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Acute heart failure: diagnosis and management Clinical guideline NICE 2022. All rights reserved. Subject to Notice of rights (https://www.nice.org.uk/terms-and- conditions#notice-of-rights). Last updated 17 November 2021 Your responsibility The recommendations in this guideline represent the view of NICE, arrived at after careful consideration of the evidence available. When exercising their judgement, professionals and practitioners are expected to take this guideline fully into account, alongside the individual needs, preferences and values of their patients or the people using their service. It is not mandatory to apply the recommendations, and the guideline does not override the responsibility to make decisions appropriate to the circumstances of the individual, in consultation with them and their families and carers or guardian. All problems (adverse events) related to a medicine or medical device used for treatment or in a procedure should be reported to the Medicines and Healthcare products Regulatory Agency using the Yellow Card Scheme. Local commissioners and providers of healthcare have a responsibility to enable the guideline to be applied when individual professionals and people using services wish to use it. They should do so in the context of local and national priorities for funding and developing services, and in light of their duties to have due regard to the need to eliminate unlawful discrimination, to advance equality of opportunity and to reduce health inequalities. Nothing in this guideline should be interpreted in a way that would be inconsistent with complying with those duties. Commissioners and providers have a responsibility to promote an environmentally sustainable health and care system and should assess and reduce the environmental impact of implementing NICE recommendations wherever possible. Contents Overview 4 Who is it for?


Commissioners and providers have a responsibility to promote an environmentally sustainable health and care system and should assess and reduce the environmental impact of implementing NICE recommendations wherever possible. Contents Overview 4 Who is it for? 4 Introduction 5 Drug recommendations 5 Key priorities for implementation 7 Organisation of care 7 Diagnosis, assessment and monitoring 7 Treatment after stabilisation 8 1.1 Organisation of care 9 1.2 Diagnosis, assessment and monitoring 10 1.3 Initial pharmacological treatment 10 1.4 Initial non-pharmacological treatment 11 1.5 Treatment after stabilisation 12 1.6 Valvular surgery and percutaneous intervention 13 1.7 Mechanical assist devices 13 2 Recommendations for research 14 2.3 Intra-aortic balloon counter-pulsation 15 Finding more information and committee details 17 Update information 18 This guideline is partially replaced by NG208. This guideline is the basis of QS103. Overview This guideline covers diagnosing and managing acute heart failure or possible acute heart failure in people aged 18 and over. It aims to improve the immediate care of someone who is acutely unwell as a result of heart failure. Heart failure may indicate acute myocardial injury in patients with COVID-19. See the recommendations on diagnosing and managing acute myocardial injury in our COVID-19 rapid guideline on managing COVID-19. Who is it for? Healthcare professionals Commissioners Adults who have a diagnosis of acute heart failure, or have possible acute heart failure, or are being investigated for acute heart failure Introduction Heart failure is a condition in which the heart does not pump enough blood to meet all the needs of the body. It is caused by dysfunction of the heart due to muscle damage (systolic or diastolic dysfunction), valvular dysfunction, arrhythmias or other rare causes. Acute heart failure can present as new-onset heart failure in people without known cardiac dysfunction, or as acute decompensation of chronic heart failure.


Acute heart failure can present as new-onset heart failure in people without known cardiac dysfunction, or as acute decompensation of chronic heart failure. Acute heart failure is a common cause of admission to hospital (over 67,000 admissions in England and Wales per year) and is the leading cause of hospital admission in people 65 years or older in the UK. This guideline includes important aspects of the diagnosis and management of acute heart failure that are not addressed by the NICE guideline on chronic heart failure. The guideline on chronic heart failure focuses on long-term management rather than on the immediate care of someone who is acutely unwell as a result of heart failure. This guideline covers the care of adults (aged 18 years or older) who have a diagnosis of acute heart failure, have possible acute heart failure, or are being investigated for acute heart failure. It includes the following key clinical areas: the role of early natriuretic peptide testing and echocardiography the role of specialist management units the use of ventilatory support, pharmacological therapy and ultrafiltration treatment after stabilisation, including selected surgical interventions and initiation of the pharmacological therapies that are used in the management of chronic heart failure. Drug recommendations The guideline will assume that prescribers will use a drug's summary of product characteristics to inform decisions made with individual patients. In memory of Christopher Jones, patient member of the GDG who ensured that the patient voice was heard during the development of this guideline. Key priorities for implementation The following recommendations have been identified as priorities for implementation. The full list of recommendations is in section 1.


Key priorities for implementation The following recommendations have been identified as priorities for implementation. The full list of recommendations is in section 1. Organisation of care All hospitals admitting people with suspected acute heart failure should provide a specialist heart failure team that is based on a cardiology ward and provides outreach services. Ensure that all people being admitted to hospital with suspected acute heart failure have early and continuing input from a dedicated specialist heart failure team. Diagnosis, assessment and monitoring In people presenting with new suspected acute heart failure, use a single measurement of serum natriuretic peptides (B-type natriuretic peptide [BNP] or N-terminal pro-B-type natriuretic peptide [NT-proBNP]) and the following thresholds to rule out the diagnosis of heart failure. BNP less than 100 ng/litre NT-proBNP less than 300 ng/litre. In people presenting with new suspected acute heart failure with raised natriuretic peptide levels (see recommendation 1.2.2), perform transthoracic Doppler 2D echocardiography to establish the presence or absence of cardiac abnormalities. In people presenting with new suspected acute heart failure, consider performing transthoracic Doppler 2D echocardiography within 48 hours of admission to guide early specialist management. Treatment after stabilisation In a person presenting with acute heart failure who is already taking beta-blockers, continue the beta-blocker treatment unless they have a heart rate less than 50 beats per minute, second or third degree atrioventricular block, or shock. Start or restart beta-blocker treatment during hospital admission in people with acute heart failure due to left ventricular systolic dysfunction, once their condition has been stabilised for example, when intravenous diuretics are no longer needed. Ensure that the person's condition is stable for typically 48 hours after starting or restarting beta-blockers and before discharging from hospital.


Ensure that the person's condition is stable for typically 48 hours after starting or restarting beta-blockers and before discharging from hospital. Offer an angiotensin-converting enzyme inhibitor (or angiotensin receptor blocker if there are intolerable side effects) and an aldosterone antagonist during hospital admission to people with acute heart failure and reduced left ventricular ejection fraction. If the angiotensin-converting enzyme inhibitor (or angiotensin receptor blocker) is not tolerated an aldosterone antagonist should still be offered. People have the right to be involved in discussions and make informed decisions about their care, as described in NICE's information on making decisions about your care. Making decisions using NICE guidelines explains how we use words to show the strength (or certainty) of our recommendations, and has information about prescribing medicines (including off-label use), professional guidelines, standards and laws (including on consent and mental capacity), and safeguarding. The following guidance is based on the best available evidence. The full guideline gives details of the methods and the evidence used to develop the guidance. 1.1 Organisation of care 1.1.1 All hospitals admitting people with suspected acute heart failure should provide a specialist heart failure team that is based on a cardiology ward and provides outreach services. 1.1.2 Ensure that all people being admitted to hospital with suspected acute heart failure have early and continuing input from a dedicated specialist heart failure team. 1.1.3 Plan the following with people with acute heart failure in line with the NICE guideline on chronic heart failure: discharge from hospital after the acute phase and subsequent management in primary care, including ongoing monitoring and care provided by the multidisciplinary team and information and communication about their condition, its treatment and prognosis.


1.1.3 Plan the following with people with acute heart failure in line with the NICE guideline on chronic heart failure: discharge from hospital after the acute phase and subsequent management in primary care, including ongoing monitoring and care provided by the multidisciplinary team and information and communication about their condition, its treatment and prognosis. 1.1.4 A follow-up clinical assessment should be undertaken by a member of the specialist heart failure team within 2 weeks of the person being discharged from hospital. 1.2 Diagnosis, assessment and monitoring 1.2.1 Take a history, perform a clinical examination and undertake standard investigations for example, electrocardiography, chest X-ray and blood tests in line with the NICE guideline on chronic heart failure. 1.2.2 In people presenting with new suspected acute heart failure, use a single measurement of serum natriuretic peptides (B-type natriuretic peptide [BNP] or N-terminal pro-B-type natriuretic peptide [NT-proBNP]) and the following thresholds to rule out the diagnosis of heart failure: BNP less than 100 ng/litre NT-proBNP less than 300 ng/litre. 1.2.3 In people presenting with new suspected acute heart failure with raised natriuretic peptide levels (see recommendation 1.2.2), perform transthoracic Doppler 2D echocardiography to establish the presence or absence of cardiac abnormalities. 1.2.4 In people presenting with new suspected acute heart failure, consider performing transthoracic Doppler 2D echocardiography within 48 hours of admission to guide early specialist management. 1.2.5 Do not routinely offer pulmonary artery catheterisation to people with acute heart failure. 1.3 Initial pharmacological treatment 1.3.1 For guidance on patient consent and capacity follow recommendations on consent and capacity in the NICE guideline on patient experience in adult NHS services. 1.3.2 Do not routinely offer opiates to people with acute heart failure. 1.3.3 Offer intravenous diuretic therapy to people with acute heart failure. Start treatment using either a bolus or infusion strategy.


1.3.3 Offer intravenous diuretic therapy to people with acute heart failure. Start treatment using either a bolus or infusion strategy. 1.3.4 For people already taking a diuretic, consider a higher dose of diuretic than that on which the person was admitted unless there are serious concerns with patient adherence to diuretic therapy before admission. 1.3.5 Closely monitor the person's renal function, weight and urine output during diuretic therapy. 1.3.6 Discuss with the person the best strategies of coping with an increased urine output. 1.3.7 Do not routinely offer nitrates to people with acute heart failure. 1.3.8 If intravenous nitrates are used in specific circumstances, such as for people with concomitant myocardial ischaemia, severe hypertension or regurgitant aortic or mitral valve disease, monitor blood pressure closely in a setting where at least level 2 care can be provided. 1.3.9 Do not offer sodium nitroprusside to people with acute heart failure. 1.3.10 Do not routinely offer inotropes or vasopressors to people with acute heart failure. 1.3.11 Consider inotropes or vasopressors in people with acute heart failure with potentially reversible cardiogenic shock. Administer these treatments in a cardiac care unit or high dependency unit or an alternative setting where at least level 2 care can be provided. Level 2 care is for people needing more detailed observation or intervention, including support for a single failing organ system or postoperative care and for those stepping down from higher levels of care. From levels of critical care for adult patients. 1.4 Initial non-pharmacological treatment 1.4.1 Do not routinely use non-invasive ventilation (continuous positive airways pressure [CPAP] or non-invasive positive pressure ventilation [NIPPV]) in people with acute heart failure and cardiogenic pulmonary oedema.


1.4 Initial non-pharmacological treatment 1.4.1 Do not routinely use non-invasive ventilation (continuous positive airways pressure [CPAP] or non-invasive positive pressure ventilation [NIPPV]) in people with acute heart failure and cardiogenic pulmonary oedema. 1.4.2 If a person has cardiogenic pulmonary oedema with severe dyspnoea and acidaemia consider starting non-invasive ventilation without delay: at acute presentation or as an adjunct to medical therapy if the person's condition has failed to respond. 1.4.3 Consider invasive ventilation in people with acute heart failure that, despite treatment, is leading to or is complicated by: respiratory failure or reduced consciousness or physical exhaustion. 1.4.4 Do not routinely offer ultrafiltration to people with acute heart failure. 1.4.5 Consider ultrafiltration for people with confirmed diuretic resistance. Diuretic resistance is defined as dose escalation beyond a person's previously recognised dose ceiling or a dose approaching the maximum recommended daily dose without incremental improvement in diuresis. From diuretics and ultrafiltration in acute decompensated heart failure. 1.5 Treatment after stabilisation 1.5.1 In a person presenting with acute heart failure who is already taking beta-blockers, continue the beta-blocker treatment unless they have a heart rate less than 50 beats per minute, second or third degree atrioventricular block, or shock. 1.5.2 Start or restart beta-blocker treatment during hospital admission in people with acute heart failure due to left ventricular systolic dysfunction, once their condition has been stabilised for example, when intravenous diuretics are no longer needed. 1.5.3 Ensure that the person's condition is stable for typically 48 hours after starting or restarting beta-blockers and before discharging from hospital. 1.5.4 Offer an angiotensin-converting enzyme inhibitor (or angiotensin receptor blocker if there are intolerable side effects) and an aldosterone antagonist during hospital admission to people with acute heart failure and reduced left ventricular ejection fraction.


1.5.4 Offer an angiotensin-converting enzyme inhibitor (or angiotensin receptor blocker if there are intolerable side effects) and an aldosterone antagonist during hospital admission to people with acute heart failure and reduced left ventricular ejection fraction. If the angiotensin-converting enzyme inhibitor (or angiotensin receptor blocker) is not tolerated an aldosterone antagonist should still be offered. In February 2016, the Medicines and Healthcare products Regulatory Agency (MHRA) published advice on the concomitant use of spironolactone and renin-angiotensin system drugs in heart failure concerning the risk of potentially fatal hyperkalaemia. See the MHRA advice for more information. 1.5.5 Closely monitor the person's renal function, electrolytes, heart rate, blood pressure and overall clinical status during treatment with beta-blockers, aldosterone antagonists or angiotensin-converting enzyme inhibitors. 1.6 Valvular surgery and percutaneous intervention The recommendations on valvular surgery and percutaneous intervention have been replaced by the NICE guideline on heart valve disease. 1.7 Mechanical assist devices 1.7.1 At an early stage, the specialist should have a discussion with a centre providing mechanical circulatory support about: people with potentially reversible severe acute heart failure or people who are potential candidates for transplantation. 2 Recommendations for research The Guideline Development Group has made the following recommendations for research, based on its review of evidence, to improve NICE guidance and patient care in the future. In people with acute heart failure, congestion and worsening renal function, does the addition of low-dose dopamine to standard therapy lead to greater diuresis and renal protection compared with adding placebo to standard therapy? Why this is important A randomised controlled trial should be conducted to investigate whether the addition of low-dose dopamine to standard therapy leads to more clinically and cost effective decongestion in people admitted to hospital for treatment of decompensated heart failure.


Why this is important A randomised controlled trial should be conducted to investigate whether the addition of low-dose dopamine to standard therapy leads to more clinically and cost effective decongestion in people admitted to hospital for treatment of decompensated heart failure. The study should aim to investigate the diuretic effect of dopamine as well as effects on renal function. One of the most common and difficult to manage problems arising during the initial treatment of people with acute heart failure is an inadequate response to intravenous diuretic therapy (that is, failure to relieve congestion), which is often associated with worsening renal function. This combination frequently leads to a prolonged inpatient stay and is associated with higher inpatient mortality rates and higher post-discharge mortality and re-admission rates. The best treatment for this combination of problems is unknown. However, theoretical and experimental evidence indicates that low-dose dopamine may improve renal blood flow, as well as enhance sodium and water excretion. Clinical trials have not yet resolved whether in some patients, the use of low-dose dopamine actually results in improved decongestion and shorter hospital stays. In people with acute heart failure and persistent congestion, does the addition of a thiazide diuretic to standard therapy lead to greater diuresis compared with adding placebo to standard therapy? Why this is important A randomised controlled trial should be conducted to investigate whether the addition of a thiazide diuretic to standard therapy leads to more clinically and cost effective decongestion in people admitted to hospital for treatment of decompensated heart failure. One of the most common and difficult to manage problems arising during the initial treatment of people with acute heart failure is an inadequate response to intravenous diuretic therapy.


One of the most common and difficult to manage problems arising during the initial treatment of people with acute heart failure is an inadequate response to intravenous diuretic therapy. This frequently leads to a prolonged inpatient stay and is associated with higher inpatient mortality and higher post-discharge mortality and re-admission rates. The best treatment for this problem is unknown. However, there is some inconsistent and non-robust evidence that addition of a thiazide or thiazide-like diuretic (metolazone) may be beneficial. The proposed study would aim to resolve this uncertainty and guide the management of a difficult clinical problem. 2.3 Intra-aortic balloon counter-pulsation In people with acute heart failure and hypoperfusion syndrome, is the use of intra-aortic balloon counter-pulsation pump (IABP) better than the use of intravenous inotropes? Why this is important A randomised controlled trial should be conducted in people with decompensated heart failure due to left ventricular systolic dysfunction and systemic hypoperfusion comparing the use of IABP with the use of inotropes/vasopressors. This would determine which strategy is more clinically and cost effective in this cohort. IABP is used in the hospital setting as an adjuvant in people with critical coronary ischaemia and in people with mechanical complications of acute myocardial infarction. It has also been used in people who develop cardiogenic shock after acute myocardial infarction. However, it is uncertain whether it can provide clinical benefit in the critically unwell patients with acute heart failure due to left ventricular systolic dysfunction and systemic hypoperfusion. In people with decompensated heart failure, fluid congestion and diuretic resistance, does ultrafiltration lead to more rapid and effective decongestion compared with continuing diuretic treatment?


In people with decompensated heart failure, fluid congestion and diuretic resistance, does ultrafiltration lead to more rapid and effective decongestion compared with continuing diuretic treatment? Why this is important A randomised controlled trial should be undertaken to determine whether ultrafiltration is more clinically and cost effective than conventional diuretic therapy for people admitted to hospital with decompensated heart failure. The study should not only investigate several clinical outcomes but also consider the impact of treatments on quality of life and provide data on safety. People who have fluid retention that is resistant to conventional diuretic therapy, with or without renal dysfunction, make up a high proportion of hospital admissions due to heart failure. Such admissions are often prolonged and therefore have important budgetary implications for the NHS. The few, relatively small scale, randomised trials of ultrafiltration performed so far have been conducted in healthcare settings very different from the UK, with less fluid retention than is usually seen in UK practice, and where length of stay is usually much shorter than in UK (and European) practice. Although technically feasible, the evidence for benefit on heart failure outcomes is inconsistent and difficult to generalise to UK practice. Therefore, a UK-based study of sufficient quality is needed. Finding more information and committee details You can see everything NICE says on this topic in the NICE Pathway on acute heart failure. To find NICE guidance on related topics, including guidance in development, see the NICE webpage on cardiovascular conditions. For full details of the evidence and the guideline committee's discussions, see the full guideline. You can also find information about how the guideline was developed, including details of the committee. NICE has produced tools and resources to help you put this guideline into practice.


NICE has produced tools and resources to help you put this guideline into practice. For general help and advice on putting our guidelines into practice, see resources to help you put NICE guidance into practice. Update information November 2021: We withdrew recommendations 1.6.1 to 1.6.4 on valvular surgery and percutaneous intervention because they have been replaced by the NICE guideline on heart valve disease. Minor changes since publication March 2016: MHRA advice on spironolactone and renin-angiotensin system drugs added to recommendation 1.5.4. Accreditation


ACC/AHA TASK FORCE MEMBERS Glenn N. Levine, MD, FACC, FAHA, Chair; Patrick T. O Gara, MD, MACC, FAHA, Chair-Elect; Jonathan L. Halperin, MD, FACC, FAHA, Immediate Past Chair; Sana M. Al-Khatib, MD, MHS, FACC, FAHA; Joshua A. Beckman, MD, MS, FAHA; Kim K. Birtcher, MS, PharmD, AACC; Biykem Bozkurt, MD, PhD, FACC, FAHA***; Ralph G. Brindis, MD, MPH, MACC***; Joaquin E. Cigarroa, MD, FACC; Lesley H. Curtis, PhD, FAHA***; Anita Deswal, MD, MPH, FACC, FAHA; Lee A. Fleisher, MD, FACC, FAHA; Federico Gentile, MD, FACC; Samuel Gidding, MD, FAHA***; Zachary D. Goldberger, MD, MS, FACC, FAHA; Mark A. Hlatky, MD, FACC, FAHA; John Ikonomidis, MD, PhD, FAHA; Jos A. Joglar, MD, FACC, FAHA; Laura Mauri, MD, MSc, FAHA; Susan J. Pressler, PhD, RN, FAHA***; Barbara Riegel, PhD, RN, FAHA; Duminda N. Wijeysundera, MD, PhD *American Society for Preventive Cardiology Representative. ACC/AHA Representative. Lay Volunteer/Patient Representative. Preventive Cardiovascular Nurses Association Representative. American Academy of Physician Assistants Representative. Task Force Liaison. #Association of Black Cardiologists Representative. **American Pharmacists Association Representative. ACC/AHA Prevention Subcommittee Liaison. American College of Preventive Medicine Representative. American Society of Hypertension Representative. Task Force on Performance Measures Liaison. American Geriatrics Society Representative. ##National Medical Association Representative. ***Former Task Force member; current member during the writing effort. This document was approved by the American College of Cardiology Clinical Policy Approval Committee and the American Heart Association Science Advisory and Coordinating Committee in September 2017, and by the American Heart Association Executive Committee in October 2017. The Comprehensive RWI Data Supplement table is available with this article at http://hyper.ahajournals.org/lookup/suppl/doi:10.1161/ HYP.0000000000000065/-/DC1. The online Data Supplement is available with this article at http://hyper.ahajournals.org/lookup/suppl/doi:10.1161/HYP.0000000000000065/-/DC2.


The online Data Supplement is available with this article at http://hyper.ahajournals.org/lookup/suppl/doi:10.1161/HYP.0000000000000065/-/DC2. The American Heart Association requests that this document be cited as follows: Whelton PK, Carey RM, Aronow WS, Casey DE Jr, Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, MacLaughlin EJ, Muntner P, Ovbiagele B, Smith SC Jr, Spencer CC, Stafford RS, Taler SJ, Thomas RJ, Williams KA Sr, Williamson JD, Wright JT Jr. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018;71:e13 e115. DOI: 10.1161/ HYP.0000000000000065. This article has been copublished in the Journal of the American College of Cardiology. Copies: This document is available on the World Wide Web sites of theAmerican College of Cardiology (www.acc.org) and theAmerican HeartAssociation (professional.heart.org). A copy of the document is available at http://professional.heart.org/statements by using either Search for Guidelines & Statements or the Browse by Topic area. To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@wolterskluwer.com. Expert peer review of AHA Scientific Statements is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines development, visit http://professional.heart.org/statements. Select the Guidelines & Statements drop-down menu, then click Publication Development. Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American Heart Association. Instructions for obtaining permission are located at http://www.heart.org/HEARTORG/General/Copyright-Permission- Guidelines_UCM_300404_Article.jsp. A link to the Copyright Permissions Request Form appears on the right side of the page.


A link to the Copyright Permissions Request Form appears on the right side of the page. ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines WRITING COMMITTEE MEMBERS Paul K. Whelton, MB, MD, MSc, FAHA, Chair; Robert M. Carey, MD, FAHA, Vice Chair; Wilbert S. Aronow, MD, FACC, FAHA*; Donald E. Casey, Jr, MD, MPH, MBA, FAHA ; Karen J. Collins, MBA ; Cheryl Dennison Himmelfarb, RN, ANP, PhD, FAHA ; Sondra M. DePalma, MHS, PA-C, CLS, AACC ; Samuel Gidding, MD, FAHA ; Kenneth A. Jamerson, MD#; Daniel W. Jones, MD, FAHA ; Eric J. MacLaughlin, PharmD**; Paul Muntner, PhD, FAHA ; Bruce Ovbiagele, MD, MSc, MAS, MBA, FAHA ; Sidney C. Smith, Jr, MD, MACC, FAHA ; Crystal C. Spencer, JD ; Randall S. Stafford, MD, PhD ; Sandra J. Taler, MD, FAHA ; Randal J. Thomas, MD, MS, FACC, FAHA ; Kim A. Williams, Sr, MD, MACC, FAHA ; Jeff D. Williamson, MD, MHS ; Jackson T. Wright, Jr, MD, PhD, FAHA## Clinical Practice Guideline 2017 by the American College of Cardiology Foundation and the American Heart Association, Inc. Hypertension is available at http://hyper.ahajournals.org DOI: 10.1161/HYP.0000000000000065 Table of Contents Preamble e15 1.1. Methodology and Evidence Review e16 1.2. Organization of the Writing Committee e17 1.3. Document Review and Approval e18 1.4. Scope of the Guideline e18 1.5. Abbreviations and Acronyms e18 2. BP and CVD Risk e19 2.4. Coexistence of Hypertension and Related Chronic Conditions e20 3. Classification of BP e21 3.1. Definition of High BP e21 3.2. Lifetime Risk of Hypertension e22 3.3. Prevalence of High BP e22 3.4. Awareness, Treatment, and Control e22 4. Measurement of BP e23 4.1.


Awareness, Treatment, and Control e22 4. Measurement of BP e23 4.1. Accurate Measurement of BP in the Office e23 4.2. Out-of-Office and Self-Monitoring of BP e24 4.3. Ambulatory BP Monitoring e25 4.4. Masked and White Coat Hypertension e26 5. Causes of Hypertension e28 5.2. Environmental Risk Factors e28 5.2.1. Overweight and Obesity e28 5.3. Childhood Risk Factors and BP Tracking e31 5.4. Secondary Forms of Hypertension e32 5.4.1. Drugs and Other Substances With Potential to Impair BP Control e32 5.4.3. Renal Artery Stenosis e34 5.4.4. Obstructive Sleep Apnea e34 7.1. Laboratory Tests and Other Diagnostic Procedures e38 7.2. Cardiovascular Target Organ Damage e38 8. Treatment of High BP e39 8.1.1. Initiation of Pharmacological BP Treatment in the Context of Overall CVD Risk e39 8.1.2. BP Treatment Threshold and the Use of CVD Risk Estimation to Guide Drug Treatment of 8.1.3. Follow-Up After Initial BP Evaluation e42 8.1.4. General Principles of Drug Therapy e42 8.1.5. BP Goal for Patients With 8.1.6. Choice of Initial Medication e46 8.2. Achieving BP Control in Individual Patients e47 8.3. Follow-Up of BP During Antihypertensive Drug Therapy e48 8.3.1. Follow-Up After Initiating Antihypertensive Drug Therapy e48 8.3.2. Monitoring Strategies to Improve Control of BP in Patients on Drug Therapy for High BP e48 9. Hypertension in Patients With Comorbidities e48 9.1. Stable Ischemic Heart Disease e49 9.2.1. Heart Failure With Reduced Ejection Fraction e50 9.2.2. Heart Failure With Preserved Ejection Fraction e51 9.3. Chronic Kidney Disease e51 9.3.1. Hypertension After Renal 9.4.1. Acute Intracerebral Hemorrhage e54 9.4.2. Acute Ischemic Stroke e54 9.4.3. Secondary Stroke Prevention e56 9.5. Peripheral Artery Disease e57 9.9. Valvular Heart Disease e60 10. Special Patient Groups e60 10.1. Race and Ethnicity e60 10.1.1. Racial and Ethnic Differences in Treatment e61 10.3.2. Children and Adolescents e64 11. Other Considerations e64 11.2.


Racial and Ethnic Differences in Treatment e61 10.3.2. Children and Adolescents e64 11. Other Considerations e64 11.2. Hypertensive Crises Emergencies and Urgencies e65 11.3. Cognitive Decline and Dementia e68 11.4. Sexual Dysfunction and Hypertension e69 11.5. Patients Undergoing Surgical Procedures e69 12. Strategies to Improve Hypertension Treatment and Control e71 12.1. Adherence Strategies for Treatment of Hypertension e71 12.1.1. Antihypertensive Medication Adherence Strategies e71 12.1.2. Strategies to Promote Lifestyle 12.1.3. Improving Quality of Care for Resource-Constrained Populations e72 12.2. Structured, Team-Based Care Interventions for Hypertension Control e73 12.3. Health Information Technology Based Strategies to Promote Hypertension Control e73 12.3.1. EHR and Patient Registries e73 12.3.2. Telehealth Interventions to Improve Hypertension Control e74 Whelton et al 2017 High Blood Pressure Clinical Practice Guideline e15 12.4. Improving Quality of Care for Patients With Hypertension e74 12.4.2. Quality Improvement Strategies e74 13. The Plan of Care for Hypertension e75 13.2. Access to Health Insurance and Medication Assistance Plans e76 13.3. Social and Community Services e76 14. Summary of BP Thresholds and Goals for Pharmacological Therapy e77 15. Evidence Gaps and Future Directions e77 References Appendix 1: Author Relationships With Industry and Other Entities (Relevant) e108 Appendix 2: Reviewer Relationships With Industry and Other Entities (Comprehensive) e110 Preamble Since 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines (guidelines) with rec- ommendations to improve cardiovascular health.


Evidence Gaps and Future Directions e77 References Appendix 1: Author Relationships With Industry and Other Entities (Relevant) e108 Appendix 2: Reviewer Relationships With Industry and Other Entities (Comprehensive) e110 Preamble Since 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines (guidelines) with rec- ommendations to improve cardiovascular health. In 2013, the National Heart, Lung, and Blood Institute (NHLBI) Advisory Council recommended that the NHLBI focus specifically on reviewing the highest-quality evidence and partner with other organizations to develop recommendations.P-1,P-2 Accordingly, the ACC and AHA collaborated with the NHLBI and stake- holder and professional organizations to complete and publish 4 guidelines (on assessment of cardiovascular risk, lifestyle modifications to reduce cardiovascular risk, management of blood cholesterol in adults, and management of overweight and obesity in adults) to make them available to the widest possible constituency. In 2014, the ACC and AHA, in partnership with several other professional societies, initiated a guideline on the prevention, detection, evaluation, and management of high blood pressure (BP) in adults. Under the management of the ACC/ AHA Task Force, a Prevention Subcommittee was appointed to help guide development of the suite of guidelines on prevention of cardiovascular disease (CVD). These guidelines, which are based on systematic methods to evaluate and classify evidence, provide a cornerstone for quality cardiovascular care. The ACC and AHA sponsor the development and publication of guide- lines without commercial support, and members of each orga- nization volunteer their time to the writing and review efforts. Guidelines are official policy of the ACC and AHA. Intended Use Practice guidelines provide recommendations applicable to patients with or at risk of developing CVD.


Intended Use Practice guidelines provide recommendations applicable to patients with or at risk of developing CVD. The focus is on medical practice in the United States, but guidelines devel- oped in collaboration with other organizations can have a global impact. Although guidelines may be used to inform regulatory or payer decisions, they are intended to improve patients quality of care and align with patients interests. Guidelines are intended to define practices meeting the needs of patients in most, but not all, circumstances and should not replace clinical judgment. Clinical Implementation Management in accordance with guideline recommendations is effective only when followed by both practitioners and patients. Adherence to recommendations can be enhanced by shared decision making between clinicians and patients, with patient engagement in selecting interventions on the basis of individual values, preferences, and associated conditions and comorbidities. Methodology and Modernization The ACC/AHA Task Force on Clinical Practice Guidelines (Task Force) continuously reviews, updates, and modifies guideline methodology on the basis of published standards from organizations, including the Institute of Medicine,P-3,P-4 and on the basis of internal reevaluation. Similarly, the pre- sentation and delivery of guidelines are reevaluated and modi- fied on the basis of evolving technologies and other factors to facilitate optimal dissemination of information to healthcare professionals at the point of care. Toward this goal, this guideline continues the introduction of an evolved format of presenting guideline recommenda- tions and associated text called the modular knowledge chunk format. Each modular chunk includes a table of related recommendations, a brief synopsis, recommendation-spe- cific supportive text, and when appropriate, flow diagrams or additional tables. References are provided within the modular chunk itself to facilitate quick review.


References are provided within the modular chunk itself to facilitate quick review. Additionally, this format will facilitate seamless updating of guidelines with focused updates as new evidence is published, as well as content tag- ging for rapid electronic retrieval of related recommendations on a topic of interest. This evolved approach format was insti- tuted when this guideline was near completion; therefore, the present document represents a transitional format that best suits the text as written. Future guidelines will fully implement this format, including provisions for limiting the amount of text in a guideline. Recognizing the importance of cost value considerations in certain guidelines, when appropriate and feasible, an analy- sis of the value of a drug, device, or intervention may be per- formed in accordance with the ACC/AHA methodology.P-5 To ensure that guideline recommendations remain current, new data are reviewed on an ongoing basis, with full guide- line revisions commissioned in approximately 6-year cycles. Publication of new, potentially practice-changing study results that are relevant to an existing or new drug, device, or man- agement strategy will prompt evaluation by the Task Force, in consultation with the relevant guideline writing committee, to determine whether a focused update should be commissioned. For additional information and policies regarding guideline development, we encourage readers to consult the ACC/AHA guideline methodology manualP-6 and other methodology Selection of Writing Committee Members The Task Force strives to avoid bias by selecting experts from a broad array of backgrounds. Writing committee members represent different geographic regions, sexes, eth- nicities, races, intellectual perspectives/biases, and scopes of clinical practice. The Task Force may also invite orga- nizations and professional societies with related inter- ests and expertise to participate as partners, collaborators, or endorsers.


The Task Force may also invite orga- nizations and professional societies with related inter- ests and expertise to participate as partners, collaborators, or endorsers. Relationships With Industry and Other Entities The ACC and AHA have rigorous policies and methods to ensure that guidelines are developed without bias or improper influence. The complete relationships with industry and other entities (RWI) policy can be found online. Appendix 1 of the present document lists writing committee members relevant RWI. For the purposes of full transparency, writing committee members comprehensive disclosure information is available online. Comprehensive disclosure information for the Task Force is available online. Evidence Review and Evidence Review Committees In developing recommendations, the writing committee uses evidence-based methodologies that are based on all available Literature searches focus on randomized controlled trials (RCTs) but also include registries, nonrandomized com- parative and descriptive studies, case series, cohort studies, systematic reviews, and expert opinion. Only key references are cited. An independent evidence review committee (ERC) is commissioned when there are 1 or more questions deemed of utmost clinical importance that merit formal systematic review. The systematic review will determine which patients are most likely to benefit from a drug, device, or treatment strategy and to what degree. Criteria for commissioning an ERC and formal systematic review include: a) the absence of a current authoritative systematic review, b) the feasibility of defining the benefit and risk in a time frame consistent with the writ- ing of a guideline, c) the relevance to a substantial number of patients, and d) the likelihood that the findings can be trans- lated into actionable recommendations. ERC members may include methodologists, epidemiologists, healthcare providers, and biostatisticians.


ERC members may include methodologists, epidemiologists, healthcare providers, and biostatisticians. The recommendations developed by the writing committee on the basis of the systematic review are marked with SR. Guideline-Directed Management and Therapy The term guideline-directed management and therapy (GDMT) encompasses clinