10 mmHg higher than itwould have been ifmeasured using the recommended standardized approach.65,6622 ESC Guidelines
+5.2.5. Comparison ofhome andambulatory blood pressure monitoring There isoverlap between home and ambulatory monitoring interms of differentiating between hypertensive phenotypes. However, around 15% ofpeople will have diagnostic disagreement, ofwhom approximately 50% will represent clinically significant differences of>5mmHg.67The ad- vantages and disadvantages ofhome and ambulatory monitoring are out- lined inTable 6. 5.3.What isthebest method for measuring blood pressure todiagnose hypertension? 5.3.1. Blood pressure measurement forhypertension screening Opportunistic screening istypically performed using office BPmeasure- ment and iskey indetecting possible hypertension. However, asingle screening office BPalone does not typically have sufficient diagnostic test performance toestablish adiagnosis, especially forBPvalues close todiagnostic thresholds. Therefore, asingle screening office BP re- quires some form ofrepeat BPassessment toconfirm adiagnosis (pref- erably out-of-office orrepeat office ifout-of-office isnot available). Relatedly, the BPthreshold foracting onascreening office BPbycon- ducting repeat BPassessments should also belower than the office BP threshold used fordiagnosing hypertension. This latter consideration is particularly relevant inthe presence ofincreased CVD risk ormarkers ofHMOD. Also ofnote, populations where masked hypertension is more prevalent include men, those who smoke, those with excessivealcohol intake, orthose with diabetes orobesity.68,69While ascreening office BPof>160/100 mmHg isalmost always consistent with adiagno- sisofhypertension, asmall proportion ofpatients will have extreme white-coat effects that motivate prompt repeat BP assessment.68 Hypertension screening approaches are discussed further inSection 7.1. 5.3.2. Blood pressure measurement fordiagnosing hypertension After detecting high BP inthe office, subsequent BP measurement for diagnosing hypertension depends on the clinical circumstances. Office BPhas lower specificity than ABPM fordetecting hypertension, sodiagnosis based onoffice BPalone isless desirable unless resources do not allow out-of-office measurements.70For screening BP of 160–179 mmHg systolic or100–109 mmHg diastolic, prompt confirm- ation (within 1month) using either office orout-of-office methods is recommended, asdelays intreatment are associated with increased CVD event rates.71For BPof≥180/110 mmHg, assessment forhyper- tensive emergency isrecommended. Inthe setting ofhypertensive emergency, immediately commencing BP-lowering treatment isrecom- mended, otherwise, prompt confirmation (preferably within aweek) can beconsidered prior tocommencing treatment (Sections 7and10). For screening BPof140–159/90–99 mmHg, out-of-office BPshould be measured toconfirm the diagnosis.72When treatment ofelevated BPis being considered (e.g. 120–139/70–89 mmHg) for individuals with high risk CVD conditions orsufficiently high 10-year predicted CVD risk, out-of-office BP measurement isrecommended, both toconfirm BP and toassess for masked hypertension. Out-of-office measurements may also behelpful for individuals with office BPof130–139/85–89 mmHg todiagnose masked hypertension. Further details onthe diag- nostic evaluation ofhypertension are provided inSection 7.2. 5.4.What isthebest method for measuring blood pressure forlong-term management ofhypertension? While repeat office measurement ofBPremains the commonest ap- proach tolong-term management ofhypertension, several lines ofin- vestigation support augmenting office BP measurements with out-of-office assessment. 5.4.1. Home monitoring There areover 50trials ofdifferent self-monitoring-based interventions.73 Self-monitoring isassociated with lower mean systolic BPat12months [−3.2 mmHg; 95% confidence interval (CI) −4.9 to−1.6 mmHg].74 Furthermore, there areknown benefits oftelemonitoring, digital interven- tions, and mobile health inmanaging BP.75–78Self-monitoring isalso likely tobecost-effective.79Unfortunately, inclinical practice, some patients may not provide reliable information ontheir home BP,and both their de- vice and measurement technique need tobechecked. 5.4.2. Ambulatory monitoring ABPM provides areference BPmeasurement but repeat ABPM testing issometimes not practical due toresource constraints and, uncom- monly, low patient acceptability.80There isapaucity ofdata ontreat- ment guided byABPM vs.that ofoffice orHBPM measurements. A trial oftreatment guided byHBPM vs.clinic and ambulatory monitoring found equivalence inBPcontrol and HMOD.81Other studies reported anon-significant trend toworse BPcontrol with ambulatory vs.office BP monitoring, though the ambulatory group also received fewerTable 6Comparison ofambulatory and home blood pressure monitoring Ambulatory monitoring Advantages •Can identify white-coat and masked hypertension •Measurement inreal-life settings and during usual activities •Stronger prognostic evidence •Night-time readings •Abundant information from asingle investigation, including short-term diurnal BPvariability •Additional BPphenotyping (e.g. nocturnal dipping status) Disadvantages •Relatively expensive and sometimes limited availability •Can beuncomfortable and affect sleep Home monitoring Advantages •Identify white-coat and masked hypertension •Cheap and widely available •Measurement athome, which may bemore relaxed than atdoctor’s office •Patient engagement inBPmeasurement and telemedicine potential •Easily repeated and used over longer periods toassess day-to-day BP variability Disadvantages •Only static BPatrest istypically available •Potential for measurement error due toimproper measurement technique orunvalidated orpoorly calibrated device •Nocturnal readings not usually possible ©ESC 2024 BP, blood pressure.ESC Guidelines 23
+medications.82Potential advantages ofABPM over HBPM include diag- nosing nocturnal hypertension orsymptomatic transient hypotension orhypertension with exertion. Assuch, ABPM and HBPM should be considered complementary and additive, rather than competing ap- proaches tolong-term BPmanagement.83 5.5.Measuring blood pressure inselected groups 5.5.1. Pregnancy Monitoring BPduring pregnancy istypically done atantenatal visits, which vary dependent ontrimester (with increasing frequency to- wards term). BPtends toreach anadir at20–30 weeks ofpregnancy before increasing towards term at40weeks.84Only asmall number ofautomated oscillometric BPmonitors have been adequately vali- dated inpregnancy and several have failed, usually due toproviding BP values that are erroneously high.85Auscultatory measurement with sphygmomanometry isconsequently the clinical standard in pregnancy.85Self-monitoring athome isnot yet proven tobeeffect- ive ingestational hypertension.86,87While norms for BP during pregnancy remain unclear, the 2022 Chronic Hypertension and Pregnancy (CHAP) trial indicated benefit oftargeting clinic BPbelow 140/90 mmHg.88Consideration ofsecondary causes ofhyperten- sion isimportant inyoung women with gestational hypertension. Further details are provided inSection 9.2 and the 2018 ESC Guideline for the management ofcardiovascular disease during pregnancy.89 5.5.2. Atrial fibrillation Hypertension isarisk factor for AF.90,91Oscillometric BPmonitors are not always accurate inthe presence ofAF, due tothe greater variability ofBPbeat tobeat, somultiple auscultatory measurements are recommended.48,92,93Some oscillometric BPmonitors include analgorithm fordetecting AF, but anelectrocardiogram (ECG) isstill required toconfirm the diagnosis.49,94 5.5.3. Orthostatic hypotension Postural ororthostatic hypotension iscommon,95,96present inap- proximately 10% ofallhypertensive adults and upto50% ofolder institutionalized adults.97,98Orthostatic hypotension isdefined as aBPdrop of≥20/10 mmHg 1and/or 3min after standing following a5-min period inthe seated orlying position.99–101Diagnosis is made inthe office. Routine ABPM isnot currently suitable for for- mally assessing orthostatic hypotension,102though itmay help in some cases, particularly when accompanied byapatient symptom diary.103 5.6.Novel methods ofmeasuring blood pressure New methods tomeasure BPare under development. Continuous of- fice and out-of-office BPrecordings and ABPM and HBPM have been developed that derive beat-to-beat, reading-to-reading, and day-to-day BPvariability. However, there isnoagreement onthe optimum ap- proach tomeasuring variability, and there isnotrial evidence that redu- cing BP variability specifically can reduce CVD events.104Other emerging technologies include wearable, wrist-based BPmeasurement devices, devices evaluating central BP,and cuffless devices implementing plethysmographic orother technologies.105,106However, there isatpresent insufficient scientific consensus on the accuracy standards and validation procedures that these cuffless devices must comply with prior tocommercialization.43,44,107–109 Inview ofthese issues, none ofthese cuffless measurement modal- ities are currently recommended for routine clinical use. Recommendation Table 1—Recommendations for measuring blood pressure (see Evidence Tables 1–8) Recommendations ClassaLevelb Itisrecommended tomeasure BPusing avalidated and calibrated device, toenforce the correct measurement technique, and toapply aconsistent approach toBPmeasurement for each patient.41,42I B Alladult patients (≥18 years) are recommended to have their office and/or out-of-office BPmeasured onanopportunistic basis and recorded intheir medical file, and betold what their current BPis.I C Out-of-office BPmeasurement isrecommended for diagnostic purposes, particularly because itcan detect both white-coat hypertension and masked hypertension. Where out-of-office measurements are not logistically and/or economically feasible, then itisrecommended that the diagnosis beconfirmed with arepeat office BPmeasurement using the correct standardized measurement technique.70I B Itisrecommended that office BPshould bemeasured inboth arms atleast atthe first visit, because a between-arm systolic BPdifference of>10 mmHg is associated with anincreased CVD risk and may indicate arterial stenosis.55,110I B Ifabetween-arm difference of>10 mmHg insystolic BPisrecorded, then itisrecommended that all subsequent BPreadings use the arm with the higher BPreading.110I B Out-of-office BPmeasurement isrecommended for ongoing management toquantify the effects of treatment and guide BP-lowering medication titration, and/or identify possible causes ofside effects (e.g. symptomatic hypotension). Where out-of-office measurements are not logistically and/ oreconomically feasible, then ongoing management isrecommended tobebased onrepeated office BP measurements using the correct standardized measurement technique.74,111,112I B Itisrecommended that allpatients undergoing BPmeasurement also undergo pulse palpation atrest todetermine heart rate and arrhythmias such asAF.113I C Most automated oscillometric monitors have not been validated for BPmeasurement inAF; BPmeasurement should beconsidered using amanual auscultatory method inthese circumstances where possible.47–49IIa C Continued24 ESC Guidelines
+6.Definition andclassification of elevated blood pressure and hypertension, andcardiovascular disease riskassessment 6.1.Definition andclassification of elevated blood pressure andhypertension Epidemiological studies demonstrate acontinuous and log-linear asso- ciation between BPand adverse CVD outcomes.22,32,33,114,115Starting atlevels aslow as90mmHg systolic, the higher the BPthe higher the relative risk ofCVD including atherosclerosis.32,114These observational data are complemented byrandomized clinical trials (RCTs),116which have provided experimental evidence regarding the BPrange forwhich BPlowering with treatment isproven toreduce CVD events. Ofnote, some studies suggest astronger relative risk for CVD for agiven BP among females compared with males.117,118 Ahealthy lifestyle should beencouraged foralladults toprevent an increase inBPand development ofhypertension.119,120Toaidpharma- cological treatment decisions, the 2024 ESC Guidelines recommend a simplified categorization ofadults according totheir BP(Figure 6).In compiling this categorization, priority was given toevidence from ran- domized trials over observational data. However, itisimportant tore- iterate that the risk ofCVD attributable toBPiscontinuous and that interpreting randomized trial data isaniterative process involving an element ofsubjectivity. Assuch, nocategorization ofBPcan beconsid- ered immutable orflawless. The 2024 Guidelines define hypertension asaconfirmed office sys- tolic BPof≥140 mmHg ordiastolic BPof≥90 mmHg. For this diagnosis tobemade, confirmation isrecommended with out-of-office measure- ments (HBPM orABPM) oratleast one repeat office measurement ata subsequent visit, asdetailed inSection 5andSection 7.2. This definition is based onseveral factors. First, meta-analyses ofrandomized trials pro- vide evidence among alladults and across various settings forthe bene- fit of BP-lowering therapy among patients with BP above this threshold.116,121,122Second, most adults with BPabove this threshold are atincreased CVD risk, typically with 10-year risk estimates of ≥10% for fatal and non-fatal CVD events.123–125The higher the pa- tient’s baseline absolute risk for CVD, the greater the net benefit from BP-lowering treatment and, atthe population level, the lower the estimated number needed totreat (NNT).126–128Third, this more traditional BPthreshold for hypertension isalready widely used bypolicymakers todefine adisease state, and maintaining this BPthreshold todefine hypertension (vs. lowering it)does not require most adults tobelabelled with what iswidely considered adisease.129 Here, we introduce anew BPcategory called ‘elevated BP’, which isdefined asanoffice systolic BPof120–139 mmHg ordiastolic BP of70–89 mmHg. Within this BPrange, the efficacy ofBP-lowering ther- apy has been established inmeta-analyses ofRCTs,116but average CVD risk inthe elevated BPgroup isnot sufficiently high tomerit drug treat- ment inallpatients.123,124,130Pharmacological treatment initiation is, however, suggested for asubgroup ofpatients within this BP range who are atincreased global risk ofCVD asidentified bythe risk strati- fication approach outlined inSections 6.3,6.4, and 8. Non-elevated BPisdefined asasystolic BPof<120 mmHg and adia- stolic BPof<70 mmHg. Fewer individuals within this BPrange are at increased risk of CVD,124and evidence for CVD benefit with BP-lowering pharmacological treatment islacking due toanabsence oftrials. We use the term ‘non-elevated BP’ todefine this BPcategory inrecognition that these are treatment categories and not prognostic categories. Because the relative risk for CVD starts toincrease atBP below this threshold (even aslow as90mmHg systolic BP), particularly among women,117,118weavoid terms like ‘normal BP’, ‘optimal BP’, or ‘normotension’ indefining this category. 6.2.Principles ofarisk-based approach for managing blood pressure andpreventing cardiovascular disease Inthe context ofBP-lowering interventions, randomized trials demon- strate aconsistent relative risk reduction inadverse CVD outcomes per unit reduction inBP.131,139However, many medical interventions in- cur costs and have side effects. Therefore, guidance isneeded onselect- ingpatients most likely tobenefit from BP-lowering treatment. This is especially true among adults with elevated BP (office systolic BP of 120–139 mmHg and/or diastolic BPof70–89 mmHg). Practical aspects forimplementing arisk-based approach arefurther discussed inSection 8. 6.2.1. Role ofcardiovascular disease riskassessment The risk ofadverse CVD outcomes increases log-linearly with constant increments insystolic BPand diastolic BP.22,32,33,114,140Concurrently, at higher BP, there isclustering ofadditional CVD risk factors.141,142 Consequently, many patients with hypertension will have anestimated 10-year risk forCVD events of≥10%,116,121,122which, forthe purposes ofthese guidelines, isconsidered sufficiently high risk tomerit consid- eration ofBP-lowering treatment inthe setting ofelevated BP.143 Using BPthresholds forhypertension alone forallocating treatment would lead tounder-treatment ofmany high-risk patients.144,145,115 Asubstantial proportion ofexcess CVD events attributable toBPoc- cur inpatients with BP levels below the traditional threshold forAnassessment for orthostatic hypotension (≥20 systolic BPand/or ≥10 diastolic BPmmHg drop at1 and/or 3min after standing) should beconsidered at least atthe initial diagnosis ofelevated BPor hypertension and thereafter ifsuggestive symptoms arise. This should beperformed after the patient is first lying orsitting for 5min.IIa C Other BPmeasures and indices (pulse pressure, BP variability, exercise BP) may beconsidered to provide additional clinical information onCVD risk in some circumstances.IIb C ©ESC 2024 AF, atrial fibrillation; BP, blood pressure; CVD, cardiovascular disease. aClass ofrecommendation. bLevel ofevidence. Recommendation Table 2—Recommendations for categorizing blood pressure (see Evidence Table 9) Recommendation ClassaLevelb Itisrecommended that BPbecategorized as non-elevated BP, elevated BP, and hypertension to aidtreatment decisions.116,121,122,131–138I B ©ESC 2024 BP, blood pressure. aClass ofrecommendation. bLevel ofevidence.ESC Guidelines 25
+hypertension diagnosis. Asthe efficacy ofBPlowering onpreventing CVD events extends down toasystolic BPof120 mmHg and adiastolic BPof70mmHg,116,135,136,146patients with elevated BPand increased CVD risk can also derive benefit from BP-lowering treatment.124,145 The heterogeneity inCVD risk among adults with elevated BPislar- ger than inthose with hypertension, assuch patients tend tobeyoung- er,and their absolute CVD risk depends more onthe prevalence of concomitant CVD risk factors.123,147Consequently, formally estimating the patient’s CVD risk, encapsulating demographics and other CVD risk factors, isrecommended toguide BP-lowering treatment decisions among patients with elevated BP.148–1516.3.Predicting cardiovascular disease risk Certain conditions ontheir own are associated with sufficient CVD risk such that patients with elevated BPalongside these conditions can be considered forBP-lowering therapy (Figure 7).These include moderate orsevere chronic kidney disease (CKD),152established clinical CVD (cor- onary heart disease, cerebrovascular disease, peripheral arterial disease, orheart failure)153–158concomitant HMOD (see Figure 7;Section 7; Supplementary data online, Table S1),31,159diabetes mellitus, and familial hypercholesterolaemia (probable ordefinite).160–163Regarding diabetes, some adults aged <60 years with type 2diabetes and elevated BPhave 10-year CVD risk of<10%. Accordingly, the diabetes-specific Non-elevated blood pressure Office BP SBP <120 mmHg and DBP <70 mmHg HBPM SBP <120 mmHg and DBP <70 mmHg ABPM Daytime SBP <120 mmHg and Daytime DBP <70 mmHgElevated blood pressure Office BP SBP 120–139 mmHg or DBP 70–89 mmHg HBPM SBP 120–134 mmHg or DBP 70–84 mmHg ABPM Daytime SBP 120–134 mmHg or Daytime DBP 70–84 mmHgHypertension Office BP SBP ≥140 mmHg or DBP ≥90 mmHg HBPM SBP ≥135 mmHg or DBP ≥85 mmHg ABPM Daytime SBP ≥135 mmHg or  Daytime DBP ≥85 mmHg Insufficient evidence confirming the efficacy and safety of BP pharmacological treatmentRisk stratify to identify individuals with high cardiovascular risk for BP pharmacological treatmentCardiovascular risk is sufficiently high to merit BP pharmacological treatment initiationBlood pressure classification The diagnosis of hypertension and elevated BP requires confirmation using out-of-office measurements  (HBPM or ABPM) or at least one additional subsequent office measurementFigure 6Blood pressure categories. ABPM, ambulatory blood pressure monitoring; BP, blood pressure; DBP, diastolic blood pressure; HBPM, home blood pressure monitoring; SBP, systolic blood pressure. We note that the respective non-daytime ABPM thresholds forelevated BPand hypertension diagnosis are listed inSection 5(Table 5).26 ESC Guidelines
+Systematic COronary Risk Evaluation 2(SCORE2)-Diabetes risk- prediction model should beconsidered toconfirm CVD risk issufficient- lyhigh (≥10%) among individuals with type 2diabetes mellitus who are aged <60 years.164 Inthe absence ofthese sufficiently high-risk conditions, risk-prediction models (SCORE2 and SCORE-OP) have been developed inthe general population topredict 10-year risk ofCVD.165,166Inadults with elevated BP without the above sufficiently high-risk conditions, risk-prediction models are recommended toinform BP-lowering treatment decisions. Risk-prediction models aremore accurate than clinical judgment ortally- ingofindividual risk factors.167–169 6.3.1. 10-year cardiovascular disease risk-prediction models Prediction models differ intheir input variables, predicted endpoints (outputs), and populations inwhich they were derived and validated. We endorse the use ofSCORE2 for individuals aged 40–69 years and SCORE2–Older Persons (SCORE2-OP) for individuals aged ≥70 years for predicting 10-year global risk offatal and non-fatal CVD events (stroke ormyocardial infarction).165,166The management ofadults aged <40 years isdiscussed inSection 9.1. The SCORE2 and SCORE2-OP models are preferred over other 10-year risk-predictionmodels, asthey predict both fatal and non-fatal CVD events, have been validated and recalibrated toEuropean populations, and because SCORE2-OP isadjusted forthe competing risk ofnon-cardiovascular mortality. Calculating SCORE2 orSCORE2-OP isrecommended for individuals with elevated BPwho are not already atsufficiently high CVD risk due toestablished CVD, moderate orsevere CKD, prob- able ordefinite familial hypercholesterolaemia, diabetes mellitus, or HMOD.165,166,170 For the purpose ofBP-lowering treatment decisions, individuals with elevated BPand apredicted 10-year CVD risk of≥10% bySCORE2 or SCORE2-OP are considered inthese guidelines tobesufficiently high risk, with details on the choice oflifestyle or drugs tofacilitate BP-lowering treatment inthis setting provided inSection 8.171,172A number ofconsiderations influenced our choice torecommend asingle risk threshold of≥10%, vs.the alternative option ofusing age-specific risk thresholds, such asthose provided inthe 2021 ESC Guidelines on cardiovascular disease prevention inclinical practice.170For ex- ample, contemporary data indicate the heightened importance ofBP control inolder adults due totheir higher absolute CVD risk (resulting inalower NNT) and concomitantly toreduce age-dependent adverse outcomes attributable toincreased BP, such asdementia. Recent treat-to-target trials (testing systolic BP targets ofapproximately 120 mmHg) used asingle CVD risk inclusion threshold and were also Moderate or severe CKDeGFR <60 mL/min/1.73 m2 or albuminuria ≥30 mg/g (≥3 mg/mmol) Familial hypercholesterolaemiaProbable or definite familial hypercholesterolaemiaDiabetes mellitusType 1 and type 2 diabetes mellituscEstablished clinical cardiovascular diseaseAtherosclerotic cardiovascular diseasea Heart failure Other forms of hypertension- mediated organ damageCardiacb VascularbFigure 7Sufficiently high cardiovascular risk conditions that warrant blood pressure-lowering treatment among adults with elevated blood pressure. CKD, chronic kidney disease; eGFR, estimated glomerular filtration rate.aCoronary heart disease, cerebrovascular disease, peripheral arterial disease. bSeeSection 7.cSCORE2-Diabetes should beconsidered toidentify lower-risk individuals (<10% 10-year CVD risk), who may not require BP-lowering medication, particularly inindividuals <60 years.ESC Guidelines 27
+enriched with older adults.135,136,146Inaddition, the average CVD event rate inthe control arm ofalandmark meta-analysis showing the bene- fits ofmore intensive BP-lowering treatment was approximately equivalent toa10% 10-year risk.116Finally, the task force, which in- cluded patient members, felt that age-specific risk thresholds could re- sult inBPtreatment decisions being made solely based onage, which is difficult tosupport scientifically orotherwise. Totrytoavoid any con- fusion with the 2021 ESC Guidelines oncardiovascular disease preven- tion inclinical practice, we use the terms ‘sufficiently high risk’ or ‘increased risk’ todescribe aperson with 10-year CVD risk of≥10% (rather than the terms ‘high risk’ or‘very high risk’).6.4.Refining cardiovascular disease risk estimation beyond riskmodels The SCORE2 and SCORE2-OP risk-prediction models incorporate traditional risk factors such asage, sex, systolic BP, cholesterol values, and smoking status topredict 10-year risk ofCVD.165,166However, they donot include ‘non-traditional’ CVD risk factors (detailed below and hereafter termed ’risk modifiers’). Non-traditional CVD risk modifiers can improve the predictive performance (i.e. discrimin- ation) ofother CVD risk-prediction models, and may also apply to SCORE2 orSCORE2-OP.173For example, among individuals with elevated BP and borderline increased 10-year predicted CVD risk bySCORE2 orSCORE2-OP (estimates of5% to<10%), these non- traditional CVD risk modifiers may help up-classify the patient’s risk and thereby prompt BP-lowering treatment (Figure 8). 6.4.1. Sex-specific non-traditional cardiovascular disease riskmodifiers Sex differences inthe distribution oftraditional and non-traditional CVD risk factors have been documented among patients with hypertension.174Although sex itself isincluded asaninput variable inthe SCORE2 and SCORE2-OP, and though these models were derived separately inmen and women, some sex-specific, non- traditional risk modifiers were not included, and their associated impact on CVD risk may not be fully captured by SCORE2, SCORE2-OP, orSCORE2-Diabetes. The relationship between BP and overall CVD risk issimilar in both sexes, though some studies even suggest astronger relative risk for CVD for agiven BP level among females compared with males.117Female-specific, non-traditional CVD risk modifiers often arise atspecific times throughout the life course, especially during pregnancy and the peri-partum period. Women with ahistory of hypertensive disorders ofpregnancy, including gestational hyperten- sion and pre-eclampsia, have atwo-fold higher long-term risk of CVD vs. women without these pregnancy conditions.175–177The relative long-term CVD risk associated with hypertensive disorders ofpregnancy may also behigher inyounger vs.older pregnant wo- men.178,179Most, but not all, ofthe excess CVD risk associated with hypertensive disorders ofpregnancy iscaptured byconvention- alCVD risk factors.176,178Gestational diabetes isindependently as- sociated with anapproximately two-fold increase inthe long-term relative risk ofCVD events.180Other complications such aspre- term delivery, recurrent miscarriage, and one ormore stillbirths are associated with a40% relative increase inlong-term CVD risk.181–185Accordingly, ahistory ofspecific pregnancy complica- tions, including gestational hypertension, pre-eclampsia, gestational diabetes, pre-term delivery, one ormore stillbirths, and recurrent miscarriage, can beconsidered asnon-traditional CVD risk modi- fiers toup-classify women with elevated BPand borderline increased 10-year predicted CVD risk (5% to<10%) tosufficiently high risk, thereby influencing the risk-based management oftheir elevated BP. Evidence whether other female-specific conditions (infertility, poly- cystic ovary syndrome, and premature menopause) and male-specific conditions (androgenic alopecia and erectile dysfunction) improve pre- diction ofCVD sufficiently toinform risk-based BP-lowering treatment decisions isinconclusive atpresent.Recommendation Table 3—Recommendations for assessing cardiovascular disease risk among individuals with elevated blood pressure (office systolic blood pressure 120–139 mmHg ordiastolic blood pressure 70–89 mmHg) (see Evidence Tables 10and11) Recommendations ClassaLevelb Itisrecommended touse arisk-based approach in the treatment ofelevated BP, and individuals with moderate orsevere CKD, established CVD, HMOD, diabetes mellitus, orfamilial hypercholesterolaemia are considered atincreased risk for CVD events.31,153–159,161–163,172I B SCORE2 isrecommended forassessing 10-year risk offatal and non-fatal CVD among individuals aged 40–69 years with elevated BPwho are not already considered atincreased risk due tomoderate or severe CKD, established CVD, HMOD, diabetes mellitus, orfamilial hypercholesterolaemia.143,165,172I B SCORE2-OP isrecommended for assessing the 10-year risk offatal and non-fatal CVD among individuals aged ≥70 years with elevated BPwho are not already considered atincreased risk due to moderate orsevere CKD, established CVD, HMOD, diabetes mellitus, orfamilial hypercholesterolaemia.143,166,172I B Itisrecommended that, irrespective ofage, individuals with elevated BPand aSCORE2 or SCORE2-OP CVD risk of≥10% beconsidered at increased risk for CVD for the purposes of risk-based management oftheir elevated BP.143,165,166,172I B SCORE2-Diabetes should beconsidered toestimate CVD risk among type 2diabetes mellitus patients with elevated BP, particularly ifthey are<60 years of age.164IIa B ©ESC 2024 BP, blood pressure; CKD, chronic kidney disease; CVD, cardiovascular disease; HMOD, hypertension-mediated organ damage; SCORE2, Systematic COronary Risk Evaluation 2; SCORE2-OP, Systematic COronary Risk Evaluation 2–Older Persons. Established CVD: coronary artery disease, cerebrovascular disease, peripheral arterial disease, orheart failure. For details onHMOD seeSection 7. aClass ofrecommendation. bLevel ofevidence.28 ESC Guidelines
+6.4.2. Non-traditional cardiovascular disease risk modifiers shared bymen andwomen Inaddition tosex-specific risk modifiers, several other non-traditional risk factors are associated with anincreased risk ofCVD, but few have been shown toimprove risk prediction ordiscrimination beyond traditional CVD risk factors. We advise considering high-CVD-risk race/ethnicity (e.g. South Asian),186–188family history ofpremature onset atherosclerotic CVD (CVD event inmales aged <55 years and/or females <65years),189,190socio-economic deprivation,191inflammatory condi- tions (e.g. systemic lupus erythematosus, rheumatoid arthritis, and psoriasis affecting 10% ormore ofbody surface area orrequir- ing systemic therapy),192–202HIV,203–205and severe mental illness (major depressive disorder, bipolar disorder, and schizophre- nia)206–208asshared non-traditional risk modifiers toup-classify the risk ofindividuals with aborderline increased 10-year pre- dicted risk using SCORE2/SCORE2-OP (5% to<10%) tosufficient- lyhigh CVD risk. Sex-specific modifiers  (Class IIa) Shared modifiers (Class IIa)  High-risk ethnicity Gestational hypertensionGestational diabetes Pre-eclampsia Pre-term delivery One or more stillbirth Recurrent miscarriageFamily history of  premature onset ASCVD Socio-economic deprivation Auto-immune inflammatory diseases Severe mental illnessRisk modifiers HIV Figure 8Cardiovascular disease risk modifiers toconsider forup-classification ofrisk. ASCVD, atherosclerotic cardiovascular disease; HIV, human immunodeficiency virus.ESC Guidelines 29
+6.4.3. Additional riskdecision tests Coronary artery calcium (CAC) scoring improves CVD risk prediction and reclassifies risk when added toconventional CVD risk factor-based estimation models.209,210ACAC score of>100 Agatston units or ≥75th percentile for age, sex, and ethnicity favours up-classification ofCVD risk.127Internal orexternal carotid plaque may also improve CVD risk prediction.211Similarly, femoral artery plaque detection may improve CVD risk prediction.212–214Arterial stiffness, asassessed bypulse wave velocity (PWV), isassociated with increased risk ofCVD events and improves CVD risk stratification.215–218Common arterial stiffness thresholds for increased risk include carotid–femoral PWV of>10 m/s and brachial–ankle PWV of>14 m/s. After assessing 10-year predicted CVD risk and non-traditional risk factors, ifarisk- based treatment decision remains uncertain forpatients with elevated BP, itisreasonable tomeasure aCAC score or,alternatively, carotid or femoral plaque, or arterial stiffness; most especially after shared decision-making with the patient and after considering cost (see Section 7for more details onthese tests). There isalso evidence that elevated cardiac biomarker levels (specifically high-sensitivity cardiac troponin and B-type natriuretic peptide/N-terminus B-type natriuretic peptide) are significant and effective risk modifiers,219,220with further supportive data from hypertensive participants.159,221,222Of note, these cardiac biomarkers can be considered markers ofHMOD (Section 7);however, wefocus onthem inthis risk modifier section be- cause they may beelevated due toother reasons besides high BP(such asatherosclerosis orheart rhythm disease).6.5.Summary ofthecardiovascular disease riskstratification approach forallocating blood pressure treatment Measured BPcombined with 10-year CVD risk-prediction models and non-traditional risk modifiers should beused forstratifying risk when allo- cating BP-lowering treatment forpersons with elevated BP(Figure 9).Itis important tostress here that patients with confirmed hypertension arere- commended toreceive BP-lowering treatment and nofurther risk strati- fication isneeded. For patients with elevated BP, the presence ofdiabetes, familial hypercholesterolaemia, established CVD (defined asprior acute or chronic coronary syndrome, cerebrovascular disease, symptomatic peripheral arterial disease, or heart failure), moderate or severe CKD, orHMOD confers increased CVD risk. One caveat isthat, spe- cifically forindividuals with elevated BPand type 2diabetes mellitus only aged <60 years, SCORE2-Diabetes should beconsidered toidentify lower CVD risk individuals (<10% over 10years). Otherwise, forpatients without these high-risk conditions, 10-year risk ofCVD should becalculated using SCORE2 (ifaged 40–69 years) and SCORE2-OP (ifaged ≥70 years). Patients with elevated BP and a 10-year predicted risk ofCVD events ≥10% are considered sufficiently high risk towarrant BP-lowering treatment (either bylifestyle ordrug treatment, seeSection 8).For patients with elevated BPand borderline in- creased predicted CVD risk bySCORE2/SCORE2-OP (5% to<10% over 10years), up-classification ofrisk may beconsidered inthe presence of sex-specific orshared non-traditional risk modifiers. After considering sex-specific and shared non-traditional risk modifiers, ifarisk-based BP-lowering treatment decision remains uncertain, itmay bereasonable tomeasure CAC score, carotid orfemoral plaque, high-sensitivity cardiac troponin orB-type natriuretic peptide biomarkers, orarterial stiffness. Risk stratification for patients with non-elevated BP(systolic BPof <120 mmHg and diastolic BPof<70 mmHg) isnot required for the purpose ofallocating BP-lowering treatment, asthe safety and efficacy ofcommencing BP-lowering treatment below this threshold isuncer- tain. Risk assessment may nonetheless beneeded inthis setting when considering other prevention therapies (e.g. lipid lowering).Recommendation Table 4—Recommendations for refining cardiovascular disease risk (see Evidence Tables 12–14) Recommendation ClassaLevelb History ofpregnancy complications (gestational diabetes, gestational hypertension, pre-term delivery, pre-eclampsia, one ormore stillbirths, and recurrent miscarriage) are sex-specific risk modifiers that should beconsidered toup-classify individuals with elevated BP and borderline increased 10-year CVD risk (5% to<10% risk). 183,184,223,224IIa B High-risk ethnicity (e.g. South Asian), family history of premature onset atherosclerotic CVD, socio-economic deprivation, auto-immune inflammatory disorders, HIV, and severe mental illness are risk modifiers shared byboth sexes that should beconsidered toup-classify individuals with elevated BPand borderline increased 10-year CVD risk (5% to<10% risk).186–191,193,198,202,204,208IIa B ContinuedAfter assessing 10-year predicted CVD risk and non-traditional CVD risk modifiers, ifarisk-based BP-lowering treatment decision remains uncertain for individuals with elevated BP, measuring CAC score, carotid orfemoral plaque using ultrasound, high-sensitivity cardiac troponin orB-type natriuretic peptide biomarkers, orarterial stiffness using pulse wave velocity, may beconsidered toimprove risk stratification among patients with borderline increased 10-year CVD risk (5% to<10% risk) after shared decision-making and considering costs.209–211,215,218,225,226IIb B ©ESC 2024 BP, blood pressure; CAC, coronary artery calcium; CVD, cardiovascular disease; HIV, human immunodeficiency virus. aClass ofrecommendation. bLevel ofevidence.30 ESC Guidelines
+Patient with elevated BPa office SBP 120–139 mmHg or DBP 70–89 mmHg YEstablished CVD, moderate/severe CKD, HMOD, DM, or FH (Class I) N Calculate  SCORE2 or SCORE2-OP (Class I)Patient with T2DM (only) and <60 years old 10-year predicted CVD risk Any of the following: Gestational diabetes Gestational hypertension Pre-eclampsia Pre-term delivery One or more still births Recurrent miscarriageN Consider shared risk modifiers (Class IIa) Any of the following: High-risk ethnicity Family history of premature onset ASCVD Socio-economic deprivation Auto-immune diseases Severe mental illness HIV N If still uncertain, shared decision-making informed by risk tools (Class IIb) Any of the following meeting abnormal criteria: CAC score Carotid or femoral plaque High-sensitivity cardiac troponin NT -proBNP Pulse wave velocity Lifestyle measures to reduce BP (Class I) Reassess risk/BP one year later (Class IIa)N Lifestyle measures to reduce BP (Class I) After 3 months of lifestyle measures, pharmacological treatment for patients with ≥130/80 mmHg  (Class I)YN Y Y Calculate SCORE2- Diabetes (Class IIa)Y  <5% 5% – <10%≥10%  Consider sex-specific risk modifiers (Class IIa) aExercise caution when considering treating persons with elevated BP and; Moderate-to-severe frailty Symptomatic orthostatic hypotension Age ≥85 yearsFigure 9Summary ofcardiovascular disease risk-stratification approach forblood pressure treatment inadults with elevated blood pressure. ASCVD, atherosclerotic cardiovascular disease; BP, blood pressure; CAC, coronary artery calcium; CKD, chronic kidney disease; CVD, cardiovascular disease; DBP, diastolic blood pressure; DM, diabetes mellitus; FH, familial hypercholesterolaemia; HMOD, hypertension-mediated organ damage; NT-proBNP, N-terminal pro-brain natriuretic peptide; SBP, systolic blood pressure; SCORE2, Systematic COronary Risk Evaluation 2;SCORE2-OP, Systematic COronary Risk Evaluation 2–Older Persons.ESC Guidelines 31
+7.Diagnosing hypertension and investigating underlying causes 7.1.Screening forhypertension Hypertension ispredominantly anasymptomatic condition that istyp- ically detected bysystematic oropportunistic screening inahealthcare setting. Systematic screening refers toany process where individuals are identified and invited toahealthcare setting solely tomeasure their BPand CVD risk profile. Opportunistic screening refers toBPbeing measured when the patient presents toahealthcare setting forany rea- son, such asaroutine check-up orthe treatment ofanacute orchronic condition. Self-screening and non-physician screening are also increas- ingly used.227–230 Few data are available onthe effectiveness ofdifferent hypertension screening strategies toreduce the morbidity and mortality associated with hypertension.231–233More evidence isneeded before systematic screening programmes with BPmeasurement can berecommended inalladults toreduce CVD events.231 Opportunistic BPscreening inaprimary care setting appears effect- ive, with anestimated 90% ofalladults aged >40 years inthe UK having aBPcheck within a5-year time period,234though these findings may not extrapolate toother countries. When patients provide HBPM re- cordings, these can also beused aspart ofanopportunistic screening programme (seeSection 5.2).235 Despite ongoing uncertainty about the effect ofhypertension screening programmes on CVD outcomes, many studies have de- monstrated that screening (mostly opportunistic screening) in- creases hypertension detection, and that the benefits ofscreening likely outweigh harms.70Global initiatives toraise BP awareness, such asthe May Measurement Month,228ortargeted initiatives, such asthe barbershop health outreach programmes,229are success- fulexamples ofBPscreening campaigns. Screening for hypertension, like for global CVD risk assessment, should beintermittently repeated, e.g. every 3years. Considering the rate ofprogression tohypertension inEuropean population samples,236itisreasonable tomeasure BP atleast every 3years inthe case ofnon-elevated BPand low–moderate CVD risk (i.e. in- dividuals aged <40 years). More frequent BP checks (i.e. yearly) should beconsidered inindividuals 40years orolder and individuals with elevated BPnot currently meeting indications for treatment170 (Figure 10).7.2.Confirming thediagnosis of hypertension Asnoted inSection 5,assessment atasingle visit byoffice BPhas lower specificity compared with ABPM for diagnosing hypertension.70,238–241 Accordingly, aprotocol for confirming the diagnosis ofhypertension is proposed (Figure 10), with out-of-office BP measurement asthe preferred method forconfirming cases ofelevated BPorhypertension. For initial screening systolic BP of>160 mmHg and/or diastolic BPof>100 mmHg, aprompt re-evaluation (within days toweeks but not >1month) preferably with ABPM or HBPM isadvisable.71 BP of>180/110 mmHg at screening requires exclusion of hypertensive emergencies, which should bemanaged asappropriate (see242andSection 10) with prompt treatment. For individuals with BPof>180/110 mmHg atscreening but without hypertensive emer- gency, prompt confirmation (preferably within aweek) can beconsid- ered prior tocommencing treatment. Recommendation Table 5—Recommendations for blood pressure screening (see Evidence Table 15) Recommendation ClassaLevelb Opportunistic screening for elevated BPand hypertension should beconsidered atleast every 3 years for adults aged <40 years.236,237IIa C Opportunistic screening for elevated BPand hypertension should beconsidered atleast annually for adults aged ≥40 years.231,237IIa C Inindividuals with elevated BPwho donot currently meet risk thresholds for BP-lowering treatment, a repeat BPmeasurement and risk assessment within 1 year should beconsidered.IIa C ContinuedOther forms ofscreening for hypertension (i.e. systematic screening, self-screening, and non-physician screening) may beconsidered, depending ontheir feasibility indifferent countries and healthcare systems.231–233IIb B ©ESC 2024 BP, blood pressure. aClass ofrecommendation. bLevel ofevidence. Recommendation Table 6—Recommendations for confirming hypertension diagnosis Recommendations ClassaLevelb Inindividuals with increased CVD risk where their screening office BPis120–139/70–89 mmHg, itis recommended tomeasure BPout ofoffice, using ABPM and/or HBPM or,ifnot logistically feasible, by making repeated office BPmeasurements onmore than one visit.70,238–241I B Where screening office BPis140–159/90–99 mmHg, itisrecommended that the diagnosis of hypertension should bebased onout-of-office BP measurement with ABPM and/or HBPM. Ifthese measurements are not logistically oreconomically feasible, then diagnosis can bemade onrepeated office BPmeasurements onmore than one visit.70,238–241I B Where screening office BPis≥160/100 mmHg: •Itisrecommended that BP160–179/100–109 mmHg beconfirmed assoon aspossible (e.g. within 1month) preferably byeither home or ambulatory BPmeasurements; •Itisrecommended when BP≥180/110 mmHg that hypertensive emergency beexcluded.I C ©ESC 2024 ABPM, ambulatory blood pressure measurement; BP, blood pressure; CVD, cardiovascular disease; HBPM, home blood pressure measurement. aClass ofrecommendation. bLevel ofevidence.32 ESC Guidelines
+7.3.Communicating thediagnosis Behavioural responses tohealth-related threats are strongly influ- enced byfive core themes (termed ‘illness representations’), which are identity, timeline, cause, consequences, and control/cure.243,244 These illness representations form the basis ofhow patients under- stand adiagnosis, and can influence their responses after being diag- nosed with hypertension.243This conceptual framework can help guide the clinical communication ofadiagnosis ofhypertension. For example, patients’ understanding ofthe chronic nature ofhyper- tension (i.e. timeline theme) iskey for ensuring long-term engage- ment with medical treatment.245Prior tocommencing treatment, itishelpful tounderstand the extent towhich patients believe that medications are necessary and ascertain ifthey have concerns.246 The core illness representations and beliefs about medicines forclin- icians toconsider are included inTable 7. The 2021 ESC Guidelines oncardiovascular disease prevention in clinical practice recommend “an informed discussion about CVD riskand treatment benefits—tailored tothe needs ofapatient” aspart ofadiagnosis communication inhypertension.170This can befacilitated using aninterdisciplinary healthcare-provided approach (seeSection 11) and byvisual information orother more accessible material that might optimally communicate hypertension-related risk.128Visualizing risk by medical imaging tomotivate risk-reducing behaviour changes may also bebeneficial.247 7.4.Baseline assessment anddiagnostic approach 7.4.1. Medical history, medication history, and physical examination The purpose ofclinical evaluation istodiagnose hypertension, delineate factors potentially contributing tohypertension, identify other CVD risk factors, define relevant comorbidities, screen forpotential second- ary causes ofhypertension (where indicated), and establish whether N Y N  YScreening for hypertension by office BP High CVD risk conditions or SCORE2/SCORE2-OP ≥10% or SCORE2/SCORE2-OP 5% – <10%  + risk modifiers  ≥40 years? Non-elevated BP <120/70 mmHgElevated BP 120–139/70–89 mmHgHypertension 140–159/90–99 mmHgHypertension 160–179/100–109 mmHgHypertension ≥180/110 mmHg Opportunistic BP screening at least every 3 years (Class IIa)Opportunistic BP screening at least every year (Class IIa)Evaluate for hypertensive emergency (Class I)Confirm BP preferably with either home or ambulatory BP measurements (Class I)Confirm BP promptly preferably with either home or ambulatory BP measurements (Class I)Figure 10 Protocol for confirming hypertension diagnosis. BP, blood pressure; CVD, cardiovascular disease; SCORE2, Systematic COronary Risk Evaluation 2;SCORE2-OP, Systematic COronary Risk Evaluation 2–Older Persons.ESC Guidelines 33
+there isevidence ofHMOD orexisting cardiac, cerebrovascular, orre- naldisease. Details onmedical history and physical examination steps are sum- marized inthe supplement (see Supplementary data online, Tables S2 andS3), aswell asdrugs orsubstances that may increase BP (see Supplementary data online, Table S4). 7.4.2. Drug adherence andpersistence with treatment Adherence isdefined asthe extent towhich apatient’s behaviour, e.g. with respect totaking medication, coincides with agreed recommenda- tions from ahealthcare provider. Persistence represents the amount of time from initiation todiscontinuation oftherapy.248Adherence tomed- icaltherapies isespecially suboptimal inasymptomatic conditions such as hypertension.249–254Non-adherence toBP-lowering therapy correlates with ahigher risk ofCVD events.255,256Objective methods toassess ad- herence, such asdetecting prescribed drugs inblood orurine samples and directly observed treatment (witnessed pillintake during ABPM), have de- monstrated their potential usefulness, particularly inthe setting ofappar- ently resistant hypertension.257However, allmethods for testing drug adherence have limitations. Non-adherence toBP-lowering therapy depends on many factors (Figure 11).253Effective patient–physician communication iscrucial toim- prove adherence.258,259Single-pill combinations improve persistence in BP-lowering treatment and areassociated with lower all-cause mortality.2607.4.3. Routine andoptional tests Routine tests include laboratory and clinical tests todetect increased CVD risk and relevant comorbidities (e.g. hyperlipidaemia and diabetes) (Table 8). Optional tests should beconsidered inthe initial assessment ifthey are likely tochange patient management, with the main rationale being toimprove CVD risk stratification.170Ashighlighted inSection 6,for adults with elevated BPwho also have a10-year estimated CVD risk of5%to<10%, optional tests including those forHMOD may becon- sidered ifup-classification ofrisk onthe basis ofanabnormal test result could prompt initiation ofBP-lowering therapy.31,170Evidence ofsub- clinical microvascular neurodegeneration and/or lacunar brain disease due tosmall-vessel pathology may also indicate HMOD.264Table 7Keyillness representations andtreatment beliefs: how these apply tocommunicating ahypertension diagnosis tothepatient (note that gender influences these representations) Illness representationExample patient question Application toahypertension diagnosis conversation Identity What isthe disease/illness label and the related symptoms?The condition where your systolic BPis≥140 and/or diastolic BP≥90 mmHg iscalled hypertension. We classify systolic BP120–139 ordiastolic BP70–89 mmHg aselevated BP. For most people, this has nonoticeable signs or symptoms, therefore, we need tomonitor your BPtoassess how medications and behavioural changes are working. Control Isthe illness controllable through medical intervention orbehavioural change?Hypertension can usually becontrolled with medication and behavioural changes such as dietary changes and regular physical activity. For some people we need totryafew different options before we get BPunder control. Timeline Isthis anacute orchronic problem? This isaserious long-term orchronic condition condition that will require long-term management. This means that itmay need tobemanaged throughout life. Consequences What are the physical and psychosocial consequences?Ifhypertension isnot controlled, then there isarisk ofaserious acute cardiovascular disease event such asastroke orheart attack; however, ifitismanaged through the right medical intervention and behavioural changes, then this risk can bereduced and the condition will have less consequences for your life. Causes What caused the condition? Multiple factors contribute tosomeone developing hypertension. These include both non-modifiable factors (e.g. genetics and age) and modifiable factors (e.g. diet, weight, and physical activity). We are best focusing onthose things that we can control to reduce your BP. Treatment beliefs Example patient question Application toahypertension diagnosis communication Necessity Towhat extent istreatment necessary? Taking BP-lowering medication every day isnecessary tokeep your BPunder control and tohelp prevent amore serious health problem developing. Do you think that these medicines will help you? Concerns Towhat extent does treatment cause concern?Some patients have concerns about taking daily medications throughout their life, e.g. about side effects. Do you have any concerns about taking your BPmedications every day? ©ESC 2024 BP, blood pressure. Recommendation Table 7—Recommendations for assessing adherence and persistence with treatment (see Evidence Table 16) Recommendation ClassaLevelb Objective evaluation ofadherence (either directly observed treatment ordetecting prescribed drugs in blood orurine samples) should beconsidered inthe clinical work-up ofpatients with apparent resistant hypertension, ifresources allow.261–263IIa B ©ESC 2024 aClass ofrecommendation. bLevel ofevidence.34 ESC Guidelines
+While the role ofoptional tests for HMOD (Table 9)inthe man- agement ofelevated BPisemphasized inthese guidelines, we also note that these tests may help tooptimize treatment inhyperten- sive adults with BP of>140/90 mmHg who are prescribed BP-lowering therapy (e.g. by facilitating patient adherence andovercoming clinician inertia inachieving anintensive BPtreatment target ofaslow as120 mmHg systolic). The role ofvisualizing HMOD inhelping motivate risk-reducing changes inpatients and overcome physician inertia has been tested ininterventional trials (Section 7.3).247,265–267 Non-adherence definition Assessment Intervention Non-adherence definition Assessments Intervention 1 2 3Patient does not initiate medication Prescription fill data and self-report Communicate benefits/safety of medication; alleviate fear of side effects/harm; discuss practicalities Patient does not take medication as prescribed Prescription refill data; self-report; electronic monitoring;  chemical adherence testing (blood/urine) Reminders; encourage habit formation; simplify drug regimen Patient discontinues medication Prescription refill data; self-report; electronic monitoring; chemical adherence testing (blood/urine) Motivational counseling on benefits/safety of medication;  discuss side effects; medication reconciliation; review practical aspects (cost and ease of access to medication)Non-adherence definition Assessment InterventionInitiation Implementation PersistenceFigure 11 Definitions, assessments, and potential interventions for the three phases ofadherence toBP-lowering medications. Table 8Routine tests recommended intheinitial work-up ofapatient with elevated blood pressure orhypertension Routine test Clinical utility Fasting blood glucose (and HbA1c iffasting blood glucose is elevated)Assessing CVD risk and comorbidities Serum lipids: total cholesterol, LDL cholesterol, HDL and non-HDL cholesterol, triglyceridesAssessing CVD risk Blood sodium and potassium, haemoglobin and/or haematocrit, calcium, and TSHScreening secondary hypertension (primary aldosteronism, Cushing’s disease, polycythaemia, hyperparathyroidism, and hyperthyroidism) Blood creatinine and eGFR; urinalysis and urinary albumin-to-creatinine ratioAssessing CVD risk and HMOD Guiding treatment choice Screening secondary hypertension (renoparenchymal and renovascular) 12-lead ECG Assessing HMOD (left atrial enlargement, left ventricular hypertrophy) Assessing irregular pulse and other comorbidities (AF, previous acute myocardial infarction) ©ESC 2024 AF, atrial fibrillation; CVD, cardiovascular disease; ECG, electrocardiogram; eGFR, estimated glomerular filtration rate; HbA1c, glycated haemoglobin; HDL, high-density lipoprotein; HMOD, hypertension-mediated organ damage; LDL, low-density lipoprotein; TSH, thyroid-stimulating hormone.ESC Guidelines 35
+HMOD assessment isalso animportant way toidentify young adults <40 years old who have increased CVD risk, since 10-year estimated CVD risk bySCORE2 cannot becalculated inthis age group (see Section 8.1). More details ondiagnostic thresholds for HMOD bythe various assessment options, including important sex differences, are provided inSupplementary data online, Tables S1andS5andFigure 12. Finally, some individuals may beatheightened risk for CVD events when cardiac and vascular HMOD measurements like LVH and increased PWV donot regress over time with appropriate treatment and BPcontrol.14,268–271 Investigations aimed atscreening for secondary hypertension are additional optional tests and aredetailed inSection 7.6. Ofnote, patients with anincidental adrenal nodule ornodules (typically detected onim- aging ofthe abdomen done forother clinical reasons) warrant screen- ing for elevated BP and hypertension. Those with adrenal incidentalomas and hypertension warrant abasic work-up forsecond- ary hypertension toinclude screening for primary aldosteronism, Cushing’s syndrome and phaeochromocytoma. 7.4.3.1. Thekidneys CKD isdefined asabnormalities ofkidney structure orfunction, pre- sent foratleast 3months with implications forhealth.272Renal function isevaluated initially using serum creatinine and anestimated glomerular filtration rate (eGFR) equation (preferably race-free CKD-EPI) and typ- ically forproteinuria.273Our definition ofmoderate-to-severe CKD re- quires aneGFR of<60 mL/min/1.73 m2oralbuminuria of≥30 mg/g (≥3 mg/mmol). Intensive BPcontrol inpatients with CKD reduces ratesofCVD events.274,275CKD can influence the choice ofBP-lowering treatment (Sections 8and9),aswell asnewer drugs forcardiovascular prevention, such assodium–glucose co-transporter 2(SGLT2) inhibi- tors and finerenone. We recommend repeat measurement ofeGFR and urine albumin: creatinine ratio (ACR) atleast annually ifclinically significant CKD isdi- agnosed. Renal ultrasound and Doppler examination toevaluate causes ofCKD and toexclude renoparenchymal and renovascular hyperten- sion (RVH) should also beconsidered.276,277 7.4.3.2. Theheart A12-lead ECG isapart ofthe initial routine work-up forallpatients with hypertension and should berepeated whenever patients present with an irregular pulse orcardiac symptoms. The ECG should beanalysed for LVH (Supplementary data online, Table S1) and AF.31,278–282 Echocardiography isrecommended inpatients with hypertension when the ECG isabnormal, murmurs are detected, orthere are cardiac symptoms. Afull, standardized, two-dimensional echocardiogram should beperformed, preferably with tissue Doppler and strain assessment. Echocardiography can beconsidered for allpatients with newly diag- nosed hypertension, iflocal resources and reimbursement policies allow. Over 5years offollow-up, subclinical leftventricular diastolic dysfunction predicts the incidence ofCVD.283–285Inaddition, LVH detected byecho- cardiography predicts total and cardiovascular mortality and CVD events inthe general population,286,287including inyoung adults.26,268,288,289 Data on the associations with CVD ofother metrics for detecting HMOD intheheart arealso available.26,268,290Since cardiac size and func- tion differ bysex, sex-specific thresholds for detecting HMOD inthe heart are used toavoid under-diagnosis inwomen.25,174,291Table 9Optional tests that may beused asclinically indi- cated intheinitial work-up ofapatient with elevated blood pressure orhypertension toassess hypertension-mediated organ damage orestablished cardiovascular disease Optional test Clinical utility Echocardiography Assessing HMOD (hypertensive heart disease) Assessing established CVD (previous acute myocardial infarction, heart failure) Assessing thoracic aorta dilation CAC bycardiac CT orcarotid or femoral artery ultrasound imagingAssessing HMOD (atherosclerotic plaque) Large artery stiffness (carotid– femoral orbrachial–ankle PWV)Assessing HMOD (arterial stiffness) High-sensitivity cardiac troponin and/or NT-proBNPAssessing HMOD Ankle–brachial index Assessing established CVD (lower-extremity arterial disease) Abdominal ultrasound Assessing established CVD (abdominal aneurysm) Fundoscopy Assessing HMOD (hypertensive retinopathy) Diagnosing hypertensive emergency/ malignant hypertension (haemorrhages and exudates, papilloedema) ©ESC 2024 CAC, coronary artery calcium; CT, computed tomography; CVD, cardiovascular disease; HMOD, hypertension-mediated organ damage; NT-proBNP, N-terminal pro-brain natriuretic peptide; PWV, pulse wave velocity.Recommendation Table 8—Recommendations for assessing renal hypertension-mediated organ damage Recommendation ClassaLevelb Itisrecommended tomeasure serum creatinine, eGFR, and urine ACR inallpatients with hypertension.170,273I A Ifmoderate-to-severe CKD isdiagnosed, itis recommended torepeat measurements ofserum creatinine, eGFR, and urine ACR atleast annually.276I C Renal ultrasound and Doppler examination should beconsidered inhypertensive patients with CKD to assess kidney structure and determine causes of CKD and toexclude renoparenchymal and renovascular hypertension.276,277CT ormagnetic resonance renal angiography are alternative testing options.IIa C ©ESC 2024 ACR, albumin:creatinine ratio; CKD, chronic kidney disease; CT, computed tomography; eGFR, estimated glomerular filtration rate. aClass ofrecommendation. bLevel ofevidence. Recommendation Table 9—Recommendations for assessing cardiac hypertension-mediated organ damage Recommendation ClassaLevelb A12-lead ECG isrecommended forallpatients with hypertension.31,281I B Continued36 ESC Guidelines
+7.4.3.3. Thearteries Cardiac computed tomography (CT) may beused tomeasure CAC and, ifintravascular contrast isadministered, fully visualize coronary artery disease to improve risk stratification.211,293As noted in Section 6,CAC scoring can reclassify CVD risk upwards ordown- wards in addition to conventional risk factors.127,170,211,233,294 Carotid ultrasound detects presence orabsence ofcarotid plaque (wall thickness ≥1.5mm) and stenosis. Presence ofplaque inthe ca- rotid orfemoral arteries improves risk prediction for CVD events in asymptomatic patients on top ofconventional risk-factor assess- ment.211,247,265,267,295,296Systematic use ofintima media thickness does not appear toconsistently improve prediction offuture CVD events.297Arterial stiffness ismeasured ascarotid–femoral PWV or brachial–ankle PWV, and can contribute topredictive value and risk reclassification.28,31,215,216PWV iscurrently used mostly forresearch purposes orinspecialist referral centres. Checking for inter-arm BP difference may identify asubclavian stenosis asvascular HMOD.38 Other tests assessing the vasculature [such asabdominal ultrasound orankle–brachial index (ABI)] should also beconsidered inpatients with hypertension, when specific cardiovascular complications (ab- dominal aneurysm, peripheral artery disease) are clinically suspected. Finally, microvascular HMOD can beassessed byfundoscopy. Asim- plified classification has been proposed and validated.298Inhyperten- sive individuals, the presence ofmild or moderate hypertensive retinopathy isassociated with anincreased risk ofCVD events.299 Fundoscopy isrecommended also inhypertensive diabetic patients and inthe work-up ofmalignant hypertension and hypertensive emergencies.7.4.4. Genetic testing Hypertension isconsidered acomplex polygenic disorder, because many genes orgene combinations influence BP.300,301However, some well-defined phenotypes relating tosingle-gene mutations (i.e. mono- genic forms ofhypertension) have been identified (see Supplementary data online, Table S6). These are rare, but knowledge ofthe genetic defect may allow targeted treatment ofthe proband and also proper management ofthe patient’s siblings.302,303As such, genetic testing should beconsidered only forthose with ahigh prior probability ofhav- ingamonogenic condition and such patients should bereferred tospe- cialized centres. Inmost patients with elevated BP orhypertension, routine genetic testing isnot recommended. Family history and apedi- gree analysis can help tofind aheritable pattern ofhypertension or hypotension.304 7.5.Resistant hypertension: definition and diagnosis Despite availability and use ofmultiple BP-lowering medications, many patients worldwide have uncontrolled hypertension.306–308 Considering this, societies have introduced the term ‘drug-resistant hypertension’, or‘treatment-resistant hypertension’, or‘resistant hypertension’,309which has been reported in10%–20% ofpatients with hypertension.310,311 Resistant hypertension isnot adisease perse.Compared with treated patients who achieve BP control, patients with resistant hypertension (by any definition) have aworse prognosis: risk of myocardial infarction, stroke, end-stage renal disease, and death inthese adults may betwo- tosix-fold higher.309Secondary causes ofhypertension are also more likely inthe presence ofresistant hypertension.312 Allresistant hypertension definitions require adiuretic intheprescribed multiple-drug regimen, because excess saltintake and saltand water reten- tion arekey players inresistance toBP-lowering treatments (Table 10).309Echocardiography isrecommended inpatients with hypertension and ECG abnormalities, orsigns or symptoms ofcardiac disease.14,31,292I B Echocardiography may beconsidered inpatients with elevated BP, particularly when itislikely to change patient management.31,291IIb B ©ESC 2024 BP, blood pressure; ECG, electrocardiogram. aClass ofrecommendation. bLevel ofevidence. Recommendation Table 10—Recommendations for assessing vascular hypertension-mediated organ dam- age(see Evidence Table 17) Recommendations ClassaLevelb Fundoscopy isrecommended ifBP>180/110 mmHg inthe work-up ofhypertensive emergency and malignant hypertension, aswell asinhypertensive patients with diabetes.I C Fundoscopy for detecting hypertensive retinopathy may beconsidered inpatients with elevated BPor hypertension.299IIb B Ultrasound examination ofthe carotid orfemoral arteries for detecting plaque may beconsidered in patients with elevated BPorhypertension when itis likely tochange patient management.211IIb B ContinuedCoronary artery calcium scoring may beconsidered inpatients with elevated BPorhypertension when it islikely tochange patient management.127,211IIb B Measurement ofPWV may beconsidered inpatients with elevated BPorhypertension when itislikely to change patient management.28,31,215,216IIb B ©ESC 2024 BP, blood pressure; PWV, pulse wave velocity. aClass ofrecommendation. bLevel ofrecommendation. Recommendation Table 11—Recommendations for genetic testing inhypertension management Recommendations ClassaLevelb Genetic testing should beconsidered inspecialist centres for patients suspected tohave rare monogenic causes ofsecondary hypertension orfor those with phaeochromocytoma/ paraganglioma.302,305IIa B Routine genetic testing for hypertension isnot recommended.III C ©ESC 2024 aClass ofrecommendation. bLevel ofevidence.ESC Guidelines 37
+Coronary artery calcium score >100 Agatston unitsCarotid-femoral PWV >10 m/s Brachial-ankle PWV >14 m/sPlaque (focal wall thickening >1.5 mm)Cornell voltage: SV3+RaVL>28 mm (men)  SV3+RaVL>20 mm (women)RaVL ≥11 mmSokolow–Lyon: SV1+RV5 >35 mm Cardiac CTPulse wave velocityCarotid or femoral ultrasoundCardiac biomarkersEchocardiographyECGeGFR ACRModerate-to-severe kidney disease LVH LVH Diastolic dysfunctionLV mass/height2.7(g/m2.7):>50 (men) >47 (women) LV mass/BSA(g/m2): >115 (men) >95 (women) RWT ≥0.43 LV concentric geometry: LA volume/height2 (mL/m2):>18.5 (men) >16.5 (women) LA volume index (mL/m2): 34 e’ <7cm; E/e’ >14 hs-cTnT or I >99th percentile upper reference limit NT -proBNP >125 pg/mL if age <75 years or >450 pg/mL if ≥75 yearseGFR <60 mL/min/1.73 m2 irrespective of albuminuria Albuminuria ≥30 mg/g irrespective of eGFR Assistance overcoming patient and physician inertiaIndividuals <40 years old with elevated blood pressureUncertain situations (i.e. BP or risk close to thresholds, masked or white-coat hypertension, non-traditional CVD risk factors)Individuals with elevated BP with SCORE2/SCORE2-OP risk of 5–<10%Support decision to start or intensify BP- lowering treatment for:Why measure? How to diagnose HMOD? What to measure? Which organ? Kidney Heart Arteries Figure 12 Tests and criteria for defining hypertension-mediated organ damage and considerations for their use inclinical practice. ACR, albumin: creatinine ratio; BP, blood pressure; BSA, body surface area; CT, computed tomography; CVD, cardiovascular disease; ECG, electrocardiogram; eGFR, estimated glomerular filtration rate; HMOD, hypertension-mediated organ damage; hs-cTnT, high-sensitivity cardiac troponin T;LA, left atrial; LV, left ventricular; LVH, left ventricular hypertrophy; NT-proBNP, N-terminal pro-brain natriuretic peptide; PWV, pulse wave velocity; RWT, relative wall thickness; SCORE2, Systematic COronary Risk Evaluation 2;SCORE2-OP, Systematic COronary Risk Evaluation 2–Older Persons. More details and references can befound inthe Supplementary data online, Tables S1andS5.38 ESC Guidelines
+Inaddition, excluding pseudo-resistance isaprerequisite. Specifically, pseudo-resistance indicates poor adherence toBP-lowering treatment, which should beverified bycareful questioning ofthe patient inthe first instance (Section 7.4.3).257Inaddition, white-coat hypertension must be excluded.263Contributors topseudo-resistance are listed inTable 11. Objective evaluation ofadherence (either directly observed treatment ordetecting prescribed drugs inblood orurine samples) should also beconsidered, ifresources allow. The work-up ofpatients presumed tohave resistant hypertension is complex and often requires technologies that are not available to GPs.257,309Accordingly, we recommend these patients are referred tospecialized centres. 7.6.Secondary hypertension: when to screen/further investigations 7.6.1. General considerations Secondary hypertension ismore prevalent than previously thought (Figures 13–15).312–317Depending on the definition used and the cohort studied, the prevalence ofsecondary hypertension is10%–35% in allhypertensive patients318,319and upto50% ofpatients with resistant hypertension (though the latter prevalence estimate included persons with eGFR <40mL/min/1.73 m2).312Primary aldosteronism isacommon cause,315,320with, e.g. ahigh prevalence ofhyperaldosteron- ism (up to12%) observed inpatients with BPof>180/110 mmHg.316 Despite these numbers, screening rates for primary aldosteronism, even inhigh-risk groups such asthose with resistant hypertension321 and hypokalaemia,322are low (around 2% and 4% ofeligible patients, respectively). Inmost healthcare systems, GPs are typically the ‘gate- keeper’ ofaccess tospecialized care and should beinvolved inscreen- ing patients for common causes ofsecondary hypertension, especially sleep apnoea and primary aldosteronism (Supplementary data online, Tables S2andS3). Primary aldosteronism isassociated with anincreased risk ofCVD events, which may bepartly independent ofBP.323,324 7.6.2. Primary aldosteronism Though spontaneous ordiuretic-induced hypokalaemia are strongly suggestive ofprimary aldosteronism, ahistory ofhypokalaemia is not present inmost patients diagnosed with this condition. The aldosterone-to-renin ratio (ARR) isthus recommended for primary aldosteronism screening (seeFigure 13).325This test can easily bedone intreatment-naïve patients, though itisfar more common for the ARR test tobeconsidered when patients are already being treated for elevated BPorhypertension. This isrelevant because ARR can beinflu- enced bythe drugs being taken atthe time oftesting. Accordingly, there are 2approaches toscreen foraldosteronism among patients who are already undergoing treatment forelevated BPorhypertension: •The first istoconduct ARR testing intreated patients with anindication foraldosteronism screening asefficiently aspossible and without chan- ging orstopping their baseline BP-lowering medications, simply tofacili- tate such testing. The ARR result then needs tobeinterpreted inthe context ofthe specific medication(s) the patient istaking. Advantages ofthis approach include reducing barriers toscreening and nochange inmedication inthese patients, many ofwhom donot have BPcon- trolled and inwhom further deterioration intheir BPcontrol bystop- ping orchanging medication may increase risk ofCVD. Disadvantages include theinterpretation oftheARR result, which depends onthespe- cific medications taken atthe time oftesting.326Input from ahyperten- sion specialist orendocrinologist may benecessary.Recommendation Table 12—Recommendations for resistant hypertension work-up (see Evidence Table 18) Recommendation ClassaLevelb Patients with resistant hypertension should be considered forreferral toclinical centres with expertise inhypertension management forfurther testing.309,312IIa B ©ESC 2024 aClass ofrecommendation. bLevel ofevidence.Table 10 Current definition ofresistant hypertension Definition ofresistant hypertension Hypertension isdefined asresistant when atreatment strategy including appropriate lifestyle measures and treatment with maximum ormaximally tolerated doses ofadiuretic (thiazide orthiazide-like), aRAS blocker, and a calcium channel blocker failtolower office systolic and diastolic BPvalues to <140 mmHg and/or <90 mmHg, respectively. These uncontrolled BPvalues must beconfirmed byout-of-office BPmeasurements (HBPM orABPM— Section 5.1 for relevant BPthresholds). Key considerations •Resistant hypertension isnot adisease, but anindicator that should be used toidentify patients athigh risk for CVD, inwhich secondary hypertension isalso frequent; •Pseudo-resistant hypertension must beexcluded, including that caused by non-adherence totreatment; •Inpatients with decreased eGFR (i.e.<30 mL/min/1.73 m2)anadequately up-titrated loop diuretic isnecessary todefine resistant hypertension; •Patients with suspected resistant hypertension should bereferred to specialized centres; •These ESC Guidelines donot include the terms ‘controlled resistant hypertension’ (BP attarget but requiring ≥4 medications) or‘refractory hypertension’ (BP not attarget despite ≥5 medications). ©ESC 2024 ABPM, ambulatory blood pressure monitoring; BP, blood pressure; CVD, cardiovascular disease; eGFR, estimated glomerular filtration rate; HBPM, home blood pressure monitoring; RAS, renin–angiotensin system.Table 11 Conditions found tocause pseudo-resistance orresistance toblood pressure-lowering treatment Causes ofpseudo-resistant hypertension Poor adherence toand persistence with treatment White-coat phenomenon Poor BPmeasurement method Marked brachial artery calcification (Osler phenomenon) Clinician inertia (inadequate doses, inappropriate combinations of BP-lowering drugs) Munchausen syndrome (rare) Causes ofresistant hypertension Behavioural factors Overweight/obesity Physical inactivity Excess daily dietary sodium Excess habitual alcohol consumption Useofdrugs orsubstances thatmayincrease BP See Supplementary data online, Table S4 Undetected secondary hypertension SeeTable 13 ©ESC 2024 BP, blood pressure.ESC Guidelines 39
+•To reliably estimate renin and aldosterone status (and therefore ARR), and tofacilitate a‘clean’ screen for aldosteronism, asecond approach istodiscontinue drugs that affect these variables when- ever feasible before ARR testing (Table 12). Such interfering drugs include, beta-blockers, centrally acting drugs (e.g., clonidine and alpha-methyldopa) renin-angiotensin system (RAS) blockers and diuretics.326Long-acting calcium channel blockers (CCBs), either di- hydropyridine ornon-dihydropyridine, and alpha-receptor antago- nists do not interfere with the ARR and can beused instead of interfering medications before ARR testing. Should drugs that do not interfere with the ARR becontraindicated orinsufficient tocon- trol BP,centrally acting sympatholytic drugs can also then beused, but atthe risk ofslightly more false positives (by renin suppression). Furthermore, when mineralocorticoid receptor antagonists (MRAs) cannot bestopped forsafety reasons (i.e. severe hypokalaemia orse- vere hypertension among patients with severe hyperaldosteronism), recent evidence suggests that the accuracy ofARR testing under this treatment isonly marginally impacted, particularly inthe presence offlorid primary aldosteronism.327 Assessing sodium intake (preferably 24hurinary sodium, orsodium- to-creatinine ratio inthe morning urine sample) isalso important for interpreting the ARR, asistime inmenstrual cycle for females. ARR cut-offs vary depending onunit ofmeasurement and bylocal labora- tory. For detailed information, readers are referred tothe latest pri- mary aldosteronism guidelines.328,329 7.6.3. Renovascular hypertension Renovascular hypertension (RVH) defines acondition where renal artery occlusion orstenosis decreases renal perfusion pressure to alevel that activates the renin–angiotensin–aldosterone system (RAAS), thereby raising BP. Major causes are atherosclerosis andfibromuscular dysplasia (Figure 14and Supplementary data online, Tables S1andS2). Atherosclerosis isthe most common form of RVH, especially inolder adults.318Fibromuscular dysplasia isasys- temic non-atherosclerotic vascular disease involving medium-sized muscular arteries. When renal arteries are involved, fibromuscular dysplasia may induce RVH (FMD-RVH), especially inchildren and younger women.330–332 Though not highly sensitive, very elevated renin levels raise the sus- picion for RVH. The work-up ofRVH (Table 13) isbased onimaging tests, such asrenal artery Doppler ultrasound, with bilateral assessment ofrenal arterial resistive index, orabdominal CT angiography, ormag- netic resonance imaging (MRI), inline with current ESC Guidelines on the diagnosis and treatment ofperipheral arterial diseases,277which will beupdated in2024. Ofnote, bystander renal artery stenosis may bepresent inpatients with essential hypertension, without causing sec- ondary hypertension due toRVH. Since fibromuscular dysplasia isasys- temic disease, CT or MRI angiography from head to pelvis is recommended inpatients with FMD-RVH.277,332 7.6.4. Obstructive sleep apnoea syndrome Obstructive sleep apnoea syndrome (OSAS) isprevalent inhyperten- sion and particularly inresistant hypertension, with studies indicating that upto60% ofpatients with resistant hypertension have features ofOSAS.314OSAS should besuspected inpatients with hypertension and suggestive symptoms (see Supplementary data online, Table S2), inallpatients with resistant hypertension, and inpatients with non- dipping orreverse-dipping pattern at24hBPmonitoring, especially if obese (Figure 15). Using validated questionnaires may help identify pa- tients athigh risk ofOSAS.333Lack ofsuggestive symptoms does not rule out OSAS. Asimplified polysomnogram confirms the diagnosis [ap- noea–hypopnoea index (AHI) >5]and can quantify the severity of OSAS (mild: AHI<15;moderate: AHI of15–30; severe: AHI>30).334 Table 12 Drugs andconditions that affect aldosterone, renin, andaldosterone-to-renin ratio Factor Effect onplasma aldosterone levels Effect onrenin levels Effect onARR Serum potassium status Hypokalaemia ↓ →↑ ↓(FN) Potassium loading ↑ →↓ ↑ Sodium restriction ↑ ↑↑ ↓(FN) Sodium loading ↓ ↓↓ ↑(FP) Drugs Beta-adrenergic blockers ↓ ↓↓ ↑(FP) Calcium channel blockers (DHPs) →↓ →↑ →↓(FN with short-acting DHPs) ACE inhibitors ↓ ↑↑ ↓(FN) ARBs ↓ ↑↑ ↓(FN) Potassium-sparing diuretics ↑ ↑↑ ↓(FN) Potassium-wasting diuretics →↑ ↑↑ ↓(FN) Alpha-2 agonists (clonidine, methyldopa) ↓ ↓↓ ↑(FP) NSAIDs ↓ ↓↓ ↑(FP) Steroids ↓ →↓ ↑(FP) Contraceptive agents (drospirenone) ↑ ↑ ↑(FP) ©ESC 2024 ↑,raised; ↓,lowered; →,noeffect; ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; ARR, aldosterone-to-renin ratio; DHPs, dihydropyridines; FN, false negative; FP, false positive; NSAID, non-steroidal anti-inflammatory drug.40 ESC Guidelines
+Primary aldosteronism Mostly asymptomatic Spontaneous or diuretic- provoked hypokalaemia AF  Disproportionate HMOD Muscle weakness and tetany Family history of primary aldosteronism, early onsethypertension and/or strokeAdrenal incidentalomaSigns and symptoms Diagnosis Pathophysiology TreatmentAldosterone-renin ratio (ARR) Confirmatory tests (e.g. saline suppression test) Adrenal vein sampling or functional imaging Genetic testing Aldosterone-producing adenoma Familial forms due to germline mutationsBilateral hyperplasia Medical: mineralocorticoid receptor antagonists Surgical: unilateral adrenalectomyFigure 13 Summary ofprimary aldosteronism asacommon form ofsecondary hypertension. AF, atrial fibrillation; HMOD, hypertension-mediated organ damage.Table 13 Optional tests that should beused toscreen forsecondary hypertension inthepresence ofsuggestive signs, symptoms, ormedical history Cause ofsecondary hypertensionScreening test Primary aldosteronism Aldosterone-to-renin ratio Helpful information can also beprovided byreviewing prior potassium levels (hypokalaemia increases the likelihood of coexistent primary hyperaldosteronism) Renovascular hypertension Renal doppler ultrasound Abdominal CT angiogram orMRI Phaeochromocytoma/paraganglioma 24hurinary and/or plasma metanephrine and normetanephrine Obstructive sleep apnoea syndrome Overnight ambulatory polysomnography Renal parenchymal disease Plasma creatinine, sodium, and potassium eGFR Urine dipstick for blood and protein Urinary albumin-to-creatinine ratio Renal ultrasound Cushing’s syndrome 24hurinary free cortisol Low-dose dexamethasone suppression test Thyroid disease (hyper- or hypothyroidism)TSH Hyperparathyroidism Parathyroid hormone Calcium and phosphate Coarctation ofthe aorta Echocardiogram Aortic CT angiogram ©ESC 2024 CT, computed tomography; eGFR, estimated glomerular filtration rate; MRI, magnetic resonance imaging; TSH, thyroid-stimulating hormone.ESC Guidelines 41
+Restless/intermittent sleep, recurrent awakenings daytime sleepiness, fatigue, impaired concentration Increased neck circumferenceApnoea, snoring ObesitySigns and symptoms Atrial fibrillation Non-dipping or reverse dipping pattern 24 h ABPMObstructive sleep apnoea Pathophysiology Intermittent upper airway obstruction during sleep Overnight ambulatory polysomnographyDiagnosis Treatment Weight loss CPAP Mandibular advancement devicesFigure 15 Summary ofobstructive sleep apnoea asacommon form ofsecondary hypertension. AF, atrial fibrillation; ABPM, ambulatory blood pres- sure monitor; CPAP, continuous positive airway pressure. Renovascular hypertension Migraine, pulsatile tinnitus (FMD) Pulmonary oedema (bilateral) Multisite atherosclerosis Unexplained small kidney or kidney asymmetry Age <40 years (FMD)Signs and symptoms Pathophysiology Diagnosis TreatmentSignificant renal artery stenosis: Atherosclerosis Fibromuscular dysplasia Rare causes Renal doppler ultrasound Abdominal CT -Angio or MRIVascular bruits Arterial dissections and/or aneurysms (FMD) Medical: optimal CV risk management Interventional: renal angioplasty without (FMD) or with stenting (atherosclerosis)Acute    eGFR after RAS blockerGFR, albuminuria,    renin Age >60 years with acute change in BP or flash pulmonary oedema (atherosclerosis)Figure 14 Summary ofrenovascular disease asacommon form ofsecondary hypertension. CT-Angio, computed tomography angiography; CV, cardiovascular; FMD, fibromuscular dysplasia; GFR, glomerular filtration rate; MRI, magnetic resonance imaging; RAS, renin–angiotensin system.42 ESC Guidelines
+7.6.5. Phaeochromocytoma/paraganglioma Phaeochromocytomas/paragangliomas (PPGLs) are arare form ofsec- ondary hypertension characterized byahighly heterogeneous clinical presentation.335,336PPGLs are usually discovered incidentally.337 APPGL should besuspected inthe presence ofsigns and symptoms of catecholamine excess orinsyndromic PPGL, inpatients with afamily his- tory ofPPGL, and incarriers ofagermline mutation inone ofthe PPGL-causing genes.338Since normetanephrine and metanephrine arese- creted constitutively, asopposed tothe highly variable nature ofcatechol- amine secretion, they arepreferred asscreening tests forPPGL (Table 13). 8.Preventing andtreating elevated blood pressure andhypertension The ultimate goal ofpreventing and treating elevated BPand hyperten- sion istoreduce CVD, toimprove quality oflife, and toprevent prema- ture death. Crucially, besides BP, other CVD risk factors need tobe comprehensively addressed (e.g. smoking, glucose, dyslipidaemia) asde- tailed inthe 2021 ESC Guidelines oncardiovascular disease prevention inclinical practice.170Indeed, itisworth emphasizing that, when com- bined, these CVD risk factors have multiplicative (not additive) effects onCVD risk.340 8.1.Prevention strategies inearly life Detailed information onthis topic isprovided inthe Supplementary data online. High BPtracks from childhood toadulthood.341,342Hypertension inchildhood was redefined ina2022 ESC Consensus Document.3438.2.Non-pharmacological interventions Amajor underlying contributor toelevated BPand hypertension inthe general adult population isunhealthy lifestyle, with severe consequences forall-cause and CVD mortality. Assuch, wegive lifestyle interventions to reduce BPaspecial status inour recommendations throughout these guidelines (Figures 16and17). This isreflected byamodified approach tothe class ofrecommendations for lifestyle interventions compared with medical interventions (pharmacological orprocedural). Given the salutary benefits ofhealthy lifestyle onarange ofoutcomes that extend well beyond BP-lowering effects,347including broad mental and physical health benefits, wedonot require lifestyle interventions tohave RCT evi- dence forefficacy inreducing CVD events through BPlowering toachieve aClass Irecommendation. Indeciding togive lifestyle interventions this status, the task force also recognizes that: (i)lifestyle interventions are less likely tobesubjected toclinical outcomes trials (e.g. due tofunding limitations and lack ofinterest from industry), and (ii)the risks ofadverse effects and toxicity relating tohealthy lifestyle interventions are low. In contrast, inthese guidelines, toachieve aClass Irecommendation (irre- spective oflevel ofevidence) there needs tobeevidence that medical in- terventions that reduce BPalso decrease CVD events byBPlowering. 8.2.1. Dietary sodium andpotassium intake 8.2.1.1. Sodium Reducing dietary salt (sodium chloride) intake inindividuals with high baseline intake lowers CVD event rates.348Extensive observational stud- ieshave reported dose–response associations between high dietary so- dium intake and CVD events.349–351The potential impact ofsalt reduction onpopulation health issignificant, particularly incountries where the population’s average salt intake ishigh. Pooled data from long- term follow-up salt-reduction trials demonstrate that reducing salt by 2.5g/day isassociated with anapproximately 20% reduction inCVD events atthe population level.349 The health benefits ofsalt reduction are likely mediated, largely, by BP-lowering effects.352–354An almost linear relationship has been de- scribed inadose–response meta-analysis between sodium intake ran- ging from 0.4 to7.6g/day and reduction ofsystolic and diastolic BPis independent ofbaseline BP.355,356Women appear tobe, onaverage, more sodium sensitive than men,357and may have greater outcome benefits when receiving comparable sodium-restricted diets.358Trial evidence for the BP-lowering benefits ofsalt reduction extend down todaily sodium intakes of<1.5 g/day.356,358–361 The task force acknowledges that the observational data linking so- dium intake toCVD outcomes are mixed and that some studies have not found alink between salt intake and CVD.362,363Inaddition, apo- tential J-curve exists between sodium intake and CVD events (where- bysome analyses suggest that sodium reduction tovery low levels could beharmful).363,364While there are differences ofopinion, the task force agreed that, onbalance, (i)observational J-curve data are often due toreverse causality orconfounding,114,348,365,366(ii)the re- lationship between dietary sodium and stroke istypically linear in shape, without any J-curve, (iii) ifthe J-curve were causal, the adverse effect ofvery low sodium onCVD would have tobemediated bysome harmful mechanism that overcomes the expected benefit mediated by BPlowering (which isunlikely), and (iv) estimation ofsodium intake using spot-urine sodium testing (which was commonly done instudies reporting aJ-curve) may not beasvalid asother methods.367For ex- ample, most (but not all)362reports measuring 24hurine sodium ex- cretion (asurrogate measure ofsodium intake) have not reported a J-curve association with CVD.350,364Furthermore the causal evidence demonstrating reduced CVD with sodium restriction (using potassium- enriched salt substitutes) inthe Salt Substitute and Stroke Study (SSaSS)Recommendation Table 13—Recommendations for screening forsecondary hypertension (see Evidence Tables 19and20) Recommendations ClassaLevelb Itisrecommended that patients with hypertension presenting with suggestive signs, symptoms ormedical history ofsecondary hypertension are appropriately screened forsecondary hypertension.312,314,315,323,339I B Screening for primary aldosteronism byrenin and aldosterone measurements should be considered inalladults with confirmed hypertension (BP≥140/90 mmHg).313,316,323,339IIa B ©ESC 2024 BP, blood pressure. aClass ofrecommendation. bLevel ofevidence. Recommendation Table 14—Recommendations for screening forhypertension inchildren andadolescents (see Evidence Table 21) Recommendation ClassaLevelb Opportunistic screening with office BP measurements tomonitor development ofBPduring late childhood and adolescence, especially ifone or both parents have hypertension, should be considered tobetter predict development ofadult hypertension and associated CVD risk.344–346IIa B ©ESC 2024 BP, blood pressure; CVD, cardiovascular disease. aClass ofrecommendation. bLevel ofevidence.ESC Guidelines 43
+and Diet, ExerCIse and carDiovascular hEalth-Salt (DECIDE-Salt) trials was compelling,348,368even though sodium restriction inthese trials was not below 2g/day. Itisrecommended torestrict total dietary sodium intake toap- proximately 2g/day orless (equivalent toapproximately 5gorabout ateaspoon ofsalt per day). This includes added salt and salt already contained infood. While the feasibility ofthis sodium target can be debated, the evidence for the benefits ofthis sodium target among patients with elevated BP orhypertension issufficient, particularly interms oflowering BP. The optimal sodium intake inthe general population with non-elevated BP isless clear (noting also that the BP-lowering effect of salt reduction among patients with non-elevated BPappears lower).353,354Amore feasible compromise inthe general population might beatarget sodium intake range of2– 4g/day.369,370Itneeds tobeemphasized that large parts ofdaily so- dium intake occur bymeans ofsodium consumption contained in processed foods.8.2.1.2. Potassium Optimal dietary potassium intake, e.g.byconsuming diets rich infruits and vegetables, has BP-lowering effects and may beassociated with lower CVD risk.348,364,368,371–373The association between potassium intake, systol- icBP,and CVD events may besex-specific, being stronger inwomen.374The World Health Organization (WHO) recommends over 3.5g/day (∼90 mmol/day) ofdietary potassium.375Excessive potassium supplementation should, however, beavoided374and CKD guidelines recommend dietary po- tassium restriction to<2.4 g/day inpersons with advanced CKD (see Supplementary data online).376 Alower urinary sodium-to-potassium ratio (Na+/K+ratio; asurro- gate forreduced dietary sodium intake complemented byincreased po- tassium intake) has been associated with agreater reduction insystolic and diastolic BPthan with ahigher ratio.348,377 Inpatients with hypertension and high dietary sodium, increased dietary intake ofpotassium (inaddition tolower dietary sodium) should becon- sidered.348,350,378Inpatients with persistently high sodium intake (>5 g/ Aerobic exercise training At least 150 min/week moderate-intensity or 75 min/week vigorousintensity: brisk walking, jogging,cycling, swimming(Class I) Isometric resistance exercise training:Low-to-moderate-intensity(3 sets of 1–2 min contraction:hand-grip, plank, wall sit) Dynamic resistance exercise training:Large muscle groups, low-to-moderate-intensity (2–3 sets with10–15 reps.: squat, push-ups, sit-up)Increase daily physical activity (steps/day, take stairs, walk/cycle) Avoid sedentary lifestyle BP ReductionCV Risk Reduction Dynamic or isometric resistance training to complement aerobic exercise training  2–3 times/week (Class I)Figure 16 Physical activity according todifferent types ofexercise and reduction ofblood pressure and overall cardiovascular disease risk. Priority is given toaerobic exercise training (green). BP, blood pressure; CVD, cardiovascular disease.44 ESC Guidelines
+day) and without moderate-to-advanced CKD, particularly women, anin- crease inpotassium intake by0.5–1.0 g/day may beconsidered toachieve a favourable Na+/K+ratio of1.5–2.0 and toreduce CVD risk. Potassium sup- plementation can beachieved bysubstituting sodium using potassium en- riched salts (75% sodium chloride and 25% potassium chloride)368,379,380 orbyincreasing dietary potassium intake [e.g. a125 g(medium) banana contains about 450 mg potassium, orunsalted boiled spinach (840 mg/ cup) ormashed avocado (710 mg/cup)]. Inpatients with CKD and/or those taking potassium-sparing medication, such assome diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) orspironolactone, serum levels ofpotassium should be monitored (noting that phlebotomy recommendations toavoid spuriously high potassium results should befollowed).8.2.2. Physical activity andexercise Inasystematic review and meta-analyses, aerobic (endurance) exercise was suggested asthe first-line exercise therapy for reducing BPinpa- tients with elevated BPand hypertension vs.alternative forms ofexercise, such asdynamic orisometric resistance training.381Inpatients with hypertension, regular aerobic exercise substantially lowers systolic BP byupto7–8 mmHg and diastolic BPbyupto4–5 mmHg.381,382For non- white patients with hypertension, dynamic resistance training elicits BP reductions that appear comparable toaerobic exercise.383Isometric re- sistance training also achieves clinically relevant BPreductions inpatients with hypertension, but results areinconsistent and more data from more high-quality intervention trials are required (see Supplementary data online).381,384,385With respect tomode and intensity ofaerobic exercise, Increase physical activityIncrease potassium intake Optimize weight management and diet No smokingReduce alcohol intakeReduce table salt (sodium chloride) intakeBP ReductionCV Risk ReductionFigure 17 Effects ofmain lifestyle factors onblood pressure and cardiovascular risk reduction. BP, blood pressure; CV, cardiovascular. Smoking ces- sation reduces overall cardiovascular risk but not BP(long arrow). Salt reduction reduces BPand (for persons with high baseline intake) reduces car- diovascular risk. Increased potassium intake and higher physical activity, aswell asoptimized weight management, reduce BPand are associated with lower overall cardiovascular risk (short arrows).ESC Guidelines 45
+high-intensity interval training elicits comparable BPreductions tomod- erate continuous exercise, with high-intensity interval training achieving greater improvement inphysical fitness.386 Inpatients with known hypertension, engaging inphysical activity is associated with reduced CVD mortality risk vs.sedentary patients with hypertension.387 Anexaggerated BPresponse toexercise may yield diagnostic merits for predicting incident hypertension and CVD. Inameta-analysis, anexagger- ated BPresponse toexercise was associated with anincreased risk for masked hypertension.388The risk ofcoronary heart disease also increases with higher systolic BPduring exercise, independent ofsystolic BPatrest.389 Prior recommendations foratleast 150 min/week ofmoderate inten- sity aerobic exercise (≥30 min, 5–7 days/week) can bemaintained.1,390 Alternatively, 75min ofvigorous-intensity exercise per week over 3days may beperformed, with additional benefits derived byachieving 300 min ofmoderate-intensity or150 min ofvigorous-intensity aerobic physical activity per week.390,391As acute aerobic exercise induces intensity- dependent short-term reductions inambulatory BPafter exercise, patients with elevated BPand hypertension may benefit from daily exercise toim- prove their 24hBPprofile and avoid BPpeaks onsedentary days.392 Aerobic exercise should becomplemented bylow- ormoderate-intensity resistance training (2–3 times per week), e.g.dynamic resistance, starting at 2–3 sets of10–15 repetitions at40%–60% ofone-repetition maximum393 orisometric resistance training with three sets of1–2 min contractions, such ashand-grip, plank, orwall sit(Figure 16).381,394 Inuncontrolled hypertension atrest, high-intensity exercise should beapplied with caution, with resting systolic BPof>200 mmHg and dia- stolic BPof>110 mmHg indicating relative contraindications.395Age, sex, gender,396ethnicity, and comorbidities, aswell asindividual prefer- ences, should be considered for individual exercise prescription. Detailed information onexercise prescription interms offrequency, in- tensity, time (duration) and type and progression are available inthe 2020 ESC Guidelines on sports cardiology and exercise inpatients with cardiovascular disease,390which include recommendations for pre-participation screening and cardiopulmonary exercise testing.390 8.2.3. Weight reduction anddiet Visceral obesity iscommon and associated with incident hyperten- sion.397,398An average weight loss of5kghas been associated with anaverage systolic and diastolic BPreduction of4.4and 3.6mmHg, re- spectively.399Data show that, starting atanindex body mass index (BMI) of40kg/m2,amedian weight loss of13% isassociated with a 22% lower risk for hypertension.400,401Maintaining even moderate weight loss of5%–10% ofinitial body weight can improve not only BP, but also glucose and lipid metabolism, and potentially reduce pre- mature all-cause mortality.402–404However, achieving long-term effects inpatients with hypertension viaweight loss ischallenging and the mag- nitude ofthese effects remains unclear.405,406Weight stabilization dur- ing middle-age appears tobe animportant and attainable goal to prevent obesity-related increase inBPlater inlife.407 Evidence-based diets, such asthe Mediterranean diet and the Dietary Approaches toStop Hypertension (DASH) diet, are established inter- ventions inpatients with hypertension toreduce their BPand CVD risk.408,409Additional information onhealthy dietary patterns ispro- vided inthe 2021 ESC Guidelines oncardiovascular disease prevention inclinical practice and Supplementary data online.170 Incombination with weight-loss and exercise interventions410and low sodium intake,411the DASH diet has added effect onBPreduc- tion.412Pharmacological treatment ofobesity with orlistat achieved aslight reduction of 2.6mmHg in systolic BP.413The greatest BP-lowering effects ofweight-loss medications may beachieved with the glucagon-like peptide 1(GLP-1) receptor agonists.414–416For ex- ample, inthe Semaglutide Treatment Effect inPeople with Obesity (STEP-1) trial, the GLP-1 analogue semaglutide resulted inamean weight reduction of12.4% and a5.1mmHg reduction insystolic BP.415 8.2.4. Alcohol, coffee, andsoft drinks Ina2020 Cochrane review, the short-term effects ofalcohol onBPwere dose dependent; low-dose alcohol (<14 g)did not affect BPwithin 6h, medium-dose (14–28 g)decreased both systolic and diastolic BP,and high- dose alcohol (>30 g)first decreased BPupto12hand then increased BP following >13 hofconsumption by3.7mmHg systolic and 2.4mmHg dia- stolic.417The trials inthis Cochrane review included small numbers ofwo- men. Inthelonger term, noevidence hasbeen found foraprotective effect ofchronic alcohol consumption onhypertension, foreither sex. Incon- trast, even low-dose alcohol consumption (10 g/day) increases chronic risk ofhypertension by14% inmen, but not inwomen.418Asper the 2021 ESC Guidelines oncardiovascular disease prevention inclinical prac- tice, men and women are recommended tostay within the upper limit of drinking alcoholic beverages (100 g/week ofpure alcohol). Defining num- ber ofdrinks depends onportion size, the standards ofwhich differ per country, but translates to8–14 g/drink.170Emerging data indicate itislikely healthiest toavoid allalcohol, where possible.419 Coffee intake isnot associated with ahigher risk ofhypertension in the general population; infact, higher coffee consumption may beasso- ciated with alower risk forincident hypertension.420Data regarding the association between tea drinking and CVD are inconclusive, though mechanistic trials have suggested benefits onBPlowering.421Incon- trast, energy drinks with high concentrations ofingredients such as taurine and caffeine increase BPand may lead toacute orchronic car- diovascular complications inyoung adults.422–424 Consuming two ormore servings per day ofsugar-sweetened bev- erages was associated with a35% higher risk ofcoronary artery disease inwomen inthe Nurses’ Health Study.425Inthe European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, both sugar- and artificially sweetened soft drinks were associated with higher all-cause mortality.426Inchildren and adolescents, sugar-sweetened beverages increased systolic BPand the risk forincident hypertension.427Itisre- commended to restrict free sugar consumption, in particular sugar-sweetened beverages, toamaximum of10% ofenergy intake. 8.2.5. Smoking Tostop smoking isarguably the most effective measure inpreventing major CVD events atthe individual level, likely through improved vas- cular health.428–431Estimated health benefits will beeven more sub- stantial looking atall-cause morbidity and mortality, e.g. including smoking cessation for cancer prevention. The effects ofelectronic cigarettes (e-cigarettes) onBPremain un- clear and todate there are norobust outcomes data. However, grow- ing evidence suggests that e-cigarettes can increase BP (see Supplementary data online).432,433 Among adults, smoking affects ambulatory BPbyraising daily BP,434but effects ofchronic smoking onoffice BPappear tobesmall.435Smoking ces- sation advice helps, but more intensive interventions aresuperior.436,437As recommended byprevious ESC Guidelines, smoking cessation isrecom- mended toreduce CVD risk and improve non-CVD health.1,17046 ESC Guidelines
+8.3.Pharmacological interventions 8.3.1. Treatment strategy toreduce adverse cardiovascular disease outcomes The main goal ofreducing BPistoprevent adverse CVD outcomes. The relative risk reduction afforded byafixed degree ofBPreduction islargely independent ofpre-treatment BP.116There isaclear relationship be- tween theintensity ofBPlowering and therelative and absolute reduction inrisk ofCVD events for alladults, regardless ofage (atleast upto 85years), sex, prior CVD, diabetes, orAF.116,131,443–445With this strong evidence forthe ‘the lower the better, but within reason’ paradigm, deci- sion rules are required forselecting patients most likely tobenefit from treatment.172Inthis section, asummary ofevidence for BP-lowering drug treatment isprovided, followed bystrategies fortheir use forpre- venting CVD. 8.3.2. Drug classes with evidence onclinical outcomes inthetarget population The major drug classes with robust evidence forBP-mediated reduction inCVD events areACE inhibitors, ARBs, dihydropyridine CCBs, diuretics (thiazides and thiazide-like diuretics such as hydrochlorothiazide, chlorthalidone, and indapamide), and beta-blockers (see Supplementary data online, Tables S7andS8).122,446,447The first four are recommended asfirst-line options for starting hypertension treatment inthe general population. Beta-blockers can beadded preferentially incircumstances such asinthe presence ofangina orheart failure, after myocardial infarc- tion, orforcontrolling heart rate, where they arethecornerstone ofther- apy.122,448,449Insuch settings, second-generation (cardioselective) and, specifically, third-generation (vasodilating) beta-blockers arepreferred.450 However, beta-blockers are less effective than ACE inhibitors, ARBs, CCBs, ordiuretics atpreventing stroke, and have ahigher discontinuation rate due toside effects.451,452Beta-blockers and diuretics, especially when combined, are associated with anincreased risk ofnew-onset diabetes in predisposed patients.453,454The effect ofRAS blockers and CCBs onpre- venting progression ofHMOD also appears tobesuperior tobeta- blockers.455–458Beta-blockers should also beavoided inpatients with iso- lated systolic hypertension ormore generally with arterial stiffness, asthey increase stroke volume (given the lower heart rate).218 When therapy and adherence with the above-mentioned drug classes isoptimized but insufficient toreach BPgoals, other drug classes can be used for treating hypertension. Ofthese, spironolactone, anMRA, ap- pears tobethe most effective atfurther lowering BPinresistant hyper- tension; however, more evidence ofCVD risk-lowering effects with MRAs among allhypertensive populations, especially those without re- sistant hypertension, isneeded.459Specifically, while use ofMRAs inpa- tients with heart failure has provided clinical evidence on the effectiveness ofMRAs for preventing CVD events, dedicated outcome trials inpatients with primary hypertension without heart failure arelack- ing. Because the present guidelines require trial evidence forCVD out- come benefit foraBP-lowering drug orprocedure toachieve aClass I recommendation, and given nooutcome trials ofMRAs have been con- ducted ingeneral samples ofpatients with primary hypertension, wehave given MRAs aClass IIarecommendation (see below). We acknowledge that spironolactone was provided aClass Irecommendation inthe 2018 ESC/ESH Guidelines on the management ofarterial hypertension. However, tobeconsistent with our requirement for trial evidence for CVD outcomes benefit inpatients with hypertension, the task force agreed toprovide aClass IIarecommendation for spironolactone in these 2024 Guidelines. Importantly, itwas also agreed that aClass IIarec- ommendation (i.e. should beconsidered) isanendorsement ofMRAs forRecommendation Table 15—Recommendations for non-pharmacological treatment ofblood pressure and cardiovascular riskreduction (see Evidence Tables 22–26) Recommendations ClassaLevelb Restriction ofsodium toapproximately 2gper day is recommended where possible inalladults with elevated BPand hypertension [this isequivalent to about 5gofsalt (sodium chloride) per day orabout a teaspoon orless].353,354I A Moderate intensity aerobic exercise of≥150 min/ week (≥30 min, 5–7 days/week) oralternatively 75min ofvigorous intensity aerobic exercise per week over 3days are recommended and should be complemented with low- ormoderate-intensity dynamic orisometric resistance training (2–3 times/ week) toreduce BPand CVD risk.1,381,390–393I A Itisrecommended toaim for astable and healthy BMI (e.g. 20–25 kg/m2)and waist circumference values (e.g.<94 cminmen and<80 cminwomen) to reduce BPand CVD risk.399–401I A Adopting ahealthy and balanced diet, such asthe Mediterranean orDASH diets, isrecommended to help reduce BPand CVD risk.412,438,439I A Men and women are recommended todrink less alcohol than the upper limit, which isabout 100 g/week ofpure alcohol. How this translates into number ofdrinks depends onportion size (the standards ofwhich differ per country), but most drinks contain 8–14 gofalcohol per drink. Preferably, itisrecommended toavoid alcohol toachieve the best health outcomes.170,419,440,441I B Itisrecommended torestrict free sugar consumption, inparticular sugar-sweetened beverages, toamaximum of10% ofenergy intake. It isalso recommended todiscourage consumption of sugar-sweetened beverages, such assoft drinks and fruit juices, starting atayoung age.425–427I B Itisrecommended tostop tobacco smoking, initiate supportive care and refer tosmoking cessation programmes, astobacco use strongly and independently causes CVD, CVD events, and all-cause mortality.428,429,431,437I A Inpatients with hypertension without moderate to advanced CKD and with high daily sodium intake, an increase ofpotassium intake by0.5–1.0 g/day—for example through sodium substitution with potassium- enriched salt (comprising 75% sodium chloride and 25% potassium chloride) orthrough diets rich infruits and vegetables—should beconsidered.348,368,373,374,442IIa A Inpatients with CKD ortaking potassium-sparing medication, such assome diuretics, ACE inhibitors, ARBs, orspironolactone, monitoring serum levels of potassium should beconsidered ifdietary potassium isbeing increased.IIa C ©ESC 2024 ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; BMI, body mass index; BP, blood pressure; CKD, chronic kidney disease; CVD, cardiovascular disease; DASH, Dietary Approaches toStop Hypertension. aClass ofrecommendation. bLevel ofevidence.ESC Guidelines 47
+treating resistant hypertension but one that acknowledges some uncer- tainty ofoutcomes benefit. Future outcome trials ofMRAs, perhaps in- cluding finerenone,460–462are encouraged inpatients with hypertension. Clinical outcome evidence from trials for other BP-lowering drug classes, such asalpha-blockers, hydralazine, minoxidil, other potassium- sparing diuretics, and centrally acting agents, isless compelling and caution regarding adverse effects iswarranted. However, they may beafinal add- ition ifallother therapeutic efforts areinsufficient todecrease BP.Ofnote, inthe Antihypertensive and Lipid-Lowering Treatment toPrevent Heart Attack (ALLHAT) trial, the alpha-blocker arm was stopped early due to futility ofbenefit forthe CVD outcome.463 8.3.3. New therapies with blood pressure-lowering properties that await supportive evidence from cardiovascular outcomes trials prior toguideline endorsement androutine useinhypertension Afew other drug classes with indication inheart failure have emerged that also have BP-lowering properties. For example, the angiotensin receptor–neprilysin inhibitor (ARNi) sacubitril/valsartan, which was ini- tially developed for hypertension,464reduces CVD mortality and morbidity inpatients with heart failure, aneffect that may have been mediated, inpart, bysuperior BP lowering compared with enalapril alone.465,466Inaposthoc subgroup analysis, sacubitril/valsartan lowered BPinadults with both heart failure with preserved ejection fraction (HFpEF) and resistant hypertension.467Inthe context ofresearch stud- ies, sacubitril/valsartan has been used inhigher doses (200 mg or 400 mg once daily) for treating hypertension.464,466,468,469 SGLT2 inhibitors have shown favourable effects onCVD events and renal haemodynamics inpatients with and without type 2diabetes, and inheart failure trials.470Inthese trials, SGLT2 inhibitors did lower BP, though only modestly.471Small trials among adults with hypertension have confirmed the potential forBPlowering with this drug class.472,473 Other new drugs with preliminary data include GLP-1 agonists and the new non-steroidal MRAs, e.g. finerenone, inmanaging hyperten- sion.415,460,461Inaddition, novel aldosterone synthase inhibitors (bax- drostat and lorundrostat) have significantly lowered BP inpatients with uncontrolled hypertension inphase 2trials.474,475 The dual endothelin-A and -Breceptor antagonist aprocitentan also reduced office and 24hBPcompared with placebo at4weeks inpa- tients with resistant hypertension inaphase 3trial.476Zilebesiran, an investigational RNA interference agent administered subcutaneously, inhibits hepatic angiotensinogen synthesis and asingle dose reduced 24hBPover approximately 6months.477 8.3.4. Drug combinations andup-titrating strategies To treat hypertension, many patients will require more than one BP-lowering medication. Combining drugs from different drug classes can have additive orsynergistic effects and lead togreater BPreduction than increasing the dose ofone drug.478–483The superior BP-lowering efficacy ofcombination therapy ismediated, atleast inpart, bythe po- tential ofcombination therapy totarget multiple pathophysiological pathways contributing toperturbed BPineach patient.484Afurther benefit ofcombination therapy isthe potential touse lower doses of each individual BP-lowering agent, which may reduce side effects and improve adherence and persistence,485though the evidence forthis hy- pothesis has been questioned.486 Upfront low-dose combination therapy istherefore recommended inpersons with hypertension, with the potential advantages offewer side effects and swifter BPcontrol being important for long-term ad- herence.487–489Ifcombination BP-lowering therapy ispursued, single- pillcombinations are preferred. For those with elevated BPwho havean indication for BP-lowering treatment, monotherapy isrecom- mended inthe first instance. One caveat tocombination therapy inhypertension isthat patient-level response toindividual BP-lowering drug classes canbeheterogeneous (sug- gesting some patients may benefit from more personalized treatment com- pared with routine combinations).490This isrelevant also with respect to race/ethnicity (seeSection 9).Another caveat isthat the evidence forre- duced CVD outcomes with BP-lowering drugs incombination therapy is based onobservational studies.491–493There are nooutcomes data from prospective trials that prove superiority ofupfront combination therapy (ei- ther assingle-pill combinations orasseparate pills) over upfront monother- apy intheisolated treatment ofhypertension.486Therefore, weconsidered giving upfront combination therapy (either asseparate pills orassingle-pill combinations) aClass IIarecommendation inthese guidelines. However, gi- ven the totality ofevidence foroutcomes benefit inobservational studies, randomized trial data forbetter BPcontrol and adherence, and importantly, also given CVD outcomes benefit forpolypills (aform ofsingle-pill combin- ation) inrandomized trials,494–496wechose toprovide aClass Irecommen- dation for upfront combination therapy inadults with confirmed hypertension, inagreement with 2018 ESC recommendations. The major four drug classes (ACE inhibitors, ARBs, dihydropyridine CCBs, and thiazide orthiazide-like diuretics) are recommended asfirst- line BP-lowering medications, either alone orincombination.122,447,484,497 Anexception isthe combination oftwo RAS blockers, which isnot re- commended.498–500For most hypertensive patients, asingle-pill com- bination, initially containing two ofthese major drug classes, and initially atlow dose, isrecommended.489,501,502Doses ofBP-lowering drugs are presented inthe Supplementary data online, Tables S7andS8. When BP isstill uncontrolled under maximally tolerated triple- combination (RAS blocker, CCB, and diuretic) therapy, and after adher- ence isassessed, the patient should be considered resistant and referred toanexpert centre for appropriate work-up (see Section 7.5). Atthe same time, the addition ofspironolactone should beconsid- ered.459Ifspironolactone isnot tolerated, eplerenone orother MRA, or beta-blockers (ifnot already indicated), should be considered. Eplerenone may need tobedosed higher (50–200 mg) for effective BP lowering. Inameta-analysis, eplerenone 25mg didnot lower BP.503Due tothe shorter time ofaction than spironolactone, eplerenone may need tobeadministered twice daily for treating hypertension. An alternative toMRA asfourth-line treatment forBPlowering istheuse ofbeta-blockers forpersons who donot already have acompelling indication. Avasodilating beta-blocker (e.g. labetalol, carvedilol, ornebivolol) ispreferred when a beta-blocker ischosen.504However, wenote that the BP-lowering effects ofbeta-blockade appears tobeless potent than spironolactone inthe set- ting ofresistant hypertension.459 Only thereafter should hydralazine, other potassium-sparing diuretics (amiloride and triamterene), centrally acting BP-lowering medications, oralpha-blockers beconsidered. Given multiple side-effects, minoxidil should only beconsidered ifallother pharmacological agents prove inef- fective inresistant hypertension.505 As noted above, polypills combining fixed doses ofBP-lowering treatment, lipid-lowering therapy and, ifindicated, aspirin are effective inmore general CVD prevention.496,506–509However, the polypill isnot available for routine clinical use inmany European countries. 8.3.5. Apractical algorithm forintensive, effective, andtolerable blood pressure lowering with drug therapy, including considerations around single-pill combinations The aim ofthe algorithm inFigure 18istointroduce alow-dose double- and then triple-combination strategy while monitoring tolerance48 ESC Guidelines
+Low-dose double combinationa therapy ACEi or ARBs / CCBs / Diuretics (Class I) BP controlled after 1–3 months (assessment at 1 month preferred if possible)Y FU at least every year Low-dose triple combination therapy  ACEi or ARBs / CCBs / Diuretics (Class I) BP controlled after 1–3 months (assessment at 1 month preferred if possible)Y FU at least every year BP controlled after 1–3 months (assessment at 1 month preferred if possible)Y FU at least every year Refer to hypertension clinic (Class IIa) At any step: add beta-blockers if compelling indications (angina, post-myocardial infarction, systolic heart failure, or heart rate control) (Class I) Maximally tolerated triple combination therapy  ACEi or ARBs / CCBs / Diuretics (Class I) T est for adherence (Class IIa) Add spironolactone (Class IIa)Apparent resistant hypertensionN N N  aInitial monotherapy preferred Elevated BP category (120/70–139/89 mmHg) Moderate-to-severe frailty Symptomatic orthostatic hypotension Age ≥85 years See section on management of resistant hypertension for further steps as neededFigure 18 Practical algorithm forpharmacological blood pressure lowering. ACEi, angiotensin-converting enzyme inhibitor; ARB, angiotensin recep- tor blocker; BP, blood pressure; CCB, calcium channel blocker; FU, follow-up.ESC Guidelines 49
+NPatient centr ed ca re Normal Abnormal≥10% <5% 5% – <10%Age <40 years, resistant hypertension, suggesti ve signs and/or symptoms Targeted seconda ry hypertension treatmentScreen for seconda ry hypertension (Class I) Calculate SCORE2/ SCORE2-OP (Class I) Assess risk modifiers (Class IIa) Consider risk tools (Class IIb)Age ≥85 y ears, moderate-to-s evere frailty ,  symptomatic OH,  short life expectancy Established CV D, moderate-to-s evere CKD , hypertension-mediated organ damag e,  diabetes mellitusa, familial hypercholester olaemiaY NN NY YYNon-ele vated BP Office SBP <120 mmHg and DBP <70 mmHgElevated BP Office SBP 120–139 mmHg and/or DBP 70–89 mmHgHyper tension Office SBP ≥140 mmHg and/or DBP ≥90 mmHg ABPM / HBPM preferred over office BPTarget SBP 120 –129 mmHg (Class I) Target DBP 70 –79 mmHg (Class IIb)Screen BP oppor tunisticall yLifestyle measu res Drug tr eatment f or confirmed BP ≥130/80 mmHg Monitor BP and medication tolerancebScreening f or hypertension Oppor tunistic:  every 3 years <40 y ears; every year ≥40 yearsHBPM/ABPM or repeated standar dized office BPConfirming h ypertension Lifestyle measur esFigure 19 Central Illustration. ABPM, ambulatory blood pressure monitoring; BP, blood pressure; CVD, cardiovascular disease; CKD, chronic kidney disease; DBP, diastolic blood pressure; HBPM, home blood pressure monitoring; OH, orthostatic hypotension; SBP, systolic blood pressure; SCORE2, Systematic COronary Risk Evaluation 2;SCORE2-OP, Systematic COronary Risk Evaluation 2–Older Persons. Summary algorithm forBPclassification and management. SeeSection 5forrecommendations onout-of-office confirmation ofthe three BPcategories.aAdults with type 2diabetes mellitus only and younger than 60years should beconsidered for SCORE2-Diabetes assessment.bThough scientific data demonstrate that, under research conditions, the optimal target BPis≤120/70 mmHg, the target BPrecommended by these guidelines inroutine practice is120–129/70–79 mmHg. Ifachieving this target isnot possible, oriftreatment isnot well tolerated, then BPshould betreated toaslow asreasonably achievable. For persons with elevated BP, treatment with lifestyle measures for3months isfirst recommended, prior toconsidering medications.50 ESC Guidelines
+among patients with hypertension, and only afterwards tostart up- titrating doses tomaximum amounts. Initiation with monotherapy, slower up-titration, and lower dosing should beconsidered inthe setting ofelevated BPand increased CVD risk, orinmoderate-to-severe frailty, limited lifeexpectancy, symptom- atic orthostatic hypotension, orolder people (aged ≥85 years). Ideally, BPshould betreated totarget within 3months toretain the confidence ofthe patient, toensure long-term adherence, and toreduce CVD risk.71 Anoverview ofthe recommended approach toBPmanagement inall adult patients isprovided inFigure 19(Central Illustration). Also, of note, teleconsultation, multidisciplinary ornurse-led care, orpatient self-monitoring can help with achieving BPcontrol incertain healthcare systems.75,510,511 8.3.6. Timing ofblood pressure-lowering drug treatment Current evidence does not show benefit of diurnal timing of BP-lowering drug administration onmajor CVD outcomes.512Itisim- portant that medication istaken atthe most convenient time ofday to improve adherence. Patients should also beencouraged totake medi- cations atthe same time each day and inaconsistent setting, tohelp ensure adherence.246,513 8.4.Selecting patients forpharmacological blood pressure-lowering treatment Commencement ofBP-lowering treatment isoften decided based on office BP measurements but, where possible, the present guidelines strongly recommend using out-of-office BPmeasurement forconfirm- ingelevated BPand hypertension (seeSection 5).Asdetailed inSection 6, anoffice BP of<120/70 mmHg iscategorized inthese guidelines as non-elevated BP. When apatient isdiagnosed with confirmed hypertension (sustained BP≥140/90 mmHg), starting BP-lowering treatment isrecommended irrespective ofCVD risk, which should consist ofasimultaneous combin- ation oflifestyle interventions and pharmacological therapy. Lifestyle in- terventions are crucial asaninitial treatment step, and must bestrongly emphasized with the patient, but concurrent pharmacological therapy is recommended. This concurrent initiation oflifestyle and pharmacological therapy should not give patients the impression that lifestyle changes are oflesser importance, and the patient should becounselled that these life- style changes may allow subsequent discontinuation ordown-titration of medication, which can beused asmotivation topersist with lifestyle changes. After treatment initiation, the patient should beseen frequently (e.g. every 1–3 months with aGP orspecialist) until BPiscontrolled. BP should becontrolled, preferably within 3months (see alsoSection 6and algorithm Figure 18). Iflifestyle changes are effective inBP lowering, pharmacological treatments may subsequently be down-titrated or stopped asappropriate. When office BPis120–139/70–89 mmHg, the patient isconsidered ashaving elevated BP, and further CVD risk stratification isrecom- mended toguide therapy (Table 14). •Inpatients with elevated BPwho are not atincreased risk for CVD (10-year CVD risk<10%) and donot have other high-risk conditions orrisk modifiers, BP-lowering lifestyle measures are recommended.Recommendation Table 16—Recommendations for pharmacological treatment ofhypertension (see Evidence Tables 27,28,and29) Recommendations ClassaLevelb Among allBP-lowering drugs, ACE inhibitors, ARBs, dihydropyridine CCBs, and diuretics (thiazides and thiazide-like drugs such aschlorthalidone and indapamide) have demonstrated the most effective reduction ofBPand CVD events, and are therefore recommended asfirst-line treatments tolower BP.122,446I A Itisrecommended that beta-blockers are combined with any ofthe other major BP-lowering drug classes when there are other compelling indications fortheir use, e.g. angina, post-myocardial infarction, heart failure with reduced ejection fraction, orfor heart rate control.122,448–450I A Itisrecommended totake medications atthe most convenient time ofday for the patient toestablish a habitual pattern ofmedication taking toimprove adherence.246,513I B Given trial evidence formore effective BPcontrol vs. monotherapy, combination BP-lowering treatment is recommended for most patients with confirmed hypertension (BP≥140/90 mmHg) asinitial therapy. Preferred combinations are aRAS blocker (either an ACE inhibitor oranARB) with adihydropyridine CCB ordiuretic. Exceptions toconsider include patients aged ≥85 years, those with symptomatic orthostatic hypotension, moderate-to-severe frailty, orelevated BP(systolic BP120–139 mmHg or diastolic BP70–89 mmHg) with aconcomitant indication for treatment.131,480,483,484,489I B ContinuedInpatients receiving combination BP-lowering treatment, fixed-dose single-pill combination treatment isrecommended.484,489,501,502,514I B IfBPisnot controlled with atwo-drug combination, increasing toathree-drug combination is recommended, usually aRAS blocker with a dihydropyridine CCB and athiazide/thiazide-like diuretic, and preferably inasingle-pill combination.489I B IfBPisnot controlled with athree-drug combination, adding spironolactone should beconsidered.459IIa B IfBPisnot controlled with athree-drug combination and inwhom spironolactone isnot effective or tolerated, treatment with eplerenone instead of spironolactone,503orthe addition ofabeta-blocker if not already indicated459and, next, acentrally acting BP-lowering medication,515analpha-blocker,515 hydralazine, orapotassium-sparing diuretic should beconsidered.516IIa B Combining two RAS blockers (ACE inhibitor and an ARB) isnot recommended.498–500,517III A ©ESC 2024 ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; BP, blood pressure; CCB, calcium channel blocker; CVD, cardiovascular disease; RAS, renin– angiotensin system. aClass ofrecommendation. bLevel ofevidence.ESC Guidelines 51
+While there are not enough outcomes data foradrug recommenda- tion inlower CVD risk adults with elevated BP, there issome evi- dence tosuggest that relative treatment effects ofBPlowering are similar across awide range ofpredicted risk categories, including among those with a<10% risk.518Therefore, while we donot pro- vide aformal recommendation forthis, ifinitial lifestyle measures are not successful after 6–12 months, drug treatment might bediscussed onanindividual basis among lower CVD-risk adults when BPisbe- tween 130/80 and<140/90 mmHg.518 •Inpatients with elevated BP (office BPof120–139/70–89 mmHg) who are atsufficiently high risk for CVD (e.g. 10-year CVD risk ≥10%) orinthe presence ofhigh-risk conditions orborderline 10-year CVD risk (5% -<10%) combined with risk modifiers or abnormal risk tool tests, BP-lowering lifestyle measures should be initiated for3months. Following this, pharmacological therapy isre- commended for persons with confirmed BP of≥130/80 mmHg, when these lifestyle changes have not worked orare not being imple- mented (Section 8.2) Prompt addition ofpharmacological therapy, if needed by3months, should beemphasized, toavoid therapeutic inertia.519For those with BP of120–129/70–79 mmHg, ongoing and intensified lifestyle intervention ispreferred. The above recommendations apply toallindividuals with elevated BP, irrespective ofage. However, recognizing the lack ofconclusive evi- dence and added risk ofside effects among certain subgroups, the task force also recommends that, among patients with elevated BP, BP-lowering treatment should always bestarted based onindividual clinical judgment and shared decision-making. Inaddition, consideration ofBP-lowering drug treatment should be deferred until BP is>140/90 mmHg inthe following settings: pre- treatment symptomatic orthostatic hypotension, age≥85 years, clinic- ally significant moderate-to-severe frailty, and/or limited predicted life- span (<3 years) due tohigh competing risk (including eGFR <30mL/ min/1.73 m2).Patients with elevated BPinthese settings are less likely toobtain sufficient net benefit from BP-lowering drug therapy ortotol- erate intensive drug therapy. Section 9contains more information on the treatment ofspecific subgroups, including older and frail adults.Table 14 Initiation ofblood pressure-lowering treatment based onconfirmed blood pressure category andcardiovas- cular disease risk Blood pressure (mmHg)Non-elevated BP (<120/70)Elevated BP(120/70 to139/89) Hypertension (≥140/90) Risk (a) All adults with SBP 120– 129 mmHg (b) SBP 130–139 AND 10-year estimated CVD risk<10% AND nohigh-risk conditions orrisk modifiers orabnormal risk tool tests(a) SBP 130–139 AND high-risk conditions (e.g. established CVD, diabetes mellitus, CKD, FHorHMOD) (b) SBP 130–139 AND 10-year estimated CVD risk≥10% (c) SBP 130–139 AND 10-year estimated CVD risk 5% -<10% AND risk modifiers orabnormal risk tool testsAssumed allatsufficiently high risk to benefit from pharmacological treatment Treatment Lifestyle measures for prevention Screen BPand CVD risk opportunisticallyLifestyle measures for treatment Monitor BPand CVD risk yearlyLifestyle measures and pharmacological treatment (after 3-month delay). Monitor BPyearly once treatment control is establishedLifestyle measures and pharmacological treatment (immediate) Monitor BPyearly once treatment control isestablished Target (mmHg) Maintain BP<120/70 Aim BP120–129/70–79 mmHga ©ESC 2024 BP, blood pressure; CKD, chronic kidney disease; CVD, cardiovascular disease; DBP, diastolic blood pressure; FH, familial hypercholesterolaemia; HMOD, hypertension-mediated organ damage; SBP, systolic blood pressure. aCaution inadults with orthostatic hypotension, moderate-to-severe frailty, limited lifeexpectancy, and older patients (aged ≥85 years). Recommendation Table 17—Recommendations for initiating blood pressure-lowering treatment (see Evidence Tables 30–32) Recommendations ClassaLevelb Inadults with elevated BPand low/medium CVD risk (<10% over 10years), BPlowering with lifestyle measures isrecommended and can reduce the risk ofCVD.119,120,348,408,411,520,521I B Inadults with elevated BPand sufficiently high CVD riskc,after 3months oflifestyle intervention, BP lowering with pharmacological treatment is recommended forthose with confirmed BP≥130/ 80mmHg toreduce CVD risk.116,522I A Itisrecommended that inhypertensive patients with confirmed BP≥140/90 mmHg, irrespective of CVD risk, lifestyle measures and pharmacological BP-lowering treatment are initiated promptly to reduce CVD risk.116,121,122I A Itisrecommended tomaintain BP-lowering drug treatment lifelong, even beyond the age of85years, ifwell tolerated.523–525I A Because the benefit inreducing CVD outcomes is uncertain inthese settings, and noting that close monitoring oftreatment tolerance isadvised, BP-lowering treatment should only beconsidered from ≥140/90 mmHg among persons meeting the following criteria: pre-treatment symptomatic orthostatic hypotension, age≥85 years, clinically significant moderate-to-severe frailty, and/or limited predicted lifespan (<3 years).131,524,526,527IIa B ©ESC 2024 BP, blood pressure; CVD, cardiovascular disease. aClass ofrecommendation. bLevel ofevidence. c10-year estimated CVD risk of≥10%; or10-year estimated CVD risk of5% -≤10% plus risk modifiers orabnormal risk tool tests; orhigh-risk conditions (e.g. established CVD, diabetes, moderate orsevere CKD, familial hypercholesterolaemia, orhypertension-mediated organ damage).52 ESC Guidelines
+8.5.Intensity ofblood pressure-lowering therapy andideal treatment targets 8.5.1. Expected degree ofblood pressure reduction with approved drugs The magnitude ofBP reduction achieved with the main classes of BP-lowering medications (ACE inhibitors, ARBs, dihydropyridine CCBs, diuretics, and beta-blockers) asmonotherapy issimilar overall.528,529BP reduction with standard doses ofany ofthese five classes can beexpected tobeapproximately 9/5mmHg with office BP and 5/3mmHg with ABPM.478These BP-lowering effects may attenuate over time.530 Combination therapy (e.g. with three drugs athalf standard dose) over the short term can lower office BPbyupto20/11 mmHg.478,531The rea- son why beta-blockers are not considered first-line BP-lowering medica- tions (outside ofcompelling indications) isnot because ofinferior BP-lowering properties (particularly for vasodilating beta-blockers),532 but because ofinferior efficacy inreducing CVD events (particularly stroke) among patients with hypertension, and tolerance issues.533–536 The BP-lowering effect ofeach BPmedication class generally increases with the dose administered, though this relationship isnot linear.537 Effects ofeach medication can also vary atthe individual level, sometimes requiring personalization bymatching the patient with the best medica- tion for them.490The magnitude ofBPreduction for any BP-lowering medication may increase asafunction ofthe pre-treatment BP, which isalso known asWilders principle.538,539 The BP-lowering effect ofpharmacological therapy istypically evi- dent after 1–2 weeks oftreatment,540but the maximum effect might take longer tomanifest. Therefore, the advised follow-up after 1–3 months (1month preferred with aGP orspecialist) allows for assess- ment oftolerance/safety, but also allows enough time togauge the fullBP-lowering effect ofeach drug titration (seeSection 8.3.4). 8.5.2. The ideal target ofblood pressure-lowering treatment Asdiscussed inSection 6,optimal control ofBPtranslates into CVD risk reduction, thereby reducing morbidity and mortality inthe population.116,478,541 BPthreshold isdefined asthe BPatwhich BP-lowering treatment is initiated, while BPtarget isthe BPgoal with treatment. The BPthreshold toinitiate BP-lowering therapy isnot necessarily the same asthe recommended BPtarget once therapy iscommenced (in other words, treatment threshold and treatment target may not bethe same foragiven patient). Specifically, forhypertensive patients inwhom BP-lowering treatment isrecommended above abaseline BPof≥140/ 90mmHg, the recommended target ofBP-lowering therapy is120–129/ 70–79 mmHg, provided treatment iswell tolerated (see Supplementary data online). Persons with elevated BPwho receive treatment arealso re- commended toachieve atarget of120–129/70–79 mmHg. Therefore, the treatment target inthe 2024 Guidelines isalways 120–129/70–79 mmHg (but only iftreatment istolerated and with cer- tain exceptions where more lenient targets are advised). Incontrast, the treatment threshold may differ based onCVD risk, specifically inthe ele- vated BPcategory. For example, inaddition tohypertensive adults with BP≥140/90 mmHg, there are individuals with anoffice systolic BPof 130–139 mmHg and/or diastolic BP of80–89 mmHg who have suffi- ciently high CVD risk torecommend BP-lowering drug treatment. The BP target range of120–129/70–79 mmHg recommended inthese guidelines reflects the most current evidence from contempor- aneous RCTs135,136,146,542–545and from meta-analyses ofRCTs.131Of note, this treatment target reduces CVD events inolder adults136,523with evidence for efficacy ofmore intensive BP-lowering treatment targets established uptoage 85years.131Furthermore, research data indicate that, tooptimally reduce CVD risk, achieving anon- treatment BPof120/70 mmHg isthe best point onthe BPtarget range provided inour guideline recommendations (Figure 20). However, while we strongly considered recommending atreatment target ofexactly 120/70 mmHg with out-of-office BPconfirmation, we instead chose a target range of120–129/70–79 mmHg (preferably with out-of-office BPconfirmation but also allowing for office BP) for the following rea- sons: providing flexibility topatients and clinicians; feedback from exter- nal peer review; feedback from patients that lifestyle ispreferred to medication unless BPisinthe hypertensive range; the knowledge that contemporary treat-to-target intensive BPtrials included only persons with baseline systolic BPof≥130 mmHg; and arecognition that the BPvalues recorded under research conditions using systematic ap- proaches tomeasurement (while strongly recommended bythese guidelines) are not always the same asBPvalues recorded under rou- tine clinical care, which can be5–10 mmHg higher.65,66 Inaddition, the trial data confirming efficacy for our recommended treatment target of120–129/70–79 mmHg donot necessarily apply tomoderately-to-severely frail adults who were generally excluded from trials. Furthermore, the data supporting this BP target among adults aged >85 years are inconclusive.131Frailty can occur atdifferent ages and is,together with tolerability ofBP-lowering treatment, anim- portant characteristic when considering the BPtarget for agiven pa- tient. Accordingly, personalized BP-lowering treatment should be instituted inpeople aged ≥85 years and/or those with significant frailty. Recommended indicators offrailty inguiding BP-lowering treatment are given inSection 9. Several important nuances are highlighted and warrant consideration prior toimplementing the new BP target of120–129/70–79 mmHg among patients receiving BP-lowering therapy: •Evidence forasystolic BP-lowering treatment target of120–129 mmHg isstrong (Class I,level ofevidence A). •Evidence for aspecific diastolic BP-lowering treatment target isless strong inthose who are treated toasystolic target of 120–129 mmHg. While most adults treated toasystolic BPtarget of120–129 mmHg will also achieve adiastolic BPof70–79 mmHg, not allwill.543,546Furthermore, adults who achieve systolic BPcon- trol are generally atlow relative risk for CVD, even when diastolic BPis70–90 mmHg.547,548Nonetheless, due inpart tothe known higher risk of isolated diastolic hypertension among younger adults,549the task force agreed that itisreasonable totarget an on-treatment diastolic BP of70–79 mmHg among patients with diastolic BPof≥80 mmHg who are already atthe systolic BPtar- get of120–129 mmHg (Class IIb, level ofevidence C). •The task force acknowledges the 2021 ESC Guidelines oncardio- vascular disease prevention inclinical practice,170which take astep- wise approach totheir recommendations forBP-lowering treatment. The 2021 Guidelines recommended anon-treatment systolic BPtar- get of130–139 mmHg asthe first step and then—based onpatient preferences, risk, and frailty—to aim for atarget on-treatment systolic BPof<130 mmHg asthe second step. While we recognize the potential value ofthis two-step approach, which many clinicians may choose tofollow, the current guidelines emphasize one on- treatment BPtarget (120–129/70–79 mmHg, provided treatment is tolerated). This one-step approach isbased onthe evidence, and mo- tivated todiscourage therapeutic inertia around BPlowering. Asan illustrative example ofthe latter concern for therapeutic inertia, anESC Guidelines 53
+on-treatment systolic BPof135 mmHg (office) may beconsidered reasonable when reviewing the 2021 ESC Guidelines oncardiovascu- lardisease prevention inclinical practice but, we hope, will not be considered reasonable tothose who follow the updated 2024 ESC Guidelines presented here. Specifically, itiswell established that an on-treatment systolic BP of135 mmHg isnot optimal relative to more intensive control.116,131,135,136,445,542,543,545 •We acknowledge that theresults from RCTs cannot always beextrapo- lated toroutine clinical care. Inaddition, werecognize theincreased risk of side effects among patients receiving more intensive BP-lowering treat- ments, compared with traditional BPtargets.545,550Accordingly, anim- portant caveat toour treatment target of120–129/70–79 mmHg is the recommendation topursue this target only when treatment iswell tolerated. Incases where BP-lowering treatment isnot well tolerated and atarget of120–129/70–79 mmHg isnot possible, itisrecommended tofollow the‘aslow asreasonably achievable’ (ALARA) principle, bytar- geting treatment toaBPthat isaslow asreasonably achievable.•Inaddition toadults with significant frailty and/or who are≥85 years ofage, the evidence for aBP-lowering treatment target of 120–129/70–79 mmHg may also not generalize topatients with: (i)pre-treatment symptomatic orthostatic hypotension, (ii)limited predicted lifespan (e.g. <3years),527and/or (iii) high levels of competing risk for non-CVD death including CKD with eGFR <30mL/min/1.73 m2)(see Section 9). Finally, asoutlined inSection 5,these guidelines endorse a‘trust but ver- ify’approach tooffice BPmeasurements, and, where possible, confirm- ingBPwith accurate out-of-office BPmeasurements (ABPM, HBPM) is recommended prior tostarting treatment, tomonitor the treatment effect ofBP-lowering medication. 8.5.3. Personalizing treatment strategies Though promising, there islittle to no evidence to date from CVD outcome trials touse novel biomarkers for individualizing BP-lowering treatment.551,552Nonetheless, different patient groups SBP 120 mmHg  is the optimal point in this range if toleratedSBP target range 120–129 mmHg  (Class I)Target SBP as low as reasonably achievable (preferably <140) if 120–129 mmHg target not tolerated or in these settings: Pre-treatment symptomatic orthostatic hypotension and/or age ≥85 years   (Class IIa) Clinically significant moderate-to-severe frailty at any age  and/or limited predicted lifespan (<3 years) (Class IIb) Exclude hypertensive emergencyAssess for symptoms or signs of hypotensionNon-elevated SBP (<120 mmHg) Elevated SBP (120–139 mmHg) 20406080120130140 160 180 200 220 240100110 260 280mmHg Systolic hypertension (≥140 mmHg)Figure 20 Systolic blood pressure categories and treatment target range. BP, blood pressure; SBP, systolic blood pressure.54 ESC Guidelines
+can beidentified, and medication initiation can betailored topre- existing conditions, such as diabetes mellitus, CKD, AF, post- myocardial infarction, heart failure, metabolic syndrome, and pro- teinuria/albuminuria (Section 9). History ofprevious side effects and possible and compelling indications also need tobeconsidered when selecting treatment (see Supplementary data online, Tables S9 andS10). Cardioselective beta-blockers may beused inlow dose in chronic asthma,553,554inline with their use inpatients with heart failure with chronic asthma. For considerations ofBP-lowering treatment among specific pa- tient populations ofinterest, including different racial/ethnic popula- tions, seeSection 9. 8.5.4. Duration andmonitoring ofdrug therapy BP-lowering treatment isusually chronic, often lifelong. This raises the question oflong-term efficiency, long-term side effects, adher- ence, and persistence with therapy. While BP-lowering therapies typically provide an overall durable effect, some attenuation ofeffect may beseen over time.66,530First-line BP-lowering medica- tion classes appear tobesafe for long-term use.555–557Once BPis controlled, atleast ayearly follow-up isadvised. Because ofthe known temporal variability inBP558,559and medication efficacy in the long term,530medication changes may be necessary over time (see Supplementary data online). 8.6.Device-based blood pressure lowering Several device-based therapies designed tolower BPhave been inves- tigated.560,561Todate, the best evidence exists forcatheter-based renal denervation. 8.6.1. Catheter-based renal denervation Sympathetic nervous system overactivity contributes tothe develop- ment and progression ofhypertension.562Renal denervation aims to interrupt afferent and efferent sympathetic nerves inthe adventitia and perivascular tissue ofthe renal arteries.563The 2018 ESC/ESH Guidelines onthe management ofarterial hypertension didnot recom- mend the use ofdevice-based therapies forroutine treatment ofhyper- tension, unless inthe context ofclinical studies and RCTs.1This was based onnegative data using first-generation radiofrequency catheters (see Supplementary data online). More recent data from sham-controlled trials investigating second- generation radiofrequency and ultrasound catheters demonstrated a BP-lowering efficacy inabroad range ofpatients, with and without con- comitant BP-lowering medications, including those with resistant hypertension.564–568Long-term, non-randomized, follow-up data from the Global Symplicity Registry,569Symplicity HTN-3 trial,570 Spyral HTN-ON MED pilot trial,571and AStudy ofthe Recor Medical Paradise System inClinical Hypertension (RADIANCE-HTN) SOLO trial572indicate asustained BP-lowering effect forupto3years. Asingle-centre open-label study suggested sustained BPreductions up to10years.573These data also highlight apotentially important advan- tage ofrenal denervation, namely that the BP-lowering effect ofthis intervention might be‘always on’, making this approach attractive for patients with suboptimal medication adherence.254Some patients may prefer aone-off procedure rather than taking daily medications chronically and may request renal denervation. Of significance, there are no reported procedure-related serious safety signals inthe first- and second-generation trials beyond the usual risk offemoral arterial access procedures (noting that most trials to date were not powered for safety outcomes and that the task force could find no published meta-analysis data on exact rates ofmajor bleeding and major femoral artery vascular access complications after renal denervation procedures). However, the rate ofmajor bleedingRecommendation Table 18—Recommendations for blood pressure targets with treatment (see Evidence Table 34) Recommendations ClassaLevelb Toreduce CVD risk, itisrecommended that treated systolic BPvalues inmost adults betargeted to120– 129 mmHg, provided the treatment iswell tolerated.22,122,131,523,541I A Incases where BP-lowering treatment ispoorly tolerated and achieving asystolic of120–129 mmHg isnot possible, itisrecommended totarget asystolic BPlevel that is‘aslow asreasonably achievable’ (ALARA principle).22,122,131,523,541I A Because the CVD benefit ofanon-treatment systolic BPtarget of120–129 mmHg may not generalize to the following specific settings, personalized and more lenient BPtargets (e.g.<140 mmHg) should be considered among patients meeting the following criteria: pre-treatment symptomatic orthostatic hypotension, and/or age≥85 years.131IIa C Because the CVD benefit ofanon-treatment systolic BPtarget of120–129 mmHg may not generalize to the following specific settings, personalized and more lenient BPtargets (e.g.<140/90 mmHg) may be considered among patients meeting the following criteria: clinically significant moderate-to-severe frailty atany age, and/or limited predicted lifespan (<3 years).IIb C Incases where on-treatment systolic BPisatorbelow target (120–129 mmHg) but diastolic BPisnot at target (≥80 mmHg), intensifying BP-lowering treatment toachieve anon-treatment diastolic BPof 70–79 mmHg may beconsidered toreduce CVD risk.IIb C ©ESC 2024 ALARA, aslow asreasonably achievable; BP, blood pressure; CVD, cardiovascular disease. aClass ofrecommendation. bLevel ofevidence.Recommendation Table 19—Recommendations for follow-up inpatients with treated hypertension (see Evidence Table 33) Recommendation ClassaLevelb Once BPiscontrolled and stable under BP-lowering therapy, atleast ayearly follow-up forBPand other CVD risk factors should beconsidered.IIa C ©ESC 2024 BP, blood pressure; CVD, cardiovascular disease. aClass ofrecommendation. bLevel ofevidence.ESC Guidelines 55
+and major femoral artery vascular access complications for coronary angiography using afemoral approach istypically reported as 1%–4%574,575but has been reported as5%–10% insome studies.575 Trials investigating radial access forrenal denervation are currently on- going (ClinicalTrials.gov identifier: NCT05234788). After renal denerv- ation, there isa0.25%–0.5% rate ofrenal artery stenosis/dissection requiring stenting.576Long-term follow-up data up to3years have not suggested worsening ofrenal function beyond the expected rates inpatients with hypertension with mildly-to-moderately reduced renal function.569,577Of note, sham-controlled trials todate excluded pa- tients with severely reduced kidney function atbaseline.564,566–568 Despite the clear promise ofrenal denervation inreducing BP, there are some concerns that warrant consideration, asweindicate inthe re- commendations. First, the effect ofcurrent renal denervation catheter technologies onBPlowering isrelatively modest foraninvasive proced- ure (meta-analyses report placebo-corrected systolic BP lowering ofapproximately 6mmHg onoffice BPassessment and 4mmHg on 24hABPM).578Assuch, the average BP-lowering effect ofrenal de- nervation appears nomore than forone standard BP-lowering medica- tion. Accordingly, many adults undergoing renal denervation will likely require ongoing, post-procedural, BP-lowering drugs. Second, the cost-effectiveness ofrenal denervation has not been fully established. Since effects ofcurrent renal denervation technologies are similar tothat ofone standard BP-lowering medication, most ofwhich are generic, itisdifficult tosee ascenario where renal denervation could beproven cost-effective for most patients. An exception might bepatients who are atvery high risk ofCVD events and who have un- controlled BP due to resistant hypertension (with or without non-adherence).579,580 Third, there are noadequately powered outcomes trials demon- strating that renal denervation reduces CVD events and issafe inthe long term. While observational reports have suggested associations be- tween renal denervation and reduced risk forCVD events,581,582these observational data have major inferential limitations including asignifi- cant potential for confounding. While BPlowering istypically agood surrogate for CVD benefit, there isno guarantee that this istrue with renal denervation and, furthermore, off-target effects independent ofBPcould influence CVD and other adverse-event rates after the pro- cedure. Because ofthe lack ofoutcomes trials, renal denervation can- not reach the Class Iindication threshold set bythis task force. Arguments that outcomes trials will not befunded are insufficient to influence guideline recommendations. However, itishoped that the position ofthese guidelines will motivate industry tosponsor the neces- sary renal denervation outcomes trials. Fourth, related tothe lack ofoutcomes data, the potentially ‘always on’ effect ofrenal denervation could backfire iflate complications emerge. Medications causing complications orside effects can simply bestopped and replaced with alternative medications when such pro- blems emerge; this isnot true with renal denervation. Fifth, the impact ofscaling uprenal denervation onusual cardiac de- partment catheterization laboratory workflows isofsome concern. Specifically, itisimportant that renal denervation procedures donot delay timely access toother elective procedures with proven efficacy inreducing CVD outcomes.583 Sixth, there isstill nodirect evidence togauge whether renal denerv- ation procedures are successful and that the kidneys are denervated and donot reinnervate over time.584Relatedly, the concept ofrespon- ders and non-responders torenal denervation (and the hypothesis that predictors ofresponse might befound tohelp identify patients most suitable for the procedure) isquestioned. Medical interventions,including drugs, are naturally subject tointer-individual variability inre- sponse.567Additionally, there are few examples inmedicine ofconsist- ent and clinically useful predictors oftreatment response for medical conditions that have complex genetic and environmental underpinnings (i.e. conditions like hypertension). Amultidisciplinary hypertension team, including experts inhyperten- sion and percutaneous cardiovascular interventions, isrecommended to evaluate the indication and toperform the procedure.585Based onthe available evidence, renal denervation may beconsidered for patients who have uncontrolled, true resistant hypertension with athree-drug combination and who express apreference toundergo renal denerv- ation.566,568,585This recommendation isinformed, inpart, bythe higher risk ofCVD events inthis subgroup, which represents amajor unmet clinical need and which also means that cost-effectiveness considerations are likely tobeoptimal inthis setting. Inpatients who are non-adherent orintolerant tomultiple BP-lowering medications, particularly first-line agents, and who have high predicted CVD risk and aBPthat isnot attar- get, renal denervation may, forthe same reasons, beconsidered ifthe pa- tients express apreference toundergo renal denervation after atailored shared decision-making process. The shared decision-making process re- quires that the patients are fully informed about the benefits, limitations, and risks associated with renal denervation. Recommendation Table 20—Recommendations for device-based treatment ofhypertension (see Evidence Table 35) Recommendations ClassaLevelb Toreduce BP, and ifperformed atamedium-to-high volume centre, catheter-based renal denervation may beconsidered for resistant hypertension patients who have BPthat isuncontrolled despite a three BP-lowering drug combination (including a thiazide orthiazide-like diuretic), and who express a preference toundergo renal denervation after a shared risk-benefit discussion and multidisciplinary assessment.564,566–568,586–590IIb B Toreduce BP, and ifperformed atamedium-to-high volume centre, catheter-based renal denervation may beconsidered for patients with both increased CVD risk and uncontrolled hypertension onfewer than three drugs, ifthey express apreference to undergo renal denervation after ashared risk-benefit discussion and multidisciplinary assessment.564,566– 568,586–590IIb A Due toalack ofadequately powered outcomes trials demonstrating itssafety and CVD benefits, renal denervation isnot recommended asafirst-line BP-lowering intervention for hypertension.III C Renal denervation isnot recommended for treating hypertension inpatients with moderate-to-severely impaired renal function (eGFR <40 mL/min/1.73 m2) orsecondary causes ofhypertension, until further evidence becomes available.III C ©ESC 2024 BP, blood pressure; CVD, cardiovascular disease; eGFR, estimated glomerular filtration rate. aClass ofrecommendation. bLevel ofevidence.56 ESC Guidelines
+8.6.2. Other devices Most device-based therapies investigated for BP-lowering therapy in hypertension have been aimed atmodulating the autonomic nervous system activity (baroreflex activation therapy, endovascular barore- flex amplification therapy, and carotid body ablation).560Cardiac neuromodulation therapy aims tolower left ventricular preload by variably altering the atrioventricular interval using adual-chamber, rate-responsive, implantable pulse generator inpatients indicated for implantation orreplacement ofadual-chamber pacemaker.591,592 Some, though not all,ofthese devices have shown promising results in non-randomized, single-arm studies. Asham-controlled trial investi- gating central iliac arteriovenous stent anastomosis was terminated early after longer-term follow-up data indicated anincrease inheart failure inthe stent group.561Therefore, the use ofthese device-based therapies isnot recommended forroutinely treating hypertension un- tilfurther evidence regarding their safety and efficacy becomes avail- able (see Supplementary data online). 8.7.Unintended andpotentially harmful consequences ofblood pressure lowering andimplications fortreatment targets 8.7.1. Adverse effects ofblood pressure-lowering medications 8.7.1.1. Symptomatic adverse effects BP-lowering medications have multiple side effects, which may bemore common infemales.536,593,594Although generally well tolerated, common side effects include headaches, cough, dizziness orlight-headedness, diar- rhoea orconstipation, fatigue, ankle swelling, and erectile problems, de- pending on the drug class (see Supplementary data online, Table S9).536,550,593–597 Inrandomized trials ofadults aged >60 years, the overall rate of symptomatic BP-lowering drug withdrawal was higher than the rate ofplacebo withdrawal (approximately 15% vs.5%).593Asystematic re- view, which included 280 638 participants in58RCTs, reported noevi- dence foranincreased relative risk offalls inthose taking BP-lowering drugs.550There was, however, anincreased relative risk ofmild hyper- kalaemia, acute kidney injury, hypotension, and syncope. Furthermore, very frail adults were excluded from BP-lowering trials, which isrele- vant because such patients are more prone toadverse effects and poly- pharmacy (see Supplementary data online).596 8.7.1.2. Renal effects Asystematic review reported anincreased risk ofacute kidney injury and hyperkalaemia associated with BP-lowering treatment.550Analyses ofoutcomes byspecific drug class showed that drugs affecting the RAAS were more likely tobeassociated with acute kidney injury and hyperkalaemia.550 Patients with significant CKD tend to be excluded from RCTs.137,545,598Itisimportant toremember these exclusion criteria, and that patients with CKD are more likely tosuffer from resistant hypertension, when extrapolating the results ofmore intensive BPlow- ering topatients with moderate-to-severe CKD (seeSection 9).599 8.7.1.3. Erectile dysfunction Older classes ofBP-lowering drugs (including diuretics, beta-blockers, and centrally acting medications) are associated with erectiledysfunction.600However, newer classes have neutral effects.601 Angiotensin receptor antagonists may have beneficial effect onerectile function.602 8.7.2. Pillburden andnon-adherence More intensive treatment ofelevated BPand hypertension may beas- sociated with anincreased risk ofpolypharmacy and pillburden, which are themselves associated with non-adherence.603,604Single-pill, fixed- dose drug combinations can help toreduce pillburden and are recom- mended toimprove adherence (refer toSection 8.3.4). Increased intensity ofBPlowering (while ultimately cost reducing in terms ofCVD reduction)605can also result inhigher upfront direct and indirect healthcare costs, with more people requiring medication and higher demand for technology-based adherence strategies, which can bechallenging toimplement, especially inresource-poor settings.604 8.7.3. Potentially harmful consequences ofblood pressure lowering forfrail older people Unintended consequences ofBPlowering (hypotension, syncope, falls) can behazardous forfrail older people inparticular.606Retrospective studies have shown that adults aged >75 years from the general population, who would have met the criteria for inclusion inthe Systolic Blood Pressure Intervention Trial (SPRINT), had arate ofinjurious falls and syn- cope that was nearly five times that ofthe standard care group inthe trial. This suggests that healthy participant bias may have contributed tothe findings ofSPRINT and other similar BP-lowering trials, and that theresults may not fully generalize toolder adults inmore routine clinical care.607 Patients’ functional ability should beconsidered inaddition toage to help negate any unintended consequences ofBPlowering inafrailer co- hort. Despite their chronological age, older patients with hypertension who are fitand can independently carry out activities ofdaily living will benefit from guideline-directed treatment similar toyounger cohorts.131 However, tailoring treatment targets and treatment plans forfrail older patients isnecessary toavoid unintended consequences. This should in- clude assessing frailty, including cognitive status, risk offalls, propensity for symptomatic orthostatic hypotension, polypharmacy, and other co- morbid conditions.608,609Of note, and asdetailed inSection 9,some data indicate abenefit ofmore intensive BP-lowering oncognitive func- tion.523,610,611For those with loss offunction but preserved activities of daily living, amore detailed geriatric assessment isrequired toexplore the risks and benefits oftreatment, aswell asconsiderations fortailoring therapeutic strategies where appropriate. For patients who areboth func- tionally impaired and unable tocarry out activities ofdaily living, the thera- peutic goals ofhypertension treatment should bepersonalized, and medications discontinued where appropriate (seeSection 9.3).596 8.7.4. Clinical inertia inblood pressure lowering The fear ofserious adverse events with BP-lowering medications isof- ten cited asareason for clinical inertia, although the evidence todate from meta-analyses ofRCTs suggests these side-effect concerns may beexaggerated.550,612However, RCTs often select populations with less frailty and multimorbidity who are more likely totolerate treat- ment.613Consequently, fewer adverse effects might be reported than would beexpected inthe general population. Itremains uptoin- dividual clinicians toinitiate shared decision-making with each patient, especially patients invulnerable groups and those who have experi- enced previous adverse events, weighing uppotential benefits against risks oftreatment.614,615ESC Guidelines 57
+9.Managing specific patient groups orcircumstances 9.1.Young adulthood (18–40 years) 9.1.1. Definition andepidemiology Inthe present guidelines ‘young adulthood’ isdefined asage 18–40 years. The prevalence ofhypertension inyoung adults isincreasing inmen and women.616–618Unhealthy lifestyle, gender, obesity, and socio-economic factors contribute.617,619–621Hypertension-attributable CVD burden in young adults, evaluated asmortality oryears ofliving with disability, has increased inthe last decades, especially inlow- and middle-income countries and inmen.622Hypertension awareness, treatment, and con- trol inyoung adults islower than inother age categories, aresult driven byworse control inyoung men.623 Systolic and diastolic hypertension and isolated diastolic hyperten- sion are associated with increased CVD risk inthe young (see Supplementary data online).624Isolated systolic hypertension inthe young isdiscussed inSection 9.4. 9.1.2. Secondary hypertension inyoung adulthood Secondary hypertension ismore frequent inyounger than inlater- onset hypertension, with aprevalence of15%–30% inhypertensive young adults reported from some referral centres.625,626Major causes ofsecondary hypertension include drug-induced hypertension (e.g. oestrogen-progesterone oral contraceptives; cold medication) and pri- mary aldosteronism. The use ofrecreational drugs/substances, aswell assupplements and energy drinks should beinvestigated (seeSection 7). Combined oestrogen-progesterone contraceptives areamong themost common causes ofdrug-induced hypertension inyoung women,627,628and should not beused inhypertensive women unless there isnoother method available oracceptable tothepatient.629Conversely, progestin-only contra- ceptives are generally considered safe inwomen with hyperten- sion.89,630,631Fibromuscular dysplasia should beconsidered asacause of secondary hypertension inyoung women,626,632whereas primary aldoster- onism, themost common form ofsecondary hypertension, isequally com- mon indifferent age classes.316Screening for secondary hypertension is thus recommended inyoung adults with hypertension. However, inobese young adults, primary hypertension ismore common, though OSAS should also beconsidered inthis instance.633 9.1.3. Measurement andmanagement ofblood pressure inyoung adults Out-of-office BPmeasurement isrecommended inyoung adults for confirming diagnosis, since the white-coat phenomenon occurs inthe young.634Because ofthe lower absolute CVD risk inthis age category compared with older adults, hard-endpoint randomized trials ofBP lowering inyoung adults have not been performed. However, since relative risk reduction byBP-lowering treatment ishomogeneous in any age group, including those <55 years old,131young adults with suit- able indications are also expected tobenefit from BP-lowering therapy. The hypertension management algorithm based onCVD risk proposed inSection 6isnot fully applicable inyoung adults, since SCORE2 has not been validated for individuals <40 years old. Even risk stratification based onlifetime risk assessment does not apply tovery young adults (e.g. 20–30 years ofage).128Inthe absence ofestablished CVD, diabetes mellitus, familial hypercholesterolaemia, and moderate orsevere CKD aBP-lowering treatment initiation threshold ofoffice 140/90 mmHg is appropriate inmost young adults. However, HMOD assessment maybeconsidered inpatients aged <40 years tostratify individuals with ele- vated BPinto ahigher risk category. For example, arterial stiffness bet- ter reclassifies CVD risk inindividuals aged <50 years than inolder individuals.28,215Echocardiographic left ventricular mass also maintains itsadded reclassification and discrimination ontop ofrisk scores in young adults (seeSection 6for discussion ofrisk modifiers).289 Irrespective ofcardiovascular risk, allyoung adults with elevated BP are recommended tofollow lifestyle guidance for BPlowering. Adis- cussion about family planning should betaken with young women of childbearing potential ateach visit.635,636 Adherence totreatment islow inyoung adults, <50% insome stud- ies.251Therefore, communicating the importance ofadherence, educa- tion, and follow-up clinics isimportant. (seeSections 7and11). 9.2.Pregnancy 9.2.1. Definition andepidemiology Hypertension inpregnancy istypically defined assystolic BP of ≥140 mmHg and/or diastolic BPof≥90 mmHg, measured using repeated BPreadings inthe office orhospital ontwo separate occasions or ≥15 min apart insevere hypertension (≥160/110 mmHg).1,637,638 Hypertension inpregnancy isthe second leading cause ofmaternal death after maternal peri-partum haemorrhage.639Approximately 7% ofpregnancies are complicated byhypertension, ofwhich 3% are due topre-eclampsia and around 1% are chronic orpre-existing hypertension.640Women with ahistory ofhypertensive disorders during pregnancy are atincreased risk ofsubsequent hypertension and CVD.640–642 9.2.2. Classifying hypertension inpregnancy Hypertension inpregnancy includes: •Chronic hypertension: precedes pregnancy, develops before 20 weeks ofgestation, persists for>6weeks post-partum, and may be associated with proteinuria. •Gestational hypertension: develops after 20weeks ofgestation and usually resolves within 6weeks post-partum.Recommendation Table 21—Recommendations for managing hypertension inyoung adults (see Evidence Tables 36and37) Recommendations ClassaLevelb Comprehensive screening for the main causes of secondary hypertension isrecommended inadults diagnosed with hypertension before the age of40 years, except for obese young adults where itis recommended tostart with anobstructive sleep apnoea evaluation.316,626I B Since SCORE2 has not been validated forindividuals <40 years, screening forHMOD may beconsidered in such young individuals with elevated BPwithout other increased CVD risk conditions toidentify additional individuals forpossible medical treatment.28,215IIb B ©ESC 2024 BP, blood pressure; CVD, cardiovascular disease; HMOD, hypertension-mediated organ damage; SCORE2, Systematic COronary Risk Evaluation 2. aClass ofrecommendation. bLevel ofevidence.58 ESC Guidelines
+•Antenatally unclassifiable hypertension: BPisfirst recorded after 20weeks ofgestation, and hypertension isdiagnosed but itis unclear ifchronic or not; reassessment isnecessary 6weeks post-partum. •Pre-eclampsia: gestational hypertension accompanied bynew- onset: (i)proteinuria (>0.3 g/day or≥30 mg/mmol ACR), (ii)other maternal organ dysfunction, including acute kidney injury (serum cre- atinine ≥1mg/dL), liver dysfunction (elevated transaminases >40 UI/L with orwithout right upper quadrant orepigastric abdominal pain), neurological complications (convulsions, altered mental status, blindness, stroke, severe headaches, and persistent visual scotomata), orhaematological complications (platelet count <150 000/µL, disse- minated intravascular coagulation, haemolysis), or(iii) uteroplacental dysfunction (such asfoetal growth restriction, abnormal umbilical ar- tery Doppler waveform analysis, orstillbirth).643The only cure for pre-eclampsia isdelivery, which isrecommended at37weeks’ gesta- tion, orearlier inhigh-risk cases. Ofnote, proteinuria isnot manda- tory for diagnosing pre-eclampsia but ispresent inabout 70% of cases.644Also, asproteinuria may be alate manifestation of pre-eclampsia, itshould besuspected when denovo hypertension is accompanied byheadache, visual disturbances, abdominal pain, or abnormal laboratory tests, specifically low platelets and/or abnormal liver function. Other potential causes forhigh BP, including pain and anxiety, must be excluded when treating hypertension during pregnancy. 9.2.3. Measuring blood pressure inpregnancy SeeSection 5.5.1 for information onBPmeasurement approaches in pregnancy.645Itisimportant torestate here that oscillometric devices tend tounder-estimate the true BPand are unreliable insevere pre- eclampsia; only afew have been validated inpregnancy. Importantly, only the relatively few devices validated formeasuring BPinpregnancy and pre-eclampsia should beused (https:/ /stridebp.org). 9.2.4. Investigating hypertension inpregnancy Basic laboratory investigations include urinalysis, blood count, haemato- crit, liver enzymes, serum creatinine, and serum uric acid. Serum uric acid isincreased inpre-eclampsia and identifies women atincreased risk of adverse maternal and foetal outcomes inhypertensive pregnancies.646 Allpregnant women should beassessed forproteinuria inearly preg- nancy (e.g. 11–14 weeks’ gestation).647Adipstick test of≥1+ should prompt further investigations, including ACR, which can bequickly de- termined inasingle spot-urine sample.648An ACR of<30 mg/mmol (<0.3 mg/mg) can rule out proteinuria.649Higher values should prompt 24hurine collection. Inone study, 10% ofpregnant women with chronic hypertension had secondary hypertension (estimated toaffect 0.24% ofallpregnan- cies).650Secondary hypertension during pregnancy isassociated with anincreased risk ofadverse outcomes.650The most common cause ofsecondary hypertension during pregnancy isCKD. The onset of hypertension during the first trimester, atthe peak ofhuman chorionic gonadotropin (HCG) secretion, should prompt consideration ofpri- mary aldosteronism.651Phaeochromocytoma inpregnant women is rare (0.002% ofallpregnancies) but highly morbid.652,653 9.2.5. Preventing hypertension andpre-eclampsia Low-to-moderate-intensity exercise, especially ifsupervised and in- itiated during the first trimester ofpregnancy, decreases the incidenceofdeveloping gestational hypertension.654Assuch, after consultation with their obstetrician, allpregnant women should participate inphys- ical activity, unless contraindicated.655Factors indicating risk ofpre- eclampsia are discussed inthe Supplementary data online. Women athigh ormoderate risk ofpre-eclampsia should beadvised totake 100–150 mgofaspirin daily atbedtime from gestational weeks 12–36.647,656,657 Oral calcium supplementation of0.5–2 gdaily isrecommended for preventing pre-eclampsia inwomen with low dietary intake ofcalcium (<600 mg daily).658,659 9.2.6. Treatment initiation andblood pressure targets Acute management ofBPinpre-eclampsia and eclampsia isdetailed in Section 10.4. Meta-analyses have found noevidence foranincreased risk fordeli- vering small-for-gestational-age babies inpregnant women with mild hypertension receiving BP-lowering medications.660Despite ahistorical paucity oftrial data, previous European guidelines1,89recommended initiating BP-lowering drug treatment (i)inallwomen with persistently elevated office BPof≥150/90 mmHg, and (ii)inwomen with gestation- alhypertension (with orwithout proteinuria), pre-existing hyperten- sion with superimposed gestational hypertension, orhypertension with subclinical HMOD, when office BPis>140/90 mmHg. Inthe CHAP trial, treating pregnant women with chronic hyperten- sion and BP of≥140/90 mmHg reduced the occurrence ofpre- eclampsia with severe features, and reduced medically indicated pre-term birth <35 weeks, compared with only treating severe hyper- tension (BP≥160/105 mmHg).88Tight BP control (target diastolic BP<85mmHg) compared with less-tight BPcontrol (target diastolic BP<100 mmHg) reduces the incidence ofsubsequent severe maternal hypertension (BP≥160/110 mmHg), but not foetal orother maternal outcomes inwomen with mild hypertension atbaseline (diastolic BPof 85–105 mmHg).661 Treatment with BP-lowering drugs inallpregnant women with con- firmed BPof≥140/90 mmHg isrecommended toreduce the progres- sion tosevere hypertension and the related risks foradverse pregnancy outcomes.660,661Inwomen with pre-existing and gestational hyperten- sion with and without pre-eclampsia, we recommend lowering BPbe- low 140 mmHg for systolic and to80–90 mmHg for diastolic BP.661 Evidence tosupport aBPtarget aslow as120–129/70–79 mmHg is lacking inpregnancy, though such evidence exists fornon-pregnant pa- tients receiving BP-lowering medication. 9.2.7. Managing mild hypertension inpregnancy (office blood pressure 140–159/90–109 mmHg) RAS inhibitors are not recommended inpregnancy due toadverse foe- taland neonatal outcomes. The BP-lowering drugs ofchoice are: beta- blockers (most data are available for labetalol, anon-selective beta- blocker that also acts asanalpha-blocker inhigher doses; metoprolol and bisoprolol are also considered safe), dihydropyridine CCBs (most data are available for nifedipine, which isgenerally considered first choice, also felodipine, nitrendipine, amlodipine, and isradipine can be used), and methyldopa.662,663Ameta-analysis suggests that beta- blockers and CCBs are more effective than methyldopa inpreventing severe hypertension.660Ofnote, however, atenolol should beavoided, asitisassociated with foetal growth restriction.664,665Methyldopa has been associated with anincreased risk ofpost-partum depression and caution istherefore advised both intra-partum and post-partum.637ESC Guidelines 59
+Hydralazine can beparticularly effective for severe hypertension in pregnancy and can beadministered intravenously inhypertensive ad- missions (Section 10).666–668While thiazide diuretics inpregnancy have limited safety data and should beused with caution, other diuretics such asfurosemide are not contraindicated and may benecessary in some situations (see Supplementary data online).669 9.2.8. Managing severe hypertension inpregnancy (>160/110 mmHg) Acute onset ofsevere hypertension persisting formore than 15min is considered ahypertensive emergency inpregnancy and iscovered in Section 10.4.2. 9.2.9. Managing blood pressure post-partum For women with hypertension during pregnancy, BPshould bemea- sured within 6hofdelivery and, ifpossible, daily foratleast aweek after discharge from the hospital.637Post-partum hypertension iscommon inthe first week and associated with prolonged hospitalization.670 Women with hypertension inpregnancy are atincreased risk of chronic hypertension,671CKD,672and CVD.177,223,640The relative risk ofchronic hypertension ishighest inthe first 6months following delivery, motivating regular screening inthese women.673Women with gestational hypertension, especially those with pre-eclampsia, have higher risk ofmasked hypertension.674BPmeasurements, ideally including out-of-office measurements, urine analyses, and CVD risk as- sessment, should atleast beperformed 6–12 weeks, 6months, and 12months post-partum and, after that, annually. Recent data indicate the potential utility ofself-monitoring ofBPduring the busy early post- partum period.675 AllBP-lowering drugs are excreted into breast milk.637Except for propranolol, atenolol, acebutolol, and nifedipine, most drugs are ex- creted invery low concentrations inbreast milk (see Supplementary data online, Table S11).637 9.2.10. Risk ofrecurrence ofhypertensive disorders inasubsequent pregnancy About 20%–30% ofwomen with hypertensive disorders inaprevious pregnancy will experience recurrence inasubsequent pregnancy.676,677 The earlier the onset ofhypertension inthe first pregnancy, the higher the risk ofrecurrence inasubsequent pregnancy.677 Further details onmanaging hypertension and other cardiovascular disorders inpregnancy are available elsewhere.89,6379.3.Very oldage(≥85 years), frailty, multimorbidity, andpolypharmacy 9.3.1. Definition offrailty The most common definition offrailty isanage-associated, biological syndrome characterized bydecreased biological reserves, due todysre- gulation ofseveral physiological systems.682This puts anindividual at risk when facing physiological stressors, and isassociated with poor outcomes, such asdisability, hospitalization, and death.683The esti- mated prevalence offrailty inpeople aged >65 years is7%–16% and isgreater inwomen than inmen.684,685Although the main determinant offrailty isage, chronological age must bedifferentiated from biological age.686An older patient can befitand robust while amultimorbid young patient can befrail. Using multiple drugs may have more unpre- dictable effects onBPinolder patients, because ofincreased competi- tion for underlying mechanisms responsible for their degradation and elimination, and because the ability ofthe baro-687and chemo-reflex688 systems inmaintaining asteady treated BPlevel can decline with ageing. With respect toBP, two issues compound interpretation ofthe frailty literature. First, frailty onitsown isastrong predictor ofmortality and cardiovascular complications689and isaccompanied byadecrease insystolic BP.690This raises the issue ofthe so-called BPJ-curve (see Section 9.8) and reverse causality, with frailty rather than excessive BPlowering being the root cause ofadverse health outcomes. Only properly randomized and controlled clinical trials can differentiate be- tween the effects offrailty vs.overly intensive BP-lowering treatment, but unfortunately, few BP-lowering trials have included asubstantial proportion offrail patients. Second, there isnoconsensus onhow to grade frailty inday-to-day clinical practice.606Complex frailty scales ex- istfor application inresearch,523,691but unless they are electronically generated,692they are typically not practical inroutine clinical care. Nonetheless, the clinical frailty scale (Figure 21) isintuitive and easy toadminister and has been validated against 5-year risk ofdeath.596,693Recommendation Table 22—Recommendations for managing hypertension inpregnancy (see Evidence Tables 38–40) Recommendations ClassaLevelb Inwomen with gestational hypertension, starting drug treatment isrecommended for those with confirmed office systolic BP≥140 mmHg ordiastolic BP≥90 mmHg.661I B Inpregnant women with chronic hypertension, starting drug treatment isrecommended for those with confirmed office systolic BP≥140 mmHg or diastolic BP≥90 mmHg.88,660,661,678I B ContinuedInwomen with chronic and gestational hypertension, itisrecommended tolower BPbelow 140/90 mmHg but not below 80mmHg for diastolic BP.I C Dihydropyridine CCBs (preferably extended-release nifedipine), labetalol, and methyldopa are recommended first-line BP-lowering medications for treating hypertension inpregnancy.I C Inconsultation with anobstetrician, low- to moderate-intensity exercise isrecommended inall pregnant women without contraindications to reduce the risk ofgestational hypertension and pre-eclampsia.654,655I B Systolic BP≥160 mmHg ordiastolic BP≥110 mmHg inpregnancy can indicate anemergency, and immediate hospitalization should beconsidered.IIa C HBPM and ABPM should beconsidered toexclude white-coat and masked hypertension, which are more common inpregnancy.679IIa C RAS blockers are not recommended during pregnancy.680,681III B ©ESC 2024 ABPM, ambulatory blood pressure monitoring; BP, blood pressure; CCB, calcium channel blocker; HBPM, home blood pressure monitoring; RAS, renin–angiotensin system. aClass ofrecommendation. bLevel ofevidence.60 ESC Guidelines
+9.3.2. Randomized controlled trials ofblood pressure lowering infrail older patients Few adults aged ≥85 years have been included intrials.131Inaddition, generalizing data from RCTs tovery frail patients may not bepos- sible.692,694–697However, the currently available evidence from RCTs has not demonstrated weakening ofthe benefits ofBP-lowering treat- ment (i.e. no effect modification) among frailer patients enrolled in these trials, although these participants likely had nomore than mild frailty (see Supplementary data online).523,694,698 Inthe absence ofrobust randomized evidence, several observational studies have suggested that lowering BPmight not bewarranted or even beharmful inpatients with significant frailty ormultimorbidity, particularly when BPisnot very high. For instance, asystematic review and meta-analysis of non-randomized studies that investigatedassociations between BPand risk ofmortality inolder patients found evidence for interaction byfrailty status, suggesting that lowering BP might beharmful inthis patient group.699However, asnoted above and inSection 9.8, these observational J-curve findings are unreliable when guiding clinical care, asunidentified biases potentially confound the results. For instance, inaddition toreverse causality, stiffness of the large arteries isassociated with both low diastolic BPand increased mortality.697Inaddition, absolute CVD risk increases with age, indicat- ingthat fewer older than younger patients with hypertension may need tobetreated toprevent one adverse health outcome.700 Therefore, given the totality of evidence from clinical trials,523,694,701,702very old and frail patients with hypertension should not bedenied the potential benefits ofBP-lowering treatment down to atarget of120–129/70–79 mmHg. However, personalized decision- Very fit1 People who are robust,  active, energetic and  motivated. These people  commonly exercise regularly. They are among  the fittest for their age.Follow BP-lowering  treatment guidelines as per  younger cohorts, ensuring  treatment is toleratedEvidence for benefit in CV  event reduction not as  strong for people with  moderate-to-severe frailty  with functional impairment  (poorly represented in  clinical trials) Evidence for benefits in  reducing CVD events with  more intensive treatment of  BPExercise caution and clinical  judgement in beginning and  intensifying BP-lowering  treatment, employing a  shared decision-making  approach Low-dose combination  therapy to achieve BP control is reasonableSingle drug therapy may be reasonable in this cohort  when initiating or maintaining  BP-lowering treatment ABPM if possible and  regular review important,  particularly if change in  frailtyMonitor for symptomatic  OH, asymptomatic OH  with falls, poor treatment  tolerance, or medication  side effects. Use clinical  judgement and APBM/HB- PM to guide deprescribing  or medication adjustment  where appropriate Well2 People who have no active  disease symptoms  but are  less fit than category I.  Often, they exercise or are  very active occasionally , e.g,  seasonally. Managing well3 People whose medical  problems are well  controlled, but are not  regularly active beyond  routine walking. Vulnerable4 While not dependent  on  others for daily help, often  symptoms limit activities. A  common complaint is  being "slowed up", and/or  being tired during the day. Mildly frail5 These people often have more  evident slowing, and need help  in high order IADLs (finances,  transportation, heavy  housework, medications).  Typically, mild frailty progres- sively impairs shopping and  walking outside alone, meal  preparation and housework. Moderately frail6 People need help with all outside activities and with  keeping house . Inside, they  often have problems with  stairs and need help with  bathing and might need  minimal assistance cueing  (prompting), standing by  with dressing. Severely frail7 Completely dependent for  personal care , from  whatever cause (physical  or cognitive). Even so, they  seem stable and not at high risk of dying (within  ~6 months). Very severely frail8 Completely dependent, approaching the end of life.  Typically, they could not recover even from a  minor illness. Terminally ill9 Approaching the end of  life. This category applies  to people with a life  expectancy <6 months ,  who are not otherwise  evidently frail.Clinical Frailty Scale 1–5Clinical Frailty Scale 6–9 Figure 21 Frailty assessment inthe management ofblood pressure. ABPM, ambulatory blood pressure monitoring; BP, blood pressure; CV, cardio- vascular; CVD, cardiovascular disease; HBPM, home blood pressure monitoring; IADLs, independent activities ofdaily living; OH, orthostatic hypoten- sion. Adapted from Rockwood etal.693ESC Guidelines 61
+making should beapriority inthe very old and frail. Together with man- agement ofBP, amajor consideration should also bewhether reversible causes offrailty can beaddressed,609e.g. bytreating underlying co- morbidities orundergoing supervised muscle-strengthening physiother- apy orsupervised exercise and co-ordination and balance training.703 9.3.3. Starting blood pressure-lowering treatment in very oldorfrail patients Allpatients must befully informed about the benefits and risks ofstart- ing BP-lowering treatment, sothat their preference isconsidered. Among 34hypertension guidelines, 18recommended 150 mmHg as the systolic goal infrailer and/or older patients, but four endorsed sys- tolic targets <130 mmHg or<120 mmHg.704Treatment can bestarted with along-acting dihydropyridine calcium channel antagonist.596,705 To achieve BP control, anACE inhibitor, orifcontraindicated, an ARB, can also beused. Thereafter, low-dose thiazides orthiazide-like diuretics are preferred unless there isaspecific contraindication, such asgout, orthostatic hypotension, ordisturbed micturition (including micturition syncope).596,705Beta-blockers are less desirable asthey reduce heart rate, cause fatigue, and increase the systolic pulse wave amplitude, which isinsufficiently buffered instiff central elastic arteries. Vasodilating beta-blockers and direct vasodilators (e.g. hydralazine and minoxidil) are associated with increased risk oforthostasis. Though data are conflicting,706alpha-blockers are also considered less desirable asthey appear tobeassociated with anincreased risk oforthostasis and falls invery old patients (aged ≥85 years).707,708Alpha-1 blockers, such asdoxazosin, prazosin, terazosin (also used totreat prostate symp- toms), are particularly prone tocausing orthostasis.98Once the appro- priate combination isfound, acombination tablet with variable composition oftwo agents may optimize adherence. Starting with com- bination therapy isnot advised inmost very oldand/or frail patients, un- less BPisvery high. 9.3.4. Maintaining blood pressure lowering invery old orfrail patients Ifvery old and frail patients tolerate BP-lowering treatment well, there isnoautomatic need todeprescribe ordiscontinue treatment; how- ever, this should bekept under review. Inthe case ofprogressive frailty, systolic BPtends todrop,709such that deprescription ofaBP-lowering drug might become necessary. Toidentify candidate drugs for depre- scribing, apatient’s current medications should bereviewed toidentify BP-lowering drugs that may have become contraindicated due tocon- comitant prescriptions ornewly developed comorbidities.705Tohelp guide deprescription ofBP-lowering agents, ABPM can beused tode- tect orthostatic hypotension orahighly variable BPnot buffered by autonomic nervous reflexes.687,6889.4.Isolated systolic anddiastolic hypertension 9.4.1. Definition ofisolated systolic hypertension Isolated systolic hypertension istypically defined assystolic BP of ≥140 mmHg with adiastolic BPof<90 mmHg. While isolated systolic hypertension isuncommon inyounger patients,713itisthemost common type ofhypertension inolder patients; >80% ofuntreated patients with hypertension aged >60 years have isolated systolic hypertension.714 9.4.2. Isolated systolic hypertension, riskfactors, and ageing Systolic BPincreases with age inmen and women until the eighth dec- ade oflife, while diastolic BPgradually increases upuntil the fifth orsixth decade oflife, after which iteither plateaus ordecreases. Asaresult, the pulse pressure (the difference between the systolic and diastolic BP) gradually widens from middle age.34These BPchanges are related to increased aortic stiffening with age.715,716 Since most older patients with hypertension have isolated systolic hypertension, and since with advancing age, risk ofCVD events isdriven bysystolic rather than diastolic BP,717management ofisolated systolic hypertension inolder adults isbroadly inline with that ofcombined systolic-diastolic hypertension seen inyounger adults.718Early isolatedRecommendation Table 23—Recommendations for managing hypertension inpatients who arevery oldor frail (see Evidence Table 41) Recommendations ClassaLevelb Itisrecommended that treatment ofelevated BPand hypertension among older patients aged <85 years who are not moderately toseverely frail follows the same guidelines asfor younger people, provided BP-lowering treatment iswell tolerated.131,523,524I A ContinuedItisrecommended tomaintain BP-lowering drug treatment lifelong, even beyond the age of85years, if well tolerated.523–525I A Because the benefit inreducing CVD outcomes is uncertain inthese settings, and noting that close monitoring oftreatment tolerance isadvised, BP-lowering treatment should only beconsidered from ≥140/90 mmHg among persons meeting the following criteria: pre-treatment symptomatic orthostatic hypotension, age≥85 years, clinically significant moderate-to-severe frailty, and/or limited predicted lifespan (<3 years).131,524,526,527IIa B Asthe safety and efficacy ofBPtreatment isless certain inindividuals with moderate orsevere frailty, clinicians should consider screening older adults for frailty using validated clinical tests; frail patients’ health priorities and ashared-decision approach should beconsidered when deciding onBP treatments and targets.523,524,613,710IIa C When initiating BP-lowering treatment for patients aged ≥85 years, and/or with moderate-to-severe frailty (atany age), long-acting dihydropyridine CCBs orRAS inhibitors should beconsidered, followed if necessary bylow-dose diuretic iftolerated, but preferably not abeta-blocker (unless compelling indications exist) oranalpha-blocker.711IIa B IfBPdrops with progressing frailty, deprescription of BP-lowering medications (and other drugs that can reduce BP, such assedatives and prostate-specific alpha-blockers) may beconsidered.712IIb C ©ESC 2024 BP, blood pressure; CCB, calcium channel blocker; CVD, cardiovascular disease; RAS, renin–angiotensin system. aClass ofrecommendation. bLevel ofevidence.62 ESC Guidelines
+systolic hypertension studies used systolic BPtreatment targets of160 or 150 mmHg.718However, results from the SPRINT and the Strategy of Blood Pressure Intervention inElderly Hypertensive Patients (STEP) trials (mean BPatstudy entry of140/78 mmHg and 146/82 mmHg, respective- ly,indicating that many ofthe patients had isolated systolic hypertension) confirm that lower systolic BP targets are effective inreducing CVD events in patients with isolated systolic hypertension (see Supplementary data online).135,136 Since relative risk reduction byBP-lowering treatment ishomoge- neous inany age group, whereas absolute risk reduction islarger with advancing age,131therapeutic inertia inolder patients with isolated systolic hypertension should beavoided (seeSection 9.3). Asnoted earl- ier, beta-blockers should beavoided inpatients with isolated systolic hypertension ormore generally with arterial stiffness, asthey increase stroke volume (given the lower heart rate).218 9.4.3. Isolated systolic hypertension inyoung adults Inyoung adults (<40 years old), the presence ofisolated systolic hyper- tension poses different pathophysiological and clinical considerations. In young patients with isolated systolic hypertension, arterial stiffness713 and relative risk ofCVD events624appear tobesimilar tothose without isolated systolic hypertension and lower than young adults with com- bined systolic-diastolic hypertension and isolated diastolic hypertension. Indeed, younger patients with isolated systolic hypertension appear to comprise aheterogeneous group.719For these reasons, itmight berea- sonable toassess central BPand arterial stiffness inthese individuals, as recommended byother scientific societies.720,721Out-of-office BPmeas- urement isrecommended toexclude white-coat hypertension, which is often associated with isolated systolic hypertension inthe young.634 9.4.4. Isolated diastolic hypertension Isolated diastolic hypertension isdefined asasystolic BPof<140 mmHg with adiastolic BPof≥90 mmHg. The isolated diastolic hypertension phenotype ismore commonly seen inyounger adults and, particularly, younger adults with obesity orother metabolic derangements.722,723In older adults with this phenotype, consideration should begiven to whether the diastolic BPwas accurately measured.724 Patients with isolated diastolic hypertension appear tohave aslightly increased relative risk for CVD of5%–30%.548,723,725However, be- cause patients with isolated diastolic hypertension are younger, they tend tohave few events, and very large samples are required to show this association. Furthermore, because the absolute risk for CVD among these individuals islow (typically <10% over 10years), it isless clear ifisolated diastolic hypertension should prompt initiation ofBP-lowering medication, particularly among persons inwhom base- line systolic BP isalready atthe target of 120–129 mmHg.723 Irrespective, patients with isolated diastolic hypertension should befol- lowed up, asthey are atincreased risk for systolic hypertension.723 Finally, itisalso worth noting that when apatient achieves atarget systolic BPof120–129 mmHg with BP-lowering treatment, there islit- tletonohigh-quality trial evidence that further intensifying BP-lowering medication toachieve both systolic BPof<120 mmHg and also diastol- icBPof<70 mmHg improves CVD prognosis.547,723 9.5.Orthostatic hypotension with supine hypertension Patients with orthostatic hypotension need not behypotensive and in- deed, many have supine elevated BP or supine hypertension. Furthermore, many patients with orthostatic hypotension are asymp- tomatic. Orthostatic hypotension ispresent inaround 10% ofalladultswith hypertension and isdefined asadrop inBPof≥20/10 mmHg after rising from either asitting orlying position toastanding position (see Section 5.5.3).97,99Assessment for orthostatic hypotension should be timed tooccur at1and/or 3min after standing. Because seated to standing assessment can lead tounder-detection oforthostatic hypo- tension, itispreferable, where possible, totest fororthostatic hypoten- sion using asupine (lying) tostanding assessment (seeSection 5).56,98,726 Assessing fororthostatic hypotension isimportant inmanaging adults with elevated BPorhypertension forseveral reasons. First, findings oftrials linking more intensive BPcontrol toimproved outcomes may not gener- alize topatients with orthostatic hypotension, particularly when itissevere inmagnitude (standing systolic BP<110 mmHg97)and/or symptomatic. Second, orthostatic hypotension may beassociated with symptoms that may limit the patient’s tolerability ofmore intensive BP-lowering approaches. Third, orthostatic hypotension may beassociated with anin- creased risk ofadverse effects commonly co-attributed topharmacological BPlowering (such ashospitalizations forhypotension).727Fourth, ortho- static hypotension isassociated with increased risk forCVD.728 However, the frequency oforthostatic hypotension isnot increased inthe more intensive BP-lowering arms ofrandomized trials compared with the less intensive BP-lowering arms.726,727,729,730Assuch, and in contrast tocommon belief, itdoes not appear that more intensive treatment ofBP (which almost always requires more BP-lowering medication) worsens orthostatic hypotension. Incontrast, there is some evidence that more intensive treatment ofhypertension may ac- tually reduce the risk oforthostatic hypotension.730,731 The aetiology oforthostatic hypotension may be considered as neurogenic ornon-neurogenic, with the latter being farmore com- mon.99Patients with orthostatic hypotension may have underlying neu- rodegenerative diseases, diabetes, B12 deficiency,732renal failure, dehydration, prolonged recumbency, deconditioning, and triggering medications (like alpha-blockers, beta-blockers, diuretics, nitrates, anti- depressants, and antipsychotics). Ofnote, ACE inhibitors, ARBs, and dihydropyridine CCBs are examples ofBP-lowering medications that appear tohave less impact onorthostatic hypotension, and their ad- verse impact, ifany, on orthostatic hypotension typically occurs in the first 2weeks orsoafter starting orintensifying treatment.733 Managing patients with supine hypertension and orthostatic hypoten- sion isacommon clinical conundrum. More detailed reviews onthis topic areavailable elsewhere.98,99The approach tomanaging orthostatic hypo- tension should benon-pharmacological atfirst. Patients with orthostatic hypotension should beasked tochange position slowly, maintain ad- equate hydration, and avoid alcohol and large meals. Compression stock- ings, crossing legs while standing, and abdominal binders may also help and should betrialled.734,735Abdominal heating pads and ahead-up bed pos- ition can reduce supine (typically nocturnal) hypertension, which may re- duce nocturnal diuresis and daytime orthostatic hypotension.736 The treatment oforthostatic hypotension among those with supine hypertension isnot toautomatically down-titrate BP-lowering medica- tions. Rather, reversible causes should besought and treated (including discontinuation of offending medications), and patients requiring BP-lowering medication should beswitched toBP-lowering medications that areless likely tocause orthostatic hypotension. When symptoms are disabling and the above interventions donot help, particularly inneuro- genic orthostatic hypotension, the best evidence exists for midodrine toreverse orthostatic hypotension, and this may begiven inconjunction with ongoing BP-lowering medications when supine hypertension ex- ists.99An alternative option tomidodrine isdroxidopa, though this is less readily available. Specialist referral isprudent when persons with su- pine hypertension are prescribed these orthostatic hypotension treat- ments, asthese agents can increase supine BPmore than standing BP.ESC Guidelines 63
+9.6.Diabetes 9.6.1. Diabetes andelevated blood pressure/ hypertension Patients with diabetes (both type 1and type 2)often have elevated BP orhypertension, and are about twice aslikely tosuffer amajor CVD event over the medium tolong term compared with those without dia- betes.737Diabetes isalso amajor cause ofmicrovascular events, such as retinopathy and nephropathy.738,739Although the risk ofCVD inpa- tients with diabetes varies byscreening and diagnostic methods,740,741 aswell aswith the presence ofother CVD risk factors,740,742onaver- age, patients with diabetes are at≥10% 10-year risk for CVD. However, formal risk estimation with the use ofSCORE2-Diabetes among type 2diabetes mellitus patients should beconsidered ifthey are aged <60 years (seeSection 6).164,739 9.6.2. J-shaped curve ofblood pressure andriskof cardiovascular disease inpatients with diabetes Evidence onthe BPthreshold and target fortreatment inpatients with diabetes has been subject todebate. Reports ofaJ-shaped association between BPand risk ofCVD indiabetes,743and the lack ofaclear bene- fit of treatment on cardiac outcomes at lower BP insome meta-analyses,744–746has led tosome cautious recommendations for intensive treatment inthis patient population. An individual patient data meta-analysis by the Blood Pressure Lowering Treatment Trialists’ Collaboration tested treatment effects in103 325 patients with diabetes and provided evidence against effect modification bycategories ofbaseline BPdown toasystolic BP of120 mmHg.445BPreduction inpatients with diabetes isexpected toreduce the risk ofdiabetes-associated complications including retin- opathy, vasculopathy, and nephropathy (albuminuria and end-stage re- nal disease), which adds weight tothe importance ofreducing BPin these patients (see Supplementary data online).745–747This task force also considered the fact that aproportion ofpatients with diabetes have orthostatic hypotension due todiabetic neuropathy,748which might affect the tolerability ofBPlowering.9.6.3. Managing blood pressure indiabetes We recommend that allpatients with diabetes are offered pharmaco- logical BP-lowering treatment with aBPtarget of120–129/70–79 mmHg, iffeasible and tolerated.136,146,445,747,749–752The task force further sees no strong evidence foradifferential BPtreatment targets inpatients with dia- betes and those without.136,146,445,746,747While the Action toControl Cardiovascular Risk inDiabetes (ACCORD) trial reported anull primary endpoint formore intensive BPtargets indiabetes, stroke was marginally re- duced.137Furthermore, extended follow-up ofACCORD,750aswell asana- lyses ofintensive BP reduction inthose randomized tothe standard glycaemic arm,749provide evidence suggesting benefit consistent with the SPRINT, STEP, and Effects ofintensive Systolic blood Pressure lowering treatment inreducing RIsk ofvascular evenTs (ESPRIT) trials.136,146,545 Overall, allmajor BP-lowering medication classes areeffective inpreventing CVD inpeople with orwithout diabetes. Ofnote, however, albuminuria is more common indiabetes and, forthis reason, ACE inhibitors and ARBs have potential advantages that may warrant consideration forBP-lowering inpatients with diabetes (see Supplementary data online, Table S10).753 Evidence for modifying BP-lowering treatment inpatients with pre-diabetes issomewhat limited. Furthermore, the relative effect ofBP lowering isrelatively consistent across different categories ofBMI asa measure ofobesity.754,755Itisalso noteworthy that elevated BPitself may increase the risk ofdiabetes,755emphasizing the potential role ofBP lowering inpreventing diabetes inaddition topreventing CVD. Among themajor classes ofBP-lowering drugs, ACE inhibitors and ARBs areeffect- iveinpreventing new-onset diabetes and can beconsidered inpatients at risk ofdiabetes and who are indicated forBP-lowering therapy.164,755 9.7.Chronic kidney disease 9.7.1. Relationship between hypertension andchronic kidney disease Approximately 850 million people worldwide have CKD, with >80% of them hypertensive, and the prevalence isexpected torise to1.56 billionRecommendation Table 24—Recommendations for managing hypertension inpatients with orthostatic hypotension Recommendation ClassaLevelb Before starting orintensifying BP-lowering medication, itisrecommended totest fororthostatic hypotension, byfirst having the patient sitorliefor5 min and then measuring BP1and/or 3min after standing.97,99I B Itisrecommended topursue non-pharmacological approaches asthe first-line treatment oforthostatic hypotension among persons with supine hypertension. For such patients, itisalso recommended toswitch BP-lowering medications that worsen orthostatic hypotension toan alternative BP-lowering therapy and not tosimply de-intensify therapy.726,727,729,730I A ©ESC 2024 BP, blood pressure. aClass ofrecommendation. bLevel ofevidence. Recommendation Table 25—Recommendations for managing hypertension inpatients with diabetes Recommendations ClassaLevelb Inmost adults with elevated BPand diabetes, after a maximum of3months oflifestyle intervention, BP lowering with pharmacological treatment is recommended for those with confirmed office BP ≥130/80 mmHg toreduce CVD risk.445,749I A BP-lowering drug treatment isrecommended for people with pre-diabetes orobesity when confirmed office BPis≥140/90 mmHg orwhen office BPis 130–139/80–89 mmHg and the patient isat predicted 10-year risk ofCVD ≥10% orwith high-risk conditions, despite amaximum of3months oflifestyle therapy.445I A Inpersons with diabetes who are receiving BP-lowering drugs, itisrecommended totarget systolic BPto120–129 mmHg, if tolerated.136,146,445,747,749–752I A ©ESC 2024 BP, blood pressure; CVD, cardiovascular disease. aClass ofrecommendation. bLevel ofevidence.64 ESC Guidelines
+by2025.756–759The pathogeneses ofhypertension and CKD are closely entwined.760Resistant hypertension, masked hypertension, HMOD, and higher night-time BPare common inpatients with CKD.761CVD isone ofthe largest contributors tomortality inpatients with CKD, with hypertension being amajor risk factor.760,762 For the purposes ofthese guidelines, adults with moderate-to-severe CKD and elevated BPare atsufficiently high risk tobeconsidered for BP-lowering drug therapy asoutlined inSection 8and the Central Illustration (Figure 19). We use Kidney Disease: Improving Global Outcomes (KDIGO) categories todefine CKD-based risk, and our def- inition ofmoderate-to-severe CKD comprises persons with aneGFR of <60 mL/min/1.73 m2and/or albuminuria of≥30 mg/g (≥3 mg/mmol).19 For persons with mild CKD and elevated BP, aCVD risk assessment should beconducted before deciding onBP-lowering treatment. 9.7.2. Blood pressure lowering inchronic kidney disease BPlowering inpatients with CKD isassociated with beneficial effect on CVD events and mortality.275,763–766BPlowering reduces progression ofCKD and the incidence ofend-stage renal disease, but this tends to beonly inthose with significant proteinuria atbaseline.766,767 9.7.3. Managing blood pressure inchronic kidney disease Patients with CKD should receive lifestyle advice, especially regarding reducing sodium intake. Dietary potassium supplementation recom- mendations are provided inSection 8,with caution required among per- sons with moderate-to-severe CKD. While exercise appears tohave little effect onimproving BPinpatients with CKD768orpatients ondia- lysis,769those with CKD onACE inhibitor monotherapy have protec- tion against adverse kidney outcomes, CVD events, cardiovascular death, and all-cause death.770,771Both ACE inhibitors and ARBs reduce the risk ofCVD events and kidney failure compared with placebo; how- ever, ACE inhibitors appear todo sowith higher probability than ARBs.772,773Patients with CKD usually require combination therapy, and this should beinitiated asacombination ofaRAS inhibitor and a CCB ordiuretic. Inpatients with eGFR <30mL/min/1.73 m2,anad- equately up-titrated loop diuretic isnecessary todefine resistant hyper- tension. Chlorthalidone, typically added toaloop diuretic, also effectively lowers BPand reduces microalbuminuria inpatients with resistant hyper- tension with stage 4CKD (eGFR of15–30 mL/min/1.73 m2).774The combination ofanACE inhibitor and anARB isnot recommended in CKD orany other BP-treatment scenario. 9.7.4. Blood pressure targets inchronic kidney disease Evidence regarding BPtargets inpatients with CKD iscomplex and con- troversial. The 2021 KDIGO Guideline suggested that adults with ele- vated BPand CKD betreated toatarget systolic BPof<120 mmHg, when tolerated, using standardized office BPmeasurement (Class of Recommendation IIb).19This suggestion was based, inpart, on the SPRINT trial.545Itshould benoted that patients with 24hurine protein excretion ≥1g/day or eGFR <20mL/min/1.73 m2were excluded from SPRINT. Inpatients with CKD, after amedian follow-up of3.3 years, the hazard ratio for the primary composite cardiovascular out- come was 0.81 (95% CI0.63–1.05) and for all-cause death itwas 0.72 (95% CI0.53–0.99). Although intensive BPlowering inSPRINT re- sulted ingreater early decline ineGFR, there was noevidence that thisreduction ineGFR attenuated the beneficial effects ofthe SPRINT intervention onCVD events ordeath.775 Several systematic reviews have examined the benefit ofintensive BP control inpatients with CKD (see Supplementary data online). Some have shown no benefit of intensive BP control on renal out- comes,764,767while others showed lower mortality inintensively trea- ted vs.non-intensively treated patients.275Highlighting the beneficial effects ofSGLT2 inhibitors inpersons with CKD776,777and finerenone inpersons with CKD and diabetes460–462,778isrelevant, though these drugs are not currently marketed for BP-lowering effects alone. 9.8.Cardiac disease 9.8.1. Blood pressure thresholds andtargets in patients with cardiac disease Recommended BPthresholds forinitiating BP-lowering therapy and re- commended BPtargets inpatients receiving therapy are provided in Sections 6and8.Allpatients with ahistory ofCVD (including coronary artery disease) are atincreased risk ofrecurrent CVD. Assuch, these patients are recommended tobetreated with BP-lowering therapy for confirmed baseline BPof≥130/80 mmHg and the recommended treatment target BPof120–129/70–79 mmHg, provided treatment is tolerated (seeSections 6and8).Asstated inSection 8,itshould bere- membered that asystolic BPof120 mmHg (especially byout-of-office assessment) islikely the optimal point inthe target range recommended inthese guidelines. Inaddition toconsidering patients with known CVD atsufficiently high risk for more intensive BPtreatment targets, theRecommendation Table 26—Recommendations for managing hypertension inpatients with chronic kidney disease Recommendations ClassaLevelb Inpatients with diabetic ornon-diabetic moderate-to-severe CKD and confirmed BP≥130/ 80mmHg, lifestyle optimization and BP-lowering medication are recommended toreduce CVD risk, provided such treatment iswell tolerated.275,766I A Inadults with moderate-to-severe CKD who are receiving BP-lowering drugs and who have eGFR >30 mL/min/1.73 m2,itisrecommended totarget systolic BPto120–129 mmHg, iftolerated. Individualized BPtargets are recommended forthose with lower eGFR orrenal transplantation.274,779I A Inhypertensive patients with CKD and eGFR >20 mL/min/1.73 m2,SGLT2 inhibitors are recommended toimprove outcomes inthe context oftheir modest BP-lowering properties.776,777I A ACE inhibitors orARBs are more effective at reducing albuminuria than other BP-lowering agents and should beconsidered aspart ofthe treatment strategy for patients with hypertension and microalbuminuria orproteinuria.780–782IIa B ©ESC 2024 ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; BP, blood pressure; CKD, chronic kidney disease, eGFR, estimated glomerular filtration rate; SGLT2, sodium–glucose co-transporter 2. aClass ofrecommendation. bLevel ofevidence.ESC Guidelines 65
+task force considers patients with both severe valvular heart disease and symptomatic heart failure toalso beatsufficiently high risk. We also note that, whether used forangina control orBPcontrol, abeta- blocker should not becombined with anon-dihydropyridine CCB. 9.8.2. Coronary artery disease with particular reference totheblood pressure J-curve Important considerations inpatients with coronary artery disease are: (i)the BPJ-curve (anobservation suggesting that over-intensive BPlow- ering may increase CVD risk insome patients), and (ii)compelling indi- cations for specific classes ofBP-lowering medications. The J-curve phenomenon describes increased risk forCVD observed among patients with the lowest and highest BPinthe dataset, with the best CVD outcome rates typically observed among those with BPinthe normal range (e.g. systolic BPof100–120 mmHg and diastolic BPof 60–80 mmHg). For this reason, the J-curve issometimes also called the U-curve, with both terms typically used interchangeably.697,783,784 However, observational data donot consistently demonstrate aBP J-curve with CVD risk.697Itismore commonly observed among pa- tients with established clinical CVD, such asthose with coronary artery disease, orinsecondary prevention cohorts.785,786Furthermore, the J-curve ismore commonly observed when analysing diastolic BPvalues vs.systolic BPvalues, though ithas been described forboth.114,697This stronger relationship with diastolic BPhas informed the hypothesis that the J-curve may becaused byreduced perfusion ofmajor organs atlow BP, which isparticularly operative fordiastolic BPinthe coronary vas- culature when considering ischaemic heart disease events (since coron- ary blood flow islargely confined todiastole).786,787 Ifexcessive lowering ofBPcauses CVD events, this needs tobe addressed intreatment recommendations provided byBPmanage- ment guidelines. The 2018 ESC/ESH Guidelines onthe management ofarterial hypertension introduced, for the first time, lower bounds of BP-lowering treatment targets, implying that treatment be de-intensified for patients with on-treatment BPbelow these bounds (i.e.<120 mmHg systolic or<70 mmHg diastolic).1The 2023 ESH docu- ment also makes this argument.788 However, since 2018, compelling evidence has demonstrated that the BPJ-curve evident inobservational datasets ishighly unlikely tore- flect acausal process and can instead beattributed toresidual con- founding and/or reverse causation.33,114,115,546,697,789–793 Accordingly, while low BPcan indicate ahigh-risk state, particularly among older adults and those with comorbidities, there isnoevidence that this isacausal phenomenon. Indeed, ifthere isanother indication forBP-lowering therapy (e.g. inapatient with wide pulse pressure and a baseline systolic BPof>140 mmHg but diastolic BPof<60 mmHg), the evidence suggests that such therapy should beprovided iftolerated to reduce CVD risk. There isalimit tohow low BPcan betreated without potentially tip- ping the scales infavour ofCVD harm vs.CVD benefit. However, itis not clear what that limit isand how much itdiffers based oncomorbid- ities. Currently, the data donot suggest that risk forCVD can becaus- ally increased bytreating any patient tothe recommended intensive BP target outlined inthese guidelines ofaslow as120/70 mmHg. We also donot recommend stopping orde-intensifying BP-lowering medication among asymptomatic patients with on-treatment BP of <120/70 mmHg. Itshould berecognized, though, that there are noro- bust data demonstrating that anon-treatment systolic BPof<90 mmHg oranon-treatment diastolic BP of<50 mmHg issafe from aCVDperspective and there isclear potential for harm. Furthermore, it must beemphasized that the above discussion ofthe BPJ-curve relates solely toCVD risk and does not consider the known non-CVD side ef- fects ofBP-lowering drugs, like, e.g. orthostatic hypotension, syncope, and renal injury. We doknow that patients treated toamore intensive BPtarget of120/70 mmHg are atincreased risk forthese side effects,550 which iswhy these guidelines stress that this more intensive target should only bepursued among those inwhom treatment isbeing toler- ated (Section 8). The second consideration inmanaging BPinpatients with coronary artery disease isthe recommended use ofBP-lowering medications with compelling indications based on outcomes trials that demon- strated CVD outcomes benefits inthe setting ofcoronary artery dis- ease. These recommendations are provided inthe recommendation table below. 9.8.3. Valvular heart disease Most patients with both severe heart valve disease and heart failure, de- fined bythe 2021 ESC/European Association for Cardio-Thoracic Surgery (EACTS) Guidelines forthe management ofvalvular heart dis- ease,794can beconsidered atincreased risk ofCVD. Accordingly, itis recommended they are treated with BP-lowering therapy for con- firmed baseline BPof>130/80 mmHg, and their recommended target oftreatment isBPof120–129/70–79 mmHg, provided treatment istol- erated. Persons with mild-to-moderate heart valve disease should have aCVD risk assessment prior todeciding their BP-lowering treatment threshold and target. Vasodilating ARBs/ACE inhibitors are preferable over vasodilating di- hydropyridine CCBs because ofthe link between valvular heart disease and subsequent heart failure and given the stronger efficacy evidence for ARBs/ACE inhibitors inthe setting ofheart failure once mani- fested.795Inaortic valve stenosis, concomitant hypertension influences both the aortic root, the aortic valve, and the left ventricular structure and function.796Inthis subgroup, treatment preferably with ARBs/ACE inhibitors should beconsidered. Abeta-blocker may beadded ifBPre- mains >140/90 mmHg.796,797 9.8.4. Heart failure Patients with symptomatic heart failure are atincreased risk ofCVD. Therefore, itisrecommended that these patients are treated with BP-lowering therapy for confirmed baseline BPof>130/80 mmHg and their recommended treatment target isBPof120–129/70–79 mmHg, provided treatment istolerated and with out-of-office confirm- ation ofon-treatment BP. Of note, many patients with systolic heart failure on maximal heart failure therapies have BP of <120/70 mmHg, and we do not recommend de-intensifying such treatment unless indicated by symptomatic side effects. Besides referencing the new evidence for ARNi and SGLT2 inhibitor ther- apies,795our 2024 recommendations for heart failure are largely unchanged from the 2018 ESC/ESH Guidelines onthe management ofarterial hypertension. Non-dihydropyridine CCBs should not be used inheart failure. Frailty and hypotension risk should be as- sessed inolder heart failure patients being considered for ARNi and SGLT2 inhibitor therapies, and older patients should beclosely followed toensure they are tolerating such treatments. For more information onthe management ofheart failure, we direct readers tothe latest ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure.79866 ESC Guidelines
+9.8.5. Heart rhythm disease (including AF) Not allpatients with heart rhythm disease, including those with AF, are atincreased risk for CVD and, assuch, the management ofBP among patients with heart rhythm disease should bethe same asfor the general adult population.443However, there isaclose relationship between increased BPand AFrisk, hence, ensuring good BPcontrol is important.801,802Management ofheart rhythm disorders should follow recommendations inguidelines specific tothese conditions.803 9.9.Chronic cerebrovascular disease and/or cognitive impairment 9.9.1. Role ofhypertension inchronic cerebrovascular disease Hypertension isarisk factor for chronic cerebrovascular disease through itsdirect effects onbrain structure and microvasculature. This manifests astransient ischaemic attack (TIA) and stroke inthe acute setting, but chronic hypertension can lead tocovert stroke and white-matter ischaemic change over time, resulting incognitive decline and progressive vascular dementia.804–808Hypertension is also associated with increased risk ofAlzheimer’s disease,809and isarisk factor for developing AF, heart failure, and CKD, allofwhich are associated with increased risk ofdeveloping cognitive impair- ment and dementia.810–813For the purposes ofthese guidelines, adults with ahistory ofstroke orTIA and elevated BPare consid- ered atsufficiently high risk tobe considered for BP-lowering drug therapy asoutlined inSection 8and the Central Illustration (Figure 19). 9.9.2. Treatment inpatients with history ofprior stroke ortransient ischaemic attack Inpatients with aprior history of TIA and ischaemic stroke, BP-lowering treatment reduces the risk ofany recurrent stroke by 20%.814–817The aetiology ofstroke can affect the degree ofrisk reduc- tion with pharmacological treatment, with greater reductions observed for intracerebral haemorrhage and lacunar ischaemic stroke syn- dromes.818–820 Most prior guidelines recommend anintensive BPtarget inpatients with aprior history ofstroke, typically using combination treatment (ACE inhibitor/ARB plus either acalcium channel antagonist orathia- zide/thiazide-like diuretic), with therapy commencing immediately after TIA and within afew days ofischaemic stroke (see Supplementary data online and seeSection 10.3 for acute BPmanagement during hospital- ization for stroke).814,815,821–824 Regimens containing anACE inhibitor and thiazide/thiazide-like diur- etic may besuperior tobeta-blockers interms ofstroke risk reduc- tion.825,826Regarding intensive BP control after stroke, typically targeting asystolic BPof<130 mmHg, individual trials were somewhat inconclusive, but ameta-analysis showed areduced risk ofrecurrent stroke of22% inthe intensive treatment group randomized toatarget systolic BPaslow as120 mmHg.543,824,827,828Caveats tothis recom- mendation would befor frail patients, who have amuch higher rate ofstroke and recurrent stroke than the general population, and who are more sensitive toadverse effects ofBP-lowering agents (see Section 9.3).596,606,607,829 9.9.3. Treatment inpatients with chronic cerebrovascular disease andcognitive impairment Treatment ofhypertension represents akey mechanism for reducing the global burden of dementia at the population level.830 Epidemiological studies have reported associations between mid-life hypertension and development ofcognitive decline inlater life, with, e.g. mid-life hypertension increasing relative risk oflifetime dementia by20%–54%.831–837Inone observational meta-analysis, anincreased risk for dementia emerged with systolic BPof>130 mmHg.831 Evidence for lowering BPtoreduce the risk ofdementia islimited due toheterogeneity inpopulations studied, cognitive testing methods used, and the varied use ofdementia orcognitive impairment orboth as aprimary outcome.838,839Findings from individual studies have mixed results (see Supplementary data online).264,839–843Studies oneffects ofBP-lowering treatment onwhite-matter intensities concluded that patients inthe intensive-control arm had less white-matter intensity ac- cumulation than inthe standard-treatment arm.841,844Studies inwhich people with stroke and TIA were included reported areduced risk of dementia and cognitive decline for the active-treatment group, but a mixed signal for dementia alone.841,845However, individual studiesRecommendation Table 27—Recommendations for managing hypertension inpatients with cardiac disease Recommendations ClassaLevelb Inpatients with ahistory ofmyocardial infarction who require BP-lowering treatment, beta-blockers and RAS blockers are recommended aspart ofthat treatment.538I A Inpatients with symptomatic angina who require BP-lowering treatment, beta-blockers and/or CCBs are recommended aspart ofthat treatment.538I A Inpatients with symptomatic HFrEF/HFmrEF, the following treatments with BP-lowering effects are recommended toimprove outcomes: ACE inhibitors (or ARBs ifACE inhibitors are not tolerated) or ARNi, beta-blockers, MRAs, and SGLT2 inhibitors.795I A Inhypertensive patients with symptomatic HFpEF, SGLT2 inhibitors are recommended toimprove outcomes inaddition totheir modest BP-lowering properties.795I A Inpatients with ahistory ofaortic valve stenosis and/ orregurgitation who require BP-lowering treatment, RAS blockers should beconsidered aspart ofthat treatment.794,796IIa C Inpatients with ahistory ofmoderate-to-severe mitral valve regurgitation who require BP-lowering treatment, RAS blockers should beconsidered as part ofthat treatment.794IIa C Inpatients with symptomatic HFpEF who have BP above target, ARBs and/or MRAs may beconsidered toreduce heart failure hospitalizations and reduce BP.795,799,800IIb B ©ESC 2024 ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; ARNi, angiotensin receptor–neprilysin inhibitor; BP, blood pressure; CCB, calcium channel blocker; HFpEF, heart failure with preserved ejection fraction; HF(m)rEF, heart failure with (mildly) reduced ejection fraction; MRA, mineralocorticoid receptor antagonist; RAS, renin–angiotensin system; SGLT2, sodium–glucose co-transporter 2. aClass ofrecommendation. bLevel ofevidence.ESC Guidelines 67
+may have been under-powered and more recent meta-analyses do convincingly support efficacy inreducing dementia with BP-lowering treatment.610,611Indeed, these meta-analyses reported areduced risk ofincident dementia orcognitive impairment with BPlowering of7%–13%.610,611While one trial suggested superiority oflong-acting CCBs,264itisunclear ifany first-line BP-lowering agent ispreferable for preventing dementia and cognitive impairment.846,847 The role ofcompeting risk mechanisms including orthostatic hypo- tension848and BPvariability849may beimportant factors intreatment decisions for people with frailty, multimorbidity, and/or chronic cere- brovascular disease. 9.10. Aortopathy 9.10.1. Coarctation oftheaorta Aortic coarctation isassociated with CVD inthe long term, even follow- ingearly surgical orpercutaneous treatment. The most common com- plications are associated with hypertension, which iscommon inaortic coarctation. When aortic coarctation isnot treated, patients often de- velop severe hypertension and HMOD (especially LVH and leftventricu- lardysfunction, aortopathy, and cerebrovascular complications).850–852 No formal RCTs todefine optimal medical treatment ofhypertension inaortic coarctation have been conducted, therefore, patients not suit- able for, orhaving undergone, intervention should betreated forhyper- tension following the core algorithm forthe general population. 9.10.2. Bicuspid aortic valve-related aortopathy Bicuspid aortic valve isthe most common congenital heart disease and is sometimes associated with aortopathy oraortic coarctation. Bicuspid aor- ticvalve disease isassociated with anincreased risk ofvalve malfunction and adverse aortic events.853,854This risk isexacerbated byhypertension. Beyond aortic dilation and aneurysm formation, bicuspid aortic valve disease isalso arisk factor for aortic dissection and rupture.855Blood pressure should becarefully monitored and controlled.856 9.10.3. Preventing aortic dilation anddissection in high-risk patients Amodest dilatation ofthe ascending aorta oraortic root isoften asso- ciated with chronic hypertension and HMOD. An additional cause of aortopathy (bicuspid valve, coarctation, Marfan orother syndromes)should beconsidered inmore severe cases.857Patients with aortic dila- tation should have their BPoptimally controlled following the core al- gorithm for the general hypertension population. Inpatients with Marfan syndrome, prophylactic use ofARBs, ACE inhi- bitors, orbeta-blockers may reduce complications orprogression ofaortic dilation.857–860More information isavailable inthe 2024 ESC Guidelines forthe management ofperipheral arterial and aortic diseases.861 9.11. Different ethnic groups Influx and settlement ofmigrant populations inEurope have contribu- ted toregional population growth and changes initscomposition.862 Ethnic minority populations are disproportionally affected byhyperten- sion and hypertension-mediated complications, compared with histor- ically native Europeans, with data suggesting migrant women are particularly vulnerable.536,863Inparticular, hypertension ismore preva- lent inthose ofAfrican descent.863,864The predominant group of European black ethnicity originates from sub-Saharan Africa,863but specific studies on the management and control ofhypertension in this population arelacking, and data areoften extrapolated from studies inthe African American population.864This assumption requires cau- tion, asdifferences likely exist between these populations interms of CVD risk, economic, and sociological status,865,866aswell asresponses toBP-lowering drugs.867 Black patients have agreater prevalence oflow-renin, salt-sensitive hypertension and may bemore predisposed toHMOD than white pa- tients, possibly inpart due toincreased vascular stiffness.864,868,869Salt restriction, thiazide orthiazide-like diuretics, and CCBs appear particu- larly useful inblack patients with hypertension, whereas RAS blocker monotherapy may beless effective.870–873Ifcombination therapy is needed, inarecent RCT conducted insub-Saharan African countries, amlodipine plus either hydrochlorothiazide orperindopril proved to beequally effective and superior, respectively, tohydrochlorothiazide plus perindopril.874When RAS blockers are used incombination ther- apy, ARBs may bepreferable toACE inhibitors, asangioedema appears more common with ACE inhibitors inblack patients. Despite some recent progress,875data onhypertension epidemi- ology and management inEuropean immigrant patients are still lacking.863,875–877 9.12. Nocturnal hypertension 9.12.1. Definition Nocturnal hypertension isdefined asnight-time BPof>120 mmHg systol- icand/or >70 mmHg diastolic by24hABPM. Nocturnal hypertension can occur asday–night sustained hypertension orisolated nocturnal hyperten- sion (daytime BP<135/85 mmHg on24hABPM). Physiologically, BPisRecommendation Table 28—Recommendations for managing hypertension inpatients with chronic cere- brovascular disease andcognitive impairment Recommendations ClassaLevelb Itisrecommended that the BP-lowering drug treatment strategy for preventing recurrent stroke should comprise aRAS blocker plus aCCB ora thiazide-like diuretic.820,823,825,826I A Inpatients with confirmed BP≥130/80 mmHg with a history ofTIA orstroke asystolic BPtarget of120– 129 mmHg isrecommended toreduce CVD outcomes, provided treatment istolerated.824,827,828I A ©ESC 2024 BP, blood pressure; CCB, calcium channel blocker; CVD, cardiovascular disease; RAS, renin–angiotensin system; TIA, transient ischaemic attack. aClass ofrecommendation. bLevel ofevidence. Recommendation Table 29—Recommendations for managing hypertension indifferent ethnic groups Recommendation ClassaLevelb Inblack patients from Sub-Saharan Africa who require BP-lowering treatment, combination therapy including aCCB combined with either athiazide diuretic oraRAS blocker should beconsidered.874IIa B ©ESC 2024 BP, blood pressure; CCB, calcium channel blocker; RAS, renin–angiotensin system. aClass ofrecommendation. bLevel ofevidence.68 ESC Guidelines
+expected todecrease during sleep by10%–20% relative todaytime BP.878 Night-time dipping patterns are classified into four groups:879,880 •Inverse dipping (riser): nocturnal increase inBP(night-to-day ra- tioof>1.0). •Non-dipper: reduced night-time BPdip of<10% (or night-to-day ratio of>0.9 and≤1.0). •Normal dipping: fall innight-time BP of>10% and<20% (or night-to-day ratio of0.8 to0.9). •Extreme dipping: marked fall innight-time BP of>20% (or night-to-day ratio of<0.8). Patients with nocturnal hypertension may bedippers ornon-dippers. Ofnote, the long-term reproducibility ofdipping patterns appears to below.881,882 9.12.2. Epidemiology Nocturnal hypertension has been observed inuptohalf ofpatients with hypertension,883–886and isassociated with increased HMOD,883im- paired renal function, and diabetes mellitus.887Nocturnal hypertension appears tobemore prevalent inblack888–890and Asian891,892popula- tions. Masked uncontrolled hypertension, which occurs in30% of patients treated for hypertension, ismore often due topoorly con- trolled nocturnal BPthan daytime BPonABPM.893 Environmental factors, including sleep duration and higher humid- ity,894nocturia,895OSAS,896obesity, high salt intake insalt-sensitive pa- tients,897orthostatic hypotension, autonomic dysfunction, CKD,898–900 diabetic neuropathy/diabetes,901and oldage62are associated with non- dipping. Moreover, nocturnal hypertension and absent night-time dip- ping pattern are more common insecondary hypertension.902,903 9.12.3. Night-time blood pressure asacardiovascular disease riskfactor Nocturnal hypertension isarisk factor for adverse CVD events,904 cerebrovascular disease, including stroke,905and cardiovascular mor- tality.891,906,907Night-time BP may provide more prognostic infor- mation than daytime BP, perhaps asitisless dependent onphysical activities. Non-dipping908–910and reverse dipping (nocturnal rise in BP) may also beassociated with increased CVD risk.62,910–913Anoc- turnal rise inBPisassociated with anincreased risk ofdementia and Alzheimer’s disease inolder men.914There isalso some evidence that extreme dipping, particularly inuntreated patients, isassociated with anincreased risk for CVD events.35,886 9.12.4. Treatment ofnocturnal hypertension There isnoreliable evidence that BP-lowering medication should be routinely dosed atbedtime. The diurnal timing ofdrug administration isdiscussed inSection 8.3.4. Inpatients with secondary hypertension, the underlying cause (OSAS, primary aldosteronism) should betreated asdiscussed inSection 9.14. 9.13. Resistant hypertension 9.13.1. Definition ofresistant hypertension Resistant hypertension isdefined asBPremaining above goal despite three ormore BP-lowering drugs ofdifferent classes atmaximally tol- erated doses, ofwhich one isadiuretic (Table 11).915Resistant hyper- tension should bemanaged atspecialized centres with the expertise and resources toexclude pseudo-resistant hypertension (adherence testing) and causes ofsecondary hypertension.9169.13.2. Non-pharmacological interventions The Treating Resistant Hypertension Using Lifestyle Modification to Promote Health (TRIUMPH) trial demonstrated significant clinic and ambulatory BPreductions inpatients with resistant hypertension par- ticipating ina4-month lifestyle intervention comprising diet and exercise interventions delivered within acardiac rehabilitation programme.917 9.13.3. Pharmacological interventions BP-lowering treatment ofresistant hypertension with single-pill combi- nations isrecommended toreduce the pillburden, thereby increasing drug adherence and persistence.492 Asresistant hypertension often, and especially inCKD,918represents a state ofsalt retention and volume expansion secondary torelative aldos- terone excess,516,919,920BPcontrol may beimproved byswitching hydro- chlorothiazide to long-acting thiazide-like diuretics, such as chlorthalidone.921,922However, arecent trial ofchlorthalidone vs. hydrochlorothiazide—which probably included asizeable proportion of adults with resistant hypertension—did not demonstrate any difference insystolic BPorCVD outcomes between thetwo medications. Inthesub- group ofpatients with prior CVD, there was astrong trend ofbenefit with chlorthalidone onCVD outcomes.447Ofnote, the risk ofhypokalaemia was higher inthe chlorthalidone group than inthe hydrochlorothiazide group.447Inpatients with eGFR <30mL/min/1.73 m2,anadequately up- titrated loop diuretic isnecessary todefine resistant hypertension. Most patients with resistant hypertension require the addition of non-first-line BP-lowering drugs (Figure 22). Ofthese, low-dose spir- onolactone (25–50 mg daily) should beconsidered first.459,515,923–925 Inpatients with resistant hypertension and type 2diabetes, spironolac- tone (25–50 mgdaily) reduced BPand albuminuria.926The use ofspirono- lactone can beprecluded bylimited tolerability due toanti-androgenic side effects resulting inbreast tenderness orgynaecomastia (inabout 6%), im- potence inmen, and menstrual irregularities inwomen.927The efficacy and safety ofspironolactone fortreating resistant hypertension have not yet been established inpatients with significant renal impairment. Moreover, spironolactone, especially inaddition toRAS inhibitors, increases the risk ofhyperkalaemia.927,928Therefore, spironolactone should berestricted topatients with aneGFR of≥30 mL/min/1.73 m2and aplasma potassium concentration of≤4.5 mmol/L.459Steroidal MRAs are contraindicated in patients with aneGFR of<30 mL/min/1.73 m2.Serum electrolytes and kid- ney function should bemonitored soon after initiation and frequently thereafter. Inpatients with resistant hypertension and CKD (eGFR of 25–45 mL/min/1.73 m2),the oral potassium binder patiromer enabled more patients tocontinue treatment with spironolactone.929 Ifspironolactone isnot tolerated due toanti-androgen side ef- fects, eplerenone may beused. Ifeplerenone isused, higher doses (i.e. 50–200 mg daily) and twice-daily dosing may benecessary to achieve aBP-lowering effect.503Ofnote, eplerenone isnot licensed for hypertension treatment inmany countries. When not already prescribed for acompelling indication, beta- blockers should beconsidered inthe treatment ofresistant hyperten- sion, though their BP-lowering effects appear tobeless potent than spironolactone inthe setting ofresistant hypertension.459 Amiloride and clonidine have data suggesting they are aseffective as spironolactone for BP lowering, though they lack outcomes data. Anon-exhaustive list ofadditional medications sometimes used for BP-lowering purposes includes other centrally acting BP-lowering med- ications (e.g. methyldopa), hydralazine, aliskiren, minoxidil, triamterene, and loop diuretics (Figure 22).515,516Asnoted earlier, minoxidil use is often limited byside effects.ESC Guidelines 69
+9.13.4. Devices forblood pressure lowering Several devices have been investigated for treating resistant hyper- tension. Ofthese, the most evidence isavailable for catheter-based renal denervation. Asdiscussed inSection 8.6.1, several randomized, sham-controlled trials have been published, demonstrating a BP-lowering efficacy over 24hfor radiofrequency and ultrasound renal denervation inabroad spectrum ofhypertension, including re- sistant hypertension.568,585Other devices are still under investiga- tion and are not recommended for routine use inclinical practice (Section 8.6.2). Intensification of pharmacotherapy If BP remains uncontrolledRenal denervationInterventional therapyShared risk-benefit discussion and multidisciplinary assessmentBeta-blocker (if not already recommended for a compelling indication)Spironolactone If spironolactone is not tolerated: eplerenoneTrue treatment-resistant hypertensionOffice BP �140/90 mmHg despite 3 or more BP-lowering medications at maximally tolerated doses, including a diuretic Referral to hypertension centre should be considered Treatment optimization of BP-lowering medications (ideally three-drug SPC)Exclusion of secondary and pseudo-resistant hypertension Alpha blockers Centrally acting BP-lowering drugs K+ sparing diuretics Others (Class IIa)  (Class IIa) (Class IIb) (Class IIa)  (Class IIa)Figure 22 Management ofresistant hypertension. BP, blood pressure; K+,potassium; SPC, single-pill combination. Recommendation Table 30—Recommendations for treating resistant hypertension (see Evidence Tables 42 and43) Recommendations ClassaLevelb Inpatients with resistant hypertension and uncontrolled BPdespite use offirst-line BPlowering therapies, the addition ofspironolactone toexisting treatment should beconsidered.459,515IIa B Continued70 ESC Guidelines
+9.14. Management ofspecific causes ofsecondary hypertension 9.14.1. General considerations These guidelines will describe only the general principles ofmanaging the most common forms ofsecondary hypertension. For the rarer forms ofsecondary hypertension, patients should bereferred tospecia- lized hypertension centres. Bydefinition, secondary hypertension should be, for the most part, cured when the underlying cause has been unambiguously identified and removed. However, inclinical practice, this isnot always the case. Vascular remodelling, acommon feature ofadelayed diagnosis ofsec- ondary hypertension, affects renal function and can account forresidual high BPinsome patients with secondary hypertension. The rate ofcure is higher when thediagnosis ismade early inthecourse ofthe disease. Most common forms ofsecondary hypertension are listed inTable 13. 9.14.2. Primary aldosteronism Primary aldosteronism (Conn syndrome) isthe most common form of secondary hypertension. The management ofprimary aldosteronism depends onitssubtype, particularly onadrenal lesions being unilateral orbilateral, because the unilateral forms are amenable tosurgical treat- ment while the latter require lifelong medical treatment. Insporadic forms, unilateral primary aldosteronism isdistinguished from bilateral primary aldosteronism byadrenal vein sampling orfunctional imaging with radiolabelled tracers.930–932Inthe much less common familial forms (necessitating afamily history betaken), genetic testing forgerm- line mutations isnecessary.933 For unilateral primary aldosteronism, surgical removal ofthe offending adrenal gland istypically considered, unless the patient isolder orhas co- morbidities ofconcern. Surgery isnot anoption for bilateral primary aldosteronism. Medical treatment iscurrently based onMRAs. Among MRAs, spironolactone isthe most widely available. The effective dose, usually 50–100 mg once daily, can betitrated upto300–400 mg once daily, ifnecessary. Eplerenone isalso used and, despite being less potent than spironolactone and requiring twice-daily administration, ithasthead- vantage ofcausing less gynaecomastia and erectile dysfunction inmen.934 Newer agents, such as the non-steroidal MRAs finerenone andexarenone, and thealdosterone synthase inhibitor baxdrostat, which low- erBPinresistant hypertension,326,474arealso being tested fortreating pri- mary aldosteronism. Ofthefamilial forms, only glucocorticoid-remediable primary aldosteronism, now reclassified asfamilial hyperaldosteronism type 1,can becorrected with dexamethasone,935usually with low doses that are free ofglucocorticoid effects and can besafely used during preg- nancy.936For detailed information, readers are referred tothe latest pri- mary aldosteronism guidelines.328,329 9.14.3. Renovascular hypertension Patients with RVH should receive medical therapy toreduce BPinthe first instance. Percutaneous transluminal renal angioplasty (PTRA) without stenting isthe treatment ofchoice forfibromuscular dysplasia, and can restore renal perfusion pressure and lower BP.937When this is not feasible, RAS blockers are the drugs ofchoice for treatment, but they require careful monitoring ofrenal function over time, asthey can cause acute renal failure inthose with tight bilateral stenoses ora stenosed solitary functioning kidney. Possible involvement ofthe ca- rotid, coronary, and other major arteries, possibly leading todissection ifBPisnot controlled, should also beconsidered, asfibromuscular dys- plasia isnow recognized asasystemic disease affecting multiple vascular beds. Patients with significant atherosclerotic renal artery stenosis are at very high risk ofCVD and renal events. Itisrecommended that PTRA and stenting are performed inexperienced centres due tothe high risk ofrestenosis. Unfortunately, though these studies didnot sole- lyrecruit patients with true significant atherosclerotic RVH, publication ofsome null trials938,939have decreased the enthusiasm forinvestigat- ingatherosclerotic renal artery stenosis. This could result inmore un- controlled hypertension, recurrent flash pulmonary oedema (Pickering syndrome), and worsening renal function ultimately leading toend- stage renal disease.940Inpatients with resistant hypertension inwhom spironolactone isnot effective ortolerated, treatment with eplerenone instead of spironolactone,503orthe addition ofabeta-blocker if not already indicated459and, next, acentrally acting BP-lowering medication,515analpha-blocker,515 hydralazine, orapotassium-sparing diuretic516 should beconsidered.IIa B Toreduce BP, and ifperformed atamedium-to-high volume centre, catheter-based renal denervation may beconsidered for resistant hypertension patients who have BPthat isuncontrolled despite a three BP-lowering drug combination, and who express apreference toundergo renal denervation after ashared risk-benefit discussion and multidisciplinary assessment.564,566–568,586–590IIb B ©ESC 2024 BP, blood pressure. aClass ofrecommendation. bLevel ofevidence. Recommendation Table 31—Recommendations for managing hypertension inpatients with renovascular hypertension (see Evidence Tables 44and45) Recommendations ClassaLevelb Renal artery angioplasty without stenting should be considered for patients with hypertension and haemodynamically significant renal artery stenosis due tofibromuscular dysplasia.941IIa C Renal artery angioplasty and stenting may be considered inpatients with haemodynamically significant, atherosclerotic, renal artery stenosis (stenosis of70%–99%, or50%–69% with post-stenotic dilatation and/or significant trans-stenotic pressure gradient) with: •Recurrent heart failure, unstable angina, orsudden onset flash pulmonary oedema despite maximally tolerated medical therapy; •Resistant hypertension; •Hypertension with unexplained unilaterally small kidney orCKD; •Bilateral renal artery stenosis orunilateral renal artery stenosis inasolitary viable kidney.942,943IIb C ContinuedESC Guidelines 71
+9.14.4. Phaeochromocytoma/paraganglioma Phaeochromocytomas are rare adrenal tumours that secrete catecho- lamines and are present in<0.2% ofpatients with hypertension. Asmall percentage (<10%) ofcatecholamine-producing tumours are extra- adrenal and are derived from sympathetic and non-sympathetic nerves. More than 35% ofthe non-syndromic PPGLs are due togermline mu- tations.338These mutations should bescreened for because, when found, they can drive management ofthe proband and the family and also inform the choice offunctional imaging. Moreover, some germline mutations, such asthose involving succinate dehydrogenase B,carry a risk ofmalignant adrenal tumours.301,336 Sympathetic PPGLs are usually secreting and present with chron- ic,episodic, orlabile hypertension. Adrenergic crises cause hyper- tensive emergencies and should be treated with anintravenous (i.v.) alpha-1-blocker, such asphentolamine, doxazosin orterazosin, orlabetalol. When given i.v.(1–2 mg/kg) twice weekly asabolus over 1min followed byacontinuous infusion, labetalol also has alpha- blocker properties and has the advantage ofallowing titration of the infusion based onthe BP response, and avoids tachycardia via beta-blockade. Identifying asingle tumour mandates surgical excision after ad- equate pharmacological preparation, because secreting PPGLs can cause fatal events with nowarning. Administering doxazosin orter- azosin, followed byabeta-blocker, usually controls BPand adrener- giccrises. AsPPGLs are associated with aredistribution ofvolume from the periphery tothe cardiopulmonary system,944patients with PPGLs have peripheral hypovolaemia that exposes them to the risk ofprofound hypotension, particularly right after tumour ex- cision. Therefore, adequate fluid administration should becarefully managed. 9.14.5. Obstructive sleep apnoea syndrome The management ofthis prevalent condition should bedriven bythe result ofapolysomnography study, which should provide the value ofthe AHI (the average number ofepisodes per hour) and the sleep position inwhich apnoeic–hypopnoeic episodes occur. For mild OSAS (AHI <15), weight loss and advice onsleep hygiene are usu- ally sufficient. For moderate (AHI of15–30) and severe (AHI >30) OSAS, continuous positive airway pressure (CPAP) isindicated and usually improves BP control and helps toresolve resistant hypertension. IfCPAP isnot tolerated, the site ofupper airway ob- struction should bedetermined byanEar, Nose, and Throat evalu- ation with drug-induced sleep endoscopy asapotential step to corrective surgery.9.14.6. Drug-induced hypertension Over-the-counter medications, prescribed drugs, and drug abuse (rec- reational substances and misuse ofdrugs) can cause hypertension (Supplementary data online, Table S4). 9.14.6.1. Anticancer drug-induced hypertension Growing evidence indicates that, while contemporary anticancer and anti-angiogenic drugs improve cancer survival, they can also cause hyper- tension (Supplementary data online, Table S4). This isespecially evident inpatients treated with vascular endothelial growth factor inhibitors, in whom BPincreases in80%–90%.945Tyrosine kinase inhibitors and pro- teasome inhibitors also increase BP, asdoadjuvant therapies (corticos- teroids, calcineurin inhibitors, non-steroidal anti-inflammatory drugs, and anti-androgen hormone therapy). Hypertension caused byanticancer drugs isoften dose limiting and may bereversible after therapy interrup- tion ordiscontinuation. Evidence-based clinical trials specifically addres- sing patients who develop hypertension due tocancer therapy are lacking. Itisrecommended that management ofhypertension inthese pa- tients follows that forthe general population.945,946Managing these com- plex patients requires multidisciplinary healthcare involving oncologists, hypertension specialists, cardiologists, and nephrologists,945,946ashigh- lighted inthe 2022 ESC Guidelines oncardio-oncology.946 9.14.7. Other forms ofsecondary hypertension Other forms ofsecondary hypertension, such asgenetic causes of hypertension (Liddle’s syndrome, glucocorticoid-remediable aldoster- onism), excess liquorice, Cushing’s syndrome, thyroid disease, hyper- parathyroidism, aortic coarctation, and acromegaly are rare. Affected patients should bereferred tospecialized centres for treatment. 10.Acute andshort-term lowering ofblood pressure 10.1. Acute blood pressure management in hypertensive emergencies 10.1.1. Definition andcharacteristics ofhypertensive emergencies Hypertensive emergency isdefined asBP of≥180/110 mmHg (see Figure 10) associated with acute HMOD, often inthe presence of symptoms. Hypertensive emergencies are potentially life-threatening and require immediate and careful intervention toreduce BP, often with i.v.therapy. Symptoms ofhypertensive emergency depend onthe organs affected but may include headache, visual disturbances, chest pain, shortness of breath, dizziness, and other neurological deficits. Inpatients with hyper- tensive encephalopathy, somnolence, lethargy, tonic–clonic seizures, and cortical blindness may precede aloss ofconsciousness; however, focal neurological lesions are rare and should raise the suspicion ofstroke. Asoutlined inSection 7,we define HMOD among patients with chronically elevated BPorhypertension asthe presence ofspecific car- diac, vascular, and renal alterations.31,159However, inthe setting of hypertensive emergency, more acute manifestations oforgan damage are relevant for management. Acute manifestations oforgan damage include: •Patients with severe acute hypertension associated with other clinical conditions likely torequire urgent reduction inBP, e.g. acute onset of aortic dissection, myocardial ischaemia, eclampsia, orheart failure.Inpatients with anindication torenal artery revascularization and technically unfeasible, orfailed, renal artery angioplasty and stenting, open surgical revascularization may beconsidered.IIb C Renal artery angioplasty isnot recommended in patients without confirmed haemodynamically significant renal artery stenosis.c938,939III A ©ESC 2024 CKD, chronic kidney disease. aClass ofrecommendation. bLevel ofevidence. cAhaemodynamically relevant stenosis isusually defined byaluminal narrowing of>70% or 50%–70% with post-stenotic dilatation.72 ESC Guidelines
+•Malignant hypertension, defined asextreme BPelevations and acute microvascular damage (microangiopathy) affecting various organs.947 The hallmark ofthis condition issmall-artery fibrinoid necrosis inthekid- neys, retina, and brain. The acute microangiopathy istypically character- ized clinically byretinopathy (flame haemorrhages, cotton wool spots, and/or papilloedema). Other manifestations ofmicroangiopathy include disseminated intravascular coagulation, encephalopathy (inabout 15% of cases), acute heart failure, and acute deterioration inrenal function. •Patients with sudden severe hypertension due tophaeochromocyto- ma, which can result insevere acute organ damage. The term ‘hypertension urgency’ describes severe hypertension inpa- tients without clinical evidence ofacute organ damage. While these pa- tients require BPreduction, they donot usually require admission to hospital, and BPreduction isbest achieved with oral medication accord- ingtothe drug treatment algorithm presented inSection 8.However, these patients may require more urgent outpatient review toensure that their BPiscontrolled. Acute and severe increases inBPcan sometimes beprecipitated by sympathomimetics such asmethamphetamine orcocaine, when cau- tion around beta-blocker use isalso needed. Many patients inanemer- gency department with acute pain ordistress may have acutely elevated BPthat will normalize when the pain and distress are relieved, rather than requiring any specific intervention tolower BP. Adiagnostic work-up isnecessary for patients with asuspected hypertensive emergency (see Supplementary data online, Table S12). 10.1.2. Acute management ofhypertensive emergencies Key considerations indefining treatment are: (1) Establishing the affected target organ(s) and whether they require any specific interventions other than BPlowering. (2) Determining whether there isaprecipitating cause for the acute rise inBPand/or another concomitant health condition present that might affect the treatment plan (e.g. pregnancy). (3) The recommended timing and magnitude ofBPlowering required for safe BPreduction. These considerations will inform the type ofBP-lowering treatment re- quired. Regarding BP-lowering drugs, i.v.treatment using ashort half- lifedrug istypically ideal toallow careful titration ofthe BPresponse totreatment. This requires ahigher dependency clinical area with facil- ities for continuous ornear-continuous haemodynamic monitoring. Recommended drug treatments forspecific hypertensive emergencies are provided inthe Supplementary data online, Table S13. Rapid and uncontrolled orexcessive BPlowering isnot recommended inhypertensive emergency asthis can lead tofurther complications. Although i.v.drug administration isrecommended formost hypertensive emergencies, oral therapy with ACE inhibitors, ARBs, orbeta-blockers (shorter-acting formulations like captopril ormetoprolol) can also beef- fective. However, low initial doses should beused because these patients can bevery sensitive tothese agents, and treatment should take place in hospital. Further comprehensive details onthe clinical management of hypertensive emergencies are available elsewhere.242 10.1.3. Prognosis andfollow-up The survival ofpatients with hypertensive emergencies has improved over the past few decades, but these patients remain athigh risk and should bescreened for secondary hypertension.10.2. Acute blood pressure management in acute intracerebral haemorrhage Inacute intracerebral haemorrhage, anincreased BPiscommon and is associated with agreater risk ofhaematoma expansion and death, and a worse prognosis for neurological recovery. Intrials testing immediate BP lowering (within <6h)toasystolic target of<140 mmHg, the achieved systolic BPinthe intervention group was typically 140–160 mmHg and was reported toreduce the risk ofhaematoma expan- sion.948,949Excessive acute drops insystolic BP(>70 mmHg) may be associated with acute renal injury and early neurological deterioration and should beavoided.950,951 10.3. Acute blood pressure management in acute ischaemic stroke The beneficial effects ofBPreduction inacute ischaemic stroke remain un- clear. Inpatients not receiving i.v.thrombolysis ormechanical thrombec- tomy, there isnoevidence foractively lowering BPunless itisextremely high (e.g.>220/120 mmHg). IfBPisextremely high, aninitial moderate relative reduction of10%–15% over aperiod ofhours may beconsid- ered.952The reason foramore conservative approach toacute BPman- agement isthat cerebral autoregulation may beimpaired inacute stroke, and maintaining cerebral perfusion relies onsystemic BP. Incontrast, patients who aretreated with i.v.thrombolysis ormechan- icalthrombectomy (orboth) should have more proactive management of severe hypertension, because they have anincreased risk ofreperfusion injury and intracranial haemorrhage. Inpatients undergoing treatment with i.v.thrombolysis, BPshould belowered to<185/110 mmHg prior tothrombolysis and then maintained at<180/105 mmHg over the following 24h.953Inpatients undergoing treatment with mechanical thrombectomy (with orwithout i.v. thrombolysis) there islimited evidence from clinical trials, but BP should also be lowered to <180/105 mmHg prior tothrombectomy and maintained over the next 24h.953,954Therefore, patients with acute ischaemic stroke and a BPof<180/105 mmHg inthefirst 72hafter stroke donot seem tobene- fitfrom theintroduction orreintroduction ofBP-lowering medication.955 For stable patients who remain hypertensive (≥140/90 mmHg) ≥3days after an acute ischaemic stroke, initiation or reintroduction of BP-lowering medication isrecommended. Recommendation Table 32—Recommendations for acutely managing blood pressure inpatients with intra- cerebral haemorrhage oracute ischaemic stroke Recommendations ClassaLevelb For patients with ischaemic stroke orTIA and an indication for BPlowering, itisrecommended that BP-lowering therapy becommenced before hospital discharge.819,820,823I B Inpatients with acute ischaemic stroke, early BPlowering with BP-lowering therapy should beconsidered inthe first 24hinthe following settings: •Inpatients who are eligible for re-perfusion therapy with intravenous thrombolysis or mechanical thrombectomy, BPshould becarefully lowered and maintained at<180/105 mmHg forat least the first 24hafter treatment.956–960IIa B ContinuedESC Guidelines 73
+10.4. Acute blood pressure management in pre-eclampsia andsevere hypertension in pregnancy 10.4.1. Pre-eclampsia Pre-eclampsia isdiscussed inSection 9.Here wefocus onitsmanagement inthe acute setting. Pre-eclampsia iscured bydelivery. Most international societies, including the ESC, recommend anintensive approach toBP lowering inpre-eclampsia.89,964,965Inwomen with pre-eclampsia and se- vere hypertension, immediately reducing systolic BPto<160 mmHg and diastolic BPto<105 mmHg using i.v.labetalol ornicardipine (with admin- istration ofmagnesium sulfate ifappropriate and consideration ofdeliv- ery ifappropriate) was recommended inthe 2018 ESC/ESH Guidelines on the management ofarterial hypertension and the 2022 ESC Guidelines for management ofcardiovascular disease inpregnancy.1,89 The objective oftreatment istolower BPwithin 150–180 min. Magnesium sulfate [4gi.v.over 5min, then 1g/hi.v.;or5gintramus- cularly (i.m.) into each buttock, then 5gi.m. every 4h]isrecommended for eclampsia treatment but also for women with pre-eclampsia who have severe hypertension and proteinuria orhypertension and neuro- logical symptoms orsigns.966There isarisk ofhypotension when mag- nesium isgiven concomitantly with nifedipine.967IfBPcontrol isnot achieved by360 min despite two medications, consulting critical care isrecommended forintensive care unit admission, stabilization, and de- livery (ifappropriate).966Since plasma volume isreduced inpre- eclampsia, diuretic therapy should beavoided. 10.4.2. Severe acute hypertension inpregnancy Severe hypertension inpregnancy (without pre-eclampsia) may neces- sitate acute BP-lowering therapies. Severe hypertension inpregnancy is defined ingeneral assystolic BPof>160 mmHg and diastolic BPof >110 mmHg and isassociated with adverse maternal and peri-natal outcomes independent ofpre-eclampsia and potentially ofthe same magnitude aseclampsia itself.89,968 There are differences inrate ofBPcontrol between i.v.labetalol and i.v.hydralazine insevere hypertension inpregnancy.969While evidence isconflicting,667,668hydralazine may beassociated with more peri-natal adverse events than other drugs.970Nifedipine seems toprovide lower BPwith lower rates ofneonatal complications than labetalol.97110.5. Peri-operative acute management of elevated blood pressure Details are provided inthe ESC Guidelines oncardiovascular assessment and management of patients undergoing non-cardiac surgery.972 Peri-operative hypertension, hypotension, and BPvariability areassociated with haemodynamic instability and poor clinical outcomes for patients undergoing surgery.973Pre-operative risk assessment forBPmanagement, therefore, should involve assessing forunderlying end-organ damage and comorbidities.974Postponing necessary non-cardiac surgery isnot usually warranted forpatients with minor ormoderate elevations inBP, asthey are not athigher CVD risk.130,975 Avoiding large fluctuations inBPinthe peri-operative course isim- portant, and planning astrategy for apatient should account for the baseline office BP.974–977 There isinsufficient evidence for reduced or increased peri- operative BP targets compared tousual care BP targets tolower peri-operative events.978No specific measure ofBP appears better than any other for predicting risk ofperi-operative events.975 10.5.1. Blood pressure-lowering drugs inthe peri-operative phase Routine initiation ofabeta-blocker peri-operatively isnot necessary.979 Pre-operative initiation ofbeta-blockers inadvance ofhigh-risk, non-cardiac surgery may be considered inpatients who have known coronary artery disease or myocardial ischaemia980or two ormore significantly elevated clinical risk factors inorder to reduce the incidence ofperi-operative myocardial infarction.979 Peri-operative continuation ofbeta-blockers isrecommended for patients currently taking beta-blockers.981 Some studies suggest that continued use ofACE inhibitors isasso- ciated with ahigher risk ofperi-operative hypotension and subsequent end-organ damage including kidney injury, myocardial infarction, and stroke.982Inthe Prospective Randomized Evaluation ofPreoperative Angiotensin-Converting Enzyme Inhibition (PREOP-ACEI) trial, transient pre-operative interruption ofACE inhibitor therapy was associated with adecreased risk ofintra-operative hypotension.983Asubsequent system- atic review also showed adecreased risk ofintra-operative hypotension with withholding ACE inhibitors/ARBs before surgery, but noassociation•Inpatients with ischaemic stroke not receiving re-perfusion treatment and BPof≥220/110 mmHg, BPshould becarefully lowered by approximately 15% during the first 24hafter stroke onset.956–960IIa C Inpatients with intracerebral haemorrhage, immediate BPlowering (within 6hofsymptom onset) should beconsidered toasystolic target 140– 160 mmHg toprevent haematoma expansion and improve functional outcome.948,949IIa A Inpatients with intracerebral haemorrhage presenting with systolic BP≥220 mmHg, acute reduction insystolic BP>70 mmHg from initial levels within 1hofcommencing treatment isnot recommended.950,951,960–963III B ©ESC 2024 BP, blood pressure; TIA, transient ischaemic attack. aClass ofrecommendation. bLevel ofevidence.Recommendation Table 33—Recommendations for acutely managing blood pressure inpatients with severe hypertension inpregnancy and pre-eclampsia (see Evidence Table 46) Recommendation ClassaLevelb Inpre-eclampsia oreclampsia with hypertensive crisis, drug treatment with i.v.labetalol ornicardipine and magnesium isrecommended.971I C Inpre-eclampsia oreclampsia associated with pulmonary oedema, nitroglycerin given asani.v. infusion isrecommended.242I C Insevere hypertension inpregnancy: •drug treatment with i.v.labetalol, oral methyldopa, ororal nifedipine isrecommended. Intravenous hydralazine isasecond-line option.666–668,969,971I C ©ESC 2024 i.v., intravenous. aClass ofrecommendation. bLevel ofevidence.74 ESC Guidelines
+with decreased mortality orCVD outcomes.984On the other hand, vigi- lance isneeded because withholding ACE inhibitors has also been shown toincrease post-operative hypertension.985Inpatients with heart failure, loop diuretics can becontinued inpatients prone tovolume overload.986 CCBs are generally considered safe pre-operatively. 11.Patient-centred care inhypertension 11.1. Definition Patient-centred care isdefined asanattitude ofthe healthcare profes- sional that closely aligns with the patient’s preferences and needs.987 Inthe patient-centred approach (Figure 23), patients are viewed asac- tive participants inhealth services, who work aspartners alongside healthcare professionals. Apatient-centred approach isassociated with higher satisfaction rates, better adherence torecommendations and prescriptions, and better treatment, particularly inthe manage- ment ofchronic illness, such ashypertension.988While there islimited evidence forthe efficacy and effectiveness ofspecific shared decision-making intervention strategies inhypertension care,989itisviewed as anethical imperative inhealthcare practice and health policy, and in clinical guidelines.130 11.2. Communicating consequences of treatment Inline with patient-centred care, itisimportant toassess whether patients understand their hypertension-related risk, therationale forany hyperten- sion treatment, the benefits and harms ofhypertension treatment, and that the treatment plan isalso centrally guided bywhat matters most to the patient. Risk communication ischallenging, and providers need tobe ledbytheindividual’s preferences when presenting more detailed numeric and visual representations ofrisk and the likely benefits and harms of hypertension treatment. Socio-demographic differences inhealthcare need tobeconsidered inpatient–provider communication.990,991 Standard approaches tocommunicate consequences oftreatment can involve 10-year risk of aCVD event with SCORE2 or SCORE2-OP. Alternatively, individual risk and risk reduction can be communicated interms of‘risk age’ or‘heart age’ (Section 7.3). PatientLifestyle (inclusive of health behaviour and social context) Medications Multidisciplinary medical team Self-care Family Figure 23 Patient-centred care.ESC Guidelines 75
+11.3. Self-measuring andmonitoring Self-care refers toindividual responsibility for healthy lifestyle beha- viours, aswell asthe actions required tocope with health condi- tions.996,997In the context of hypertension, italso includes self-management and self-measurement ofBP. Self-management includes lifestyle behaviour (diet, exercise, smoking, alcohol), co-management ofmedical treatments, and support foradher- ingtoprescribed medication.998Self-monitoring allows high BPtobede- tected early,999and enables patients toco-manage medications with their healthcare provider.1000,1001Suitably validated and correctly used digital devices have the potential tosupport co-management,1002,1003 and facilitate remote monitoring ofBP.76,81,100411.4. Facilitating medication adherence andpersistence Adherence (Figure 24) toBP-lowering drug regimens inclinical practice isalmost always lower than seen inclinical trials.1007Most apparent treatment-resistant hypertension is accounted for by non- adherence.1008Adherence should always beassessed with ano-blame approach. Various methods are available toassess adherence and, along with details on barriers to adherence, are described in the Supplementary data online andTable S14.1009 Adherence may also befacilitated byanoptimal therapeutic regi- men, which can beachieved bymedication reviews carried out at appropriate intervals. Several factors should beconsidered: (i)identify- ingdrug-related adverse events and appropriate dosing levels, (ii)using long-acting drugs that require once-daily dosing (preferably drugs that are long-acting due topharmacokinetic properties rather than galenic formulation), (iii) avoiding complex dosing schedules, (iv) using single- pillcombinations whenever feasible, (v)taking into account the financial capacity ofthe patient topay foragiven regimen inthe longer term, if relevant, orother pertinent aspects ofthe local ornational healthcare systems, and (vi) enlisting support ofafamily member orother social support to facilitate medication adherence and persistence (see Supplementary data online, Table S15).1010 While there have been advancements indigital tools tosupport self- management ofchronic illness including hypertension, there islittle efficacy evidence evaluating these interventions. Therefore, itisprema- ture tomake recommendations about specific digital tools. 11.5. Multidisciplinary management Acollaborative approach tomanaging hypertension, using team-based care among physicians, nurses, pharmacists, dietitians, and physiothera- pists, offers significant benefits over physician-only care. Multidisciplinary care isintended tobecollaborative and complemen- tary toregular medical care1011and isassociated with lower systolic and diastolic BP227,229,1012,1013and improved outcomes.230,1014 Task-shifting away from physicians isnecessary tomeet the huge need forthe management ofelevated BPand hypertension inthe popu- lation.1015Prescribing remains aphysician duty, but prescribing can be conducted under collaborative practice agreements with the multidis- ciplinary team inmany countries. Further details onpatient-centred care inhypertension isprovided in the Supplementary data online.Recommendation Table 34—Recommendations for communicating consequences of treatment (see Evidence Table 47) Recommendation ClassaLevelb Aninformed discussion about CVD risk and treatment benefits tailored tothe needs ofapatient isrecommended aspart ofhypertension management.992I C Motivational interviewing should beconsidered for patients with hypertension athospitals and community health centres toassist patients in controlling their BPand toenhance treatment adherence.993,994IIa B Physician–patient web communications are an effective tool that should beconsidered inprimary care, including reporting onhome BPreadings.995IIa C ©ESC 2024 BP, blood pressure; CVD, cardiovascular disease. aClass ofrecommendation. bLevel ofevidence. Recommendation Table 35—Recommendations for self-measuring and monitoring blood pressure (see Evidence Table 48) Recommendations ClassaLevelb Home BPmeasurement for managing hypertension byusing self-monitored BPisrecommended to achieve better BPcontrol.I B Self-measurement, when properly performed, is recommended due topositive effects onthe acceptance ofadiagnosis ofhypertension, patient empowerment, and adherence totreatment.1001I C Enhanced self-monitoring ofBPusing adevice paired with aconnected smartphone application may be considered, though evidence todate suggests that this may benomore effective than standard self-monitoring.1005,1006IIb B ©ESC 2024 BP, blood pressure. aClass ofrecommendation. bLevel ofevidence.Recommendation Table 36—Recommendations for multi/interdisciplinary blood pressure management (see Evidence Table 49) Recommendation ClassaLevelb Multidisciplinary approaches inthe management of patients with elevated BPand hypertension, including appropriate and safe task-shifting away from physicians, are recommended toimprove BP control.227,229,230,1012–1014,1016I A ©ESC 2024 BP, blood pressure. aClass ofrecommendation. bLevel ofevidence.76 ESC Guidelines
+12.Key messages (1) Given the demographic transition and the worldwide ageing of populations, the number ofindividuals with elevated BPorhyper- tension isincreasing worldwide. (2) The trajectory ofBPcontrol appears tobeworsening inNorth America, insome (but not all)European countries, and elsewhere around the world. (3) The risk forCVD attributable toBPisonacontinuous log-linear exposure variable scale, not abinary scale ofnormotension vs. hypertension. (4) BP-lowering drugs can reduce CVD risk even among individuals not traditionally classified ashypertensive. Accordingly, anewBPcategory called ‘elevated BP’ isintroduced. Elevated BPisde- fined asanoffice systolic BPof120–139 mmHg ordiastolic BPof 70–89 mmHg. Hypertension remains defined asoffice BP of ≥140/90 mmHg. (5) Hypertension inwomen isunder-studied inbasic, clinical, and popu- lation research. (6) HMOD suggests long-standing orsevere hypertension and is associated with increased CVD risk. (7) Absolute CVD risk must beconsidered when assessing and man- aging elevated BP. (8) Despite the growing number ofhypertension guidelines, the rates ofdiagnosis, treatment, and control ofhypertension (and elevated BP) remain suboptimal. Amajor factor underlying this ispoor e.g. affordability of medications and lack of social support to manage medicationsSocio-economic factors e.g. experience of side-effects and challenges of polypharmacy (treatment burden)Therapy-related factors e.g. beliefs about hypertension and related medications, persistence of medication taking habits and emotional distressPatient-related factors e.g. hypertension is a disease without an illness (asymptomatic) and often one among many morbiditiesCondition-related factorse.g. clarity and consistency of communication with patient, quality of ongoing relationship with healthcare providersHealth system/healthcare team factorsFigure 24 The five dimensions ofadherence (WHO, 2003) applied tohypertension.ESC Guidelines 77
+implementation ofevidence-based guidelines inreal-world clinical practice. (9) One ofthe most important changes inthe 2024 Guidelines isthe focus onevidence related toCVD outcomes ofBP-lowering in- terventions rather than BPlowering alone. (10) Irrespective ofthe threshold BPabove which BP-lowering treat- ment (lifestyle orpharmacological orother treatment) isre- commended, the on-treatment BP target is120–129/70–79 mmHg for alladults, provided this treatment iswell tolerated. There are several important exceptions tothese targets and in- dividualized decision-making isalways the most important priority. 13.Gaps intheevidence (1) Drivers ofworsening trajectories ofBPcontrol inwomen and men. (2) Need for sex-specific data on epidemiology, risk factors, and pathophysiology ofhypertension. Need for more prospective studies toassess women’s and men’s specific CVD risk factors pertinent toadults with elevated BPand hypertension, due tobio- logical and socio-cultural conditions. This includes sex-specific weighting oftraditional risk factors, aswell asinclusion ofsex- dependent, non-traditional, vascular risk factors such asstress, socio-economic conditions, and others.1017,1018We are also lack- ing data onsex-specific hormonal and genetic mechanisms and pathophysiology inthe human.1019Another important area in need ofinvestigation isabetter understanding ofthe role ofgen- der inthe management ofelevated BPand hypertension (including gender-driven barriers inaccessing medical care and adherence). (3) More widespread validation ofhome BP measuring devices. Validation protocols for cuffless BPmeasurement devices have just recently been proposed and need tobetested. (4) Clinical effectiveness ofHMOD indirecting intensity ofcare and personalized approaches inmanaging elevated BPand hypertension. (5) Best practice toscreen and manage primary aldosteronism. (6) Clinical benefits oftreating low CVD-risk individuals with elevated BP and further data strengthening the use ofBP-lowering medication among high-risk persons with baseline systolic BP of120–129 mmHg. (7) Need for more data onthe sex-specific optimal dosing, effects, and adverse effects ofBP-lowering drugs,1020inparticular from specifically planned prospective randomized trials. (8) More consideration for overall CVD outcomes ofBP-lowering interventions.(9) More European data (RCTs, real life) about the beneficial effect of treating patients with elevated BPand hypertension with polypills (inclusive ofnon-BP lowering medications). (10) CVD outcomes-based data onMRAs asadd-on therapy solely for resistant hypertension. (11) Trials on the BP-lowering effects ofnewer antidiabetic drugs (such asSGLT2 inhibitors and GLP-1 receptor agonists) ordrugs that now have indications forother conditions, such asfinerenone orsacubitril-valsartan. (12) Beneficial BPand CVD effects ofincreasing dietary potassium in- take and other lifestyle interventions. Studies todisentangle the effect ofsodium reduction vs.the effect ofpotassium supplemen- tation onBPcontrol and CVD outcomes. (13) RCTs comparing single-pill combination therapy with fixed doses vs.multiple monotherapies and their effects onCVD outcomes. (14) Cardiovascular outcomes trials ofrenal denervation. (15) BP-lowering treatment RCTs on different ethnic and migrant groups established inEurope. (16) Pharmacological BPmanagement inyoung adults (aged <40 years) and better data onthe efficacy ofalife-course approach for the drug management ofBP.1021 (17) CVD outcomes inmoderately toseverely frail and/or very elderly persons where BPmedications have been deprescribed, and the impact ofcompeting risks. (18) Management ofrenal artery disease with haemodynamically stable but severe stenosis (i.e. without high-risk features). (19) Need forclinical trials onmanaging hypertension inpatients trea- ted with anticancer drugs oranti-rejection drugs inrecipients of anallograft transplant. (20) Hypertension management inthe setting ofclimate changes, glo- bal warming, airand other forms ofpollution, pandemics, war zones, and inthe context ofdrug restrictions experienced in some low-to-middle-income countries. (21) Need toimprove implementation ofguidelines byhealthcare providers. (22) How todevelop sustainable hypertension care atthe intersection ofgrowing numbers ofpatients and limited resources. (23) Treat-to-target trials specifically testing BP-lowering drugs among drug-naïve persons with baseline BPof120–129 mmHg and in- creased CVD risk. 14.‘What todo’and‘what notto do’messages from theguidelines Aselected sample ofthe main messages from these guidelines are pro- vided inTable 15. Table 15 What todoandwhat nottodo Recommendations Class Level 5.Measuring blood pressure Itisrecommended tomeasure BPusing avalidated and calibrated device, toenforce the correct measurement technique, and toapply a consistent approach toBPmeasurement for each patient.I B Alladult patients (≥18 years orolder) are recommended tohave their office and/or out-of-office BPmeasured onanopportunistic basis and recorded intheir medical file, and betold what their current BPis.I C Continued78 ESC Guidelines
+Out-of-office BPmeasurement isrecommended fordiagnostic purposes, particularly because itcan detect both white-coat hypertension and masked hypertension. Where out-of-office measurements are not logistically and/or economically feasible, then itisrecommended that the diagnosis beconfirmed with arepeat office BPmeasurement using the correct standardized measurement technique.I B Itisrecommended that office BPshould bemeasured inboth arms atleast atthe first visit, because abetween-arm systolic BPdifference of >10 mmHg isassociated with anincreased CVD risk and may indicate arterial stenosis.I B Ifabetween-arm difference of>10 mmHg insystolic BPisrecorded, then itisrecommended that allsubsequent BPreadings use the arm with the higher BPreading.I B Out-of-office BPmeasurement isrecommended for ongoing management toquantify the effects oftreatment and guide BP-lowering medication titration, and/or identify possible causes ofside effects (e.g. symptomatic hypotension). Where out-of-office measurements are not logistically and/or economically feasible then ongoing management isrecommended tobebased onrepeated office BPmeasurements using the correct standardized measurement technique.I B Itisrecommended that allpatients undergoing BPmeasurement also undergo pulse palpation atrest todetermine heart rate and arrhythmias such asAF.I C 6.Definition andclassification ofelevated blood pressure andhypertension Itisrecommended that BPbecategorized asnon-elevated BP, elevated BP, and hypertension toaidtreatment decisions. I B Itisrecommended touse arisk-based approach inthe treatment ofelevated BP, and individuals with moderate orsevere CKD, established CVD, HMOD, diabetes mellitus, orfamilial hypercholesterolaemia are considered atincreased risk for CVD events.I B SCORE2 isrecommended forassessing 10-year risk offatal and non-fatal CVD among individuals aged 40–69 years with elevated BPwho are not already considered atincreased risk due tomoderate orsevere CKD, established CVD, HMOD, diabetes mellitus, orfamilial hypercholesterolaemia.I B SCORE2-OP isrecommended forassessing the 10-year risk offatal and non-fatal CVD among individuals aged ≥70 years with elevated BP who are not already considered atincreased risk due tomoderate orsevere CKD, established CVD, HMOD, diabetes mellitus, orfamilial hypercholesterolaemia.I B Itisrecommended that, irrespective ofage, individuals with elevated BPand aSCORE2 orSCORE2-OP CVD risk of≥10% beconsidered at increased risk for CVD for the purposes ofrisk-based management oftheir elevated BP.I B 7.Diagnosing hypertension andinvestigating underlying causes Inindividuals with increased CVD risk where their screening office BPis120–139/70–89 mmHg, itisrecommended tomeasure BP out-of-office, using ABPM and/or HBPM or,ifnot logistically feasible, make repeated office BPmeasurements onmore than one visit.I B Where screening office BPis140–159/90–99 mmHg, itisrecommended that the diagnosis ofhypertension should bebased onout-of-office BPmeasurement with ABPM and/or HBPM. Ifthese measurements are not logistically oreconomically feasible, then diagnosis can bemade on repeated office BPmeasurements onmore than one visit.I B Where screening BPis≥160/100 mmHg: •Itisrecommended that BP160–179/100–109 mmHg isconfirmed assoon aspossible (e.g. within 1month) preferably byeither home or ambulatory BPmeasurements. •Itisrecommended when BPis≥180/110 mmHg that hypertensive emergency beexcluded.I C Itisrecommended tomeasure serum creatinine, eGFR, and urine ACR inallpatients with hypertension. I A Ifmoderate-to-severe CKD isdiagnosed, itisrecommended torepeat measurements ofserum creatinine, eGFR, and urine ACR atleast annually.I C A12-lead ECG isrecommended for allpatients with hypertension. I B Echocardiography isrecommended inpatients with hypertension and ECG abnormalities, orsigns orsymptoms ofcardiac disease. I B Fundoscopy isrecommended ifBP>180/110 mmHg inthe work-up ofhypertensive emergency and malignant hypertension, aswell asin hypertensive patients with diabetes.I C Routine genetic testing for patients with hypertension isnot recommended. III C Itisrecommended that patients with hypertension presenting with suggestive signs, symptoms, ormedical history ofsecondary hypertension are appropriately screened for secondary hypertension.I B 8.Preventing andtreating elevated blood pressure Restriction ofsodium toapproximately 2gper day isrecommended where possible inalladults with elevated BPand hypertension [this is equivalent toabout 5gofsalt (sodium chloride) per day orabout ateaspoon orless].I A Moderate-intensity aerobic exercise of≥150 min/week [moderate aerobic exercise (≥30 min, 5–7 days/week) oralternatively 75min of vigorous exercise per week over 3days] isrecommended and should becomplemented with low- ormoderate-intensity dynamic or isometric resistance training (2–3 times/week) toreduce BPand CVD risk.I A Itisrecommended toaim forastable and healthy BMI (20–25 kg/m2)and waist circumference values (<94 cminmen and<80 cminwomen) toreduce BPand CVD risk.I A ContinuedESC Guidelines 79
+Adopting ahealthy and balanced diet such asthe Mediterranean orDASH diets isrecommended tohelp reduce BPand CVD risk. I A Men and women are recommended todrink less alcohol than the upper limit, which isabout 100 g/week ofpure alcohol. How this translates into number ofdrinks depends onportion size (the standards ofwhich differ per country), but most drinks contain 8–14 gofalcohol per drink. Preferably, itisrecommended toavoid alcohol consumption toachieve best health outcomes.I B Itisrecommended torestrict free sugar consumption, inparticular sugar-sweetened beverages, toamaximum of10% ofenergy intake. Itis also recommended todiscourage consumption ofsugar-sweetened beverages, such assoft drinks and fruit juices, starting atyoung age.I B Itisrecommended tostop tobacco smoking, initiate supportive care, and refer tosmoking cessation programmes, astobacco use strongly and independently causes CVD, CVD events, and all-cause mortality.I A Among allBP-lowering drugs, ACE inhibitors, ARBs, dihydropyridine CCBs, and diuretics (thiazides and thiazide-like drugs such as chlorthalidone and indapamide) have demonstrated the most effective reduction ofBPand CVD events, and are therefore recommended as first-line treatments tolower BP.I A Itisrecommended that beta-blockers are combined with any ofthe other major BP-lowering drug classes when there are other compelling indications for their use, e.g. angina, post-myocardial infarction, HFrEF, orfor heart rate control.I A Itisrecommended totake medications atthe most convenient time ofday forthe patient toestablish ahabitual pattern ofmedication taking toimprove adherence.I B Given trial evidence formore effective BPcontrol vs.monotherapy, combination BP-lowering treatment isrecommended formost patients with confirmed hypertension (BP≥140/90 mmHg) asinitial therapy. Preferred combinations are aRAS blocker (either anACE inhibitor oran ARB) with adihydropyridine CCB ordiuretic. Exceptions toconsider include patients aged ≥85 years, symptomatic orthostatic hypotension, moderate-to-severe frailty, and those with elevated BP(systolic BP120–139 mmHg ordiastolic BP70–89 mmHg) with aconcomitant indication for treatment.I B Inpatients receiving combination BP-lowering treatment, fixed-dose single-pill combination treatment isrecommended. I B IfBPisnot controlled with atwo-drug combination, increasing toathree-drug combination isrecommended, usually aRAS blocker with a dihydropyridine CCB and athiazide/thiazide-like diuretic, and preferably inasingle-pill combination.I B Combining two RAS blockers (ACE inhibitor and anARB) isnot recommended. III A Inadults with elevated BPand low/medium CVD risk (<10% over 10years), BPlowering with lifestyle measures isrecommended and can reduce the risk ofCVD.I B Inadults with elevated BPand sufficiently high CVD risk, after 3months oflifestyle intervention, BPlowering with pharmacological treatment isrecommended for those with confirmed BP≥130/80 mmHg toreduce CVD risk.I A Itisrecommended that inhypertensive patients with confirmed BP≥140/90 mmHg, irrespective ofCVD risk, lifestyle measures and pharmacological BP-lowering treatment isinitiated promptly toreduce CVD risk.I A Itisrecommended tomaintain BP-lowering drug treatment lifelong, even beyond the age of85years, ifwell tolerated. I A 8.Preventing andtreating elevated blood pressure (blood pressure targets) Toreduce CVD risk, itisrecommended that treated systolic BPvalues inmost adults betargeted to120–129 mmHg, provided the treatment iswell tolerated.I A Incases where BP-lowering treatment ispoorly tolerated and achieving atarget systolic of120–129 mmHg isnot possible, itisrecommended totarget asystolic BPlevel that is‘aslow asreasonably achievable’ (ALARA principle).I A 8.Preventing andtreating elevated blood pressure (renal denervation) Due toalack ofadequately powered outcomes trials demonstrating itssafety and CVD benefits, renal denervation isnot recommended asa first-line BP-lowering intervention for hypertension.III C Renal denervation isnot recommended fortreating hypertension inpatients with moderate-to-severely impaired renal function (eGFR <40 mL/min/1.73 m2)orsecondary causes ofhypertension, until further evidence becomes available.III C 9.Managing specific patient groups orcircumstances Young adults Comprehensive screening forthe main causes ofsecondary hypertension isrecommended inadults diagnosed with hypertension before the age of40years, except for obese young adults where itisrecommended tostart with anobstructive sleep apnoea evaluation.I B Hypertension inpregnancy Inwomen with gestational hypertension, starting drug treatment isrecommended forthose with confirmed office systolic BP≥140 mmHg or diastolic BP≥90 mmHg.I B Inpregnant women with chronic hypertension, starting drug treatment isrecommended forthose with confirmed office systolic BP≥140 mmHg ordiastolic BP≥90 mmHg.I B Inwomen with chronic and gestational hypertension, itisrecommended tolower BPbelow 140/90 mmHg but not below 80mmHg for diastolic BP.I C Continued80 ESC Guidelines
+Dihydropyridine CCBs (preferably extended-release nifedipine), labetalol, and methyldopa are recommended first-line BP-lowering medications for treating hypertension inpregnancy.I C Inconsultation with anobstetrician, low- tomoderate-intensity exercise isrecommended inallpregnant women without contraindications to reduce the risk ofgestational hypertension and pre-eclampsia.I B RAS blockers are not recommended during pregnancy. III B Very oldandfrail patients; orthostatic hypotension Itisrecommended that treatment ofelevated BPand hypertension among older patients aged <85 years who are not moderately toseverely frail follows the same guidelines asfor younger people, provided BP-lowering treatment iswell tolerated.I A Itisrecommended tomaintain BP-lowering drug treatment lifelong, even beyond the age of85years, ifwell tolerated. I A Before starting orintensifying BP-lowering medication, itisrecommended totest fororthostatic hypotension, byfirst having the patient sitor liefor 5min and then measuring BP1and/or 3min after standing.I B Itisrecommended topursue non-pharmacological approaches asthe first-line treatment oforthostatic hypotension among persons with supine hypertension. For such patients, itisalso recommended toswitch BP-lowering medications that worsen orthostatic hypotension toan alternative BP-lowering therapy and not tosimply de-intensify therapy.I A Diabetes Inmost adults with elevated BPand diabetes, after amaximum of3months oflifestyle intervention, BPlowering with pharmacological treatment isrecommended for those with confirmed BP≥130/80 mmHg toreduce CVD risk.I A BP-lowering drug treatment isrecommended forpeople with pre-diabetes orobesity when confirmed office BPis≥140/90 mmHg orwhen office BPis130–139/80–89 mmHg and the patient isatpredicted 10-year risk ofCVD ≥10% orwith high-risk conditions, despite amaximum of3months oflifestyle therapy.I A Inpersons with diabetes who are receiving BP-lowering drugs, itisrecommended totarget systolic BPto120–129 mmHg, iftolerated. I A Chronic kidney disease Inpatients with diabetic ornon-diabetic moderate-to-severe CKD and confirmed BP≥130/80 mmHg, lifestyle optimization and BP-lowering medication are recommended toreduce CVD risk, provided such treatment iswell tolerated.I A Inadults with moderate-to-severe CKD who arereceiving BP-lowering drugs and who have eGFR >30 mL/min/1.73 m2,itisrecommended to target systolic BPto120–129 mmHg, iftolerated. Individualized BPtargets are recommended for those with lower eGFR orrenal transplantation.I A Inhypertensive patients with CKD and eGFR >20 mL/min/1.73 m2,SGLT2 inhibitors are recommended toimprove outcomes inthe context oftheir modest BP-lowering properties.I A Cardiac disease Inpatients with ahistory ofmyocardial infarction who require BP-lowering treatment, beta-blockers and RAS blockers are recommended as part ofthat treatment.I A Inpatients with symptomatic angina who require BP-lowering treatment, beta-blockers and/or CCBs are recommended aspart ofthat treatment.I A Inpatients with symptomatic HFrEF/HFmrEF, the following treatments with BP-lowering effects are recommended toimprove outcomes: ACE inhibitors (or ARBs ifACE inhibitors are not tolerated) orARNi, beta-blockers, MRAs, and SGLT2 inhibitors.I A Inhypertensive patients with symptomatic HFpEF, SGLT2 inhibitors are recommended toimprove outcomes inthe context oftheir modest BP-lowering properties.I A Other conditions Itisrecommended that the BP-lowering drug treatment strategy for preventing stroke should comprise aRAS blocker plus aCCB ora thiazide-like diuretic.I A Inpatients with confirmed BP≥130/80 mmHg with ahistory ofTIA orstroke asystolic BPtarget 120–129 mmHg isrecommended toreduce CVD outcomes, provided treatment istolerated.I A Renal artery angioplasty isnot recommended inpatients without confirmed haemodynamically significant renal artery stenosis. III A 10.Acute andshort-term lowering ofblood pressure Intracerebral haemorrhage oracute ischaemic stroke For patients with ischaemic stroke orTIA and anindication for BPlowering, itisrecommended that BPlowering therapy should be commenced before hospital discharge.I B Inpatients with intracerebral haemorrhage presenting with systolic BP≥220 mmHg, acute reduction insystolic BP>70 mmHg from initial levels within 1hofcommencing treatment isnot recommended.III B ContinuedESC Guidelines 81
+15.Evidence tables Evidence tables are available atEuropean Heart Journal online. 16.Data availability statement No new data were generated oranalysed insupport ofthis research. 17.Author information Author/task force Member Affiliations: Cian P.McCarthy, Cardiovascular Division Massachusetts General Hospital and Harvard Medical School Boston, MA, United States ofAmerica; Rosa Maria Bruno, PARCC, Université Paris Cité, Inserm, Paris, France, and Pharmacology &Hypertension, AP-HP, Hôpital Européen Georges Pompidou, Paris, France; Sofie Brouwers, Cardiovascular Center Aalst, Department ofCardiology, OLV Clinic Aalst, Aalst, Belgium, and Department ofExperimental Pharmacology, Faculty ofMedicine and Pharmacy, Vrije Universiteit Brussel, Brussels, Belgium; Michelle D.Canavan, School ofMedicine, College ofMedicine, Nursing and Health Sciences, University of Galway, Galway, Ireland, and Department ofGeriatric Medicine, University Hospital Galway, Saolta Hospitals Group, Galway, Ireland; Claudio Ceconi, Motusmed Clinic, Brescia, Italy; Ruxandra Maria Christodorescu, Department VInternal Medicine, University of Medicine and Pharmacy VBabes, Timisoara, Romania, and Research Center, Institute ofCardiovascular Diseases, Timisoara, Romania; Stella S.Daskalopoulou, Medicine Research Institute of the McGill University Health Centre, McGill University, Montreal, Canada; Charles J.Ferro, Department of Renal Medicine, University Hospitals Birmingham, Birmingham, United Kingdom, and Institute of Cardiovascular Sciences University of Birmingham, Birmingham, United Kingdom; Eva Gerdts, Department ofClinical Science, University ofBergen, Bergen, Norway, and Department ofHeart Disease, Haukeland University Hospital, Bergen, Norway; Henner Hanssen, Department Sport, Exercise and Health, Medical Faculty, University of Basel, Basel, Switzerland; Julie Harris (UnitedKingdom), ESC Patient Forum, Sophia Antipolis, France; Lucas Lauder, Department ofcardiology, University hospital Basel, Basel, Switzerland, and Department ofinternal medicine III,Cardiology, Angiology, and Intensive Care Medicine, Saarland university medical center, Homburg, Germany; Richard J.McManus, Nuffield Department ofPrimary Care Health Sciences, University ofOxford, Oxford, United Kingdom; Gerard J.Molloy, School ofPsychology, University of Galway, Galway, Ireland; Kazem Rahimi, Deep Medicine, Nuffield Department of Women’s and Reproductive Health, University of Oxford, Oxford, United Kingdom; Vera Regitz-Zagrosek, Charite, University Medicine Berlin, Gender in Medicine, Berlin, Germany; Gian Paolo Rossi, Department of Medicine, DIMED, University ofPadua, Padua, Italy; Else Charlotte Sandset, Department ofNeurology, Oslo University Hospital, Oslo, Norway, The Norwegian Air Ambulance Foundation, Oslo, Norway, and Institute ofClinical Medicine University ofOslo, Oslo, Norway; Bart Scheenaerts (Belgium), ESC Patient Forum, Sophia Antipolis, France; JanA.Staessen, Non-Profit Research Association Alliance for the Promotion ofPreventive Medicine, Mechelen, Belgium, and Biomedical Research Group, Faculty of Medicine, University of Leuven, Leuven, Belgium; Izabella Uchmanowicz, Department of Nursing and Obstetrics, Faculty ofHealth Sciences, Wroclaw Medical University, Wroclaw, Poland; andMaurizio Volterrani, Exercise Science and Medicine San Raffaele Open University, Rome, Italy, and Cardiopulmonary Department, IRCCS San Raffaele, Rome, Italy. 18.Appendix ESC Scientific Document Group Includes Document Reviewers and ESC National Cardiac Societies. Document Reviewers: Ana Abreu (CPG Review Co-ordinator) (Portugal), Michael Hecht Olsen (CPG Review Co-ordinator) (Denmark), Marco Ambrosetti (Italy), Emmanuel Androulakis (United Kingdom), LiaEviBang (Denmark), Jesper Nørgaard Bech (Denmark), Michael A. Borger (Germany), Pierre Boutouyrie (France), Luís Bronze (Portugal), Sergio Buccheri (Sweden), Regina Dalmau (Spain), Maria Carmen De Pablo Zarzosa (Spain), Christian Delles (UnitedSevere hypertension inpregnancy andpre-eclampsia Inpre-eclampsia oreclampsia with hypertensive crisis, drug treatment with i.v.labetalol ornicardipine and magnesium isrecommended. I C Inpre-eclampsia oreclampsia associated with pulmonary oedema, nitroglycerin given asani.v.infusion isrecommended. I C Insevere hypertension inpregnancy: •drug treatment with i.v.labetalol, oral methyldopa, ororal nifedipine isrecommended. Intravenous hydralazine isasecond-line option.I C 11.Patient-centred care inhypertension Aninformed discussion about CVD risk and treatment benefits tailored tothe needs ofapatient isrecommended aspart ofhypertension management.I C Home BPmeasurement for managing hypertension byusing self-monitored BPisrecommended toachieve better BPcontrol. I B Self-measurement, when properly performed, isrecommended due topositive effects onthe acceptance ofadiagnosis ofhypertension, patient empowerment, and adherence totreatment.I C Multidisciplinary approaches inthe management ofpatients with elevated BPand hypertension, including appropriate and safe task-shifting away from physicians are recommended toimprove BPcontrol.I A ©ESC 2024 ABPM, ambulatory blood pressure monitoring; ACE, angiotensin-converting enzyme; ACR, albumin:creatinine ratio; AF, atrial fibrillation; ALARA, aslow asreasonably achievable; ARB, angiotensin receptor blocker; ARNi, angiotensin receptor–neprilysin inhibitor; BMI, body mass index; BP, blood pressure; CCB, calcium channel blocker; CKD, chronic kidney disease; CVD, cardiovascular disease; DASH, Dietary Approaches toStop Hypertension; ECG, electrocardiogram; eGFR, estimated glomerular filtration rate; ESC, European Society of Cardiology; HBPM, home blood pressure monitoring; HFpEF, heart failure with preserved ejection fraction; HF(m)rEF, heart failure with (mildly) reduced ejection fraction; HMOD, hypertension-mediated organ damage; i.v., intravenous; MRA, mineralocorticoid receptor antagonist; RAS, renin–angiotensin system; SCORE2, Systematic COronary Risk Evaluation 2; SCORE2-OP, Systematic COronary Risk Evaluation 2-Older Persons; SGLT2, sodium–glucose co-transporter 2;TIA, transient ischaemic attack.82 ESC Guidelines
+Kingdom), Maria Manuela Fiuza (Portugal), Rahima Gabulova (Azerbaijan), Bjørn Olav Haugen (Norway), Christian Heiss (United Kingdom), Borja Ibanez (Spain), Stefan James (Sweden), Vikas Kapil (United Kingdom), Meral Kayikçioglu (Turkey), Lars Køber (Denmark), Konstantinos C.Koskinas (Switzerland), Emanuela Teresa Locati (Italy), Sharon MacDonald (United Kingdom), Anastasia S.Mihailidou (Australia), Borislava Mihaylova (United Kingdom), Richard Mindham (United Kingdom) Martin Bodtker Mortensen (Denmark), Sandor Nardai (Hungary), Lis Neubeck (United Kingdom), Jens Cosedis Nielsen (Denmark), Peter M. Nilsson (Sweden), Agnes A. Pasquet (Belgium), Mónica Mendes Pedro (Portugal), Eva Prescott (Denmark), Amina Rakisheva (Kazakhstan), Ernst Rietzschel (Belgium), Bianca Rocca (Italy), Xavier Rossello (Spain), Jean-Paul Schmid (Switzerland), Eduard Shantsila (United Kingdom), Isabella Sudano (Switzerland), Ana Teresa Timóteo (Portugal), Georgios Tsivgoulis (Greece), Andrea Ungar (Italy), Ilonca Vaartjes (Netherlands), Frank Visseren (Netherlands), Heinz Voeller (Germany), Christiaan Vrints (Belgium), Adam Witkowski (Poland), Maria-Christina Zennaro (France), and Katja Zeppenfeld (Netherlands). ESC National Cardiac Societies actively involved inthe review process ofthe2024 ESC Guidelines forthemanage- ment ofelevated blood pressure andhypertension: Albania: Albanian Society ofCardiology, Naltin Shuka; Algeria: Algerian Society ofCardiology, Nadia Laredj; Austria: Austrian Society ofCardiology, Noemi Pavo; Azerbaijan: Azerbaijan Society of Cardiology, Ulvi Mirzoyev; Belgium: Belgian Society of Cardiology, Philippe van de Borne; Bosnia and Herzegovina: Association of Cardiologists of Bosnia and Herzegovina, Šekib Sokolović; Bulgaria: Bulgarian Society of Cardiology, Arman Postadzhiyan; Croatia: Croatian Cardiac Society, Jure Samardzic; Cyprus: Cyprus Society of Cardiology, Petros Agathangelou; Czechia: Czech Society ofCardiology, Jiri Widimsky; Denmark: Danish Society ofCardiology, Michael Hecht Olsen; Egypt: Egyptian Society ofCardiology, Wael M.El-Kilany; Estonia: Estonian Society ofCardiology, Priit Pauklin; Finland: Finnish Cardiac Society, Jari A. Laukkanen; France: French Society of Cardiology, Romain Boulestreau; Georgia: Georgian Society of Cardiology, Bezhan Tsinamdzgvrishvili; Germany: German Cardiac Society, Ulrich Kintscher; Greece: Hellenic Society ofCardiology, Maria Marketou; Hungary: Hungarian Society ofCardiology, Dénes Páll;Iceland: Icelandic Society ofCardiology, Þórdís Jóna Hrafnkelsdóttir; Ireland: Irish Cardiac Society, Eamon Dolan; Israel: Israel Heart Society, Talya Wolak; Italy: Italian Federation ofCardiology, Grzegorz Bilo; Kazakhstan: Association ofCardiologists ofKazakhstan, Meiramgul Kapsimetovna Tundybayeva; Kyrgyzstan: Kyrgyz Society of Cardiology, Erkin Mirrakhimov, Latvia: Latvian Society of Cardiology, Karlis Trusinskis; Lebanon: Lebanese Society of Cardiology, Ghassan Kiwan; Libya: Libyan Cardiac Society, Omar Msalem; Lithuania: Lithuanian Society of Cardiology, Jolita Badarienė; Luxembourg: Luxembourg Society of Cardiology, Cristiana-Astra Banu; Malta: Maltese Cardiac Society, Matthew Mercieca Balbi; Moldova (Republic of): Moldavian Society of Cardiology, Alexandru Caraus; Montenegro: Montenegro Society ofCardiology, Aneta Boskovic; Morocco: Moroccan Society of Cardiology, Najat Mouine; Netherlands: Netherlands Society of Cardiology, Tom Vromen; North Macedonia: National Society of Cardiology of North Macedonia, Marijan Bosevski; Norway: Norwegian Society ofCardiology, Helga B.Midtbø; Poland: Polish Cardiac Society, Adrian Doroszko; Portugal: Portuguese Society of Cardiology, Hélder Dores; Romania: Romanian Society ofCardiology, Elisabeta Badila; San Marino: San Marino Society of Cardiology, Roberto Bini; Serbia: Cardiology Society ofSerbia, Dragan Vojislav Simić; Slovenia: Slovenian Society ofCardiology, Zlatko Fras; Spain: Spanish Society ofCardiology, Pilar Mazón; Sweden: Swedish Society ofCardiology, Jonas Spaak; Switzerland: Swiss Society ofCardiology, Thilo Burkard; Syrian Arab Republic: Syrian Cardiovascular Association, Elias Barakat; Tunisia: Tunisian Society ofCardiology and Cardiovascular Surgery, Salem Abdessalem; Türkiye: Turkish Society ofCardiology, Yilmaz Gunes; Ukraine: Ukrainian Association of Cardiology, Yurij M. Sirenko; United Kingdom ofGreat Britain and Northern Ireland: British Cardiovascular Society, Adrian J.B.Brady; andUzbekistan: Association ofCardiologists ofUzbekistan, Gulnoz Abdusattarovna Khamidullaeva. ESC Clinical Practice Guidelines (CPG) Committee: Eva Prescott (Chairperson) (Denmark), Stefan James (Co-Chairperson) (Sweden), Elena Arbelo (Spain), Colin Baigent (United Kingdom), Michael A. Borger (Germany), Sergio Buccheri (Sweden), Borja Ibanez (Spain), Lars Køber (Denmark), Konstantinos C. 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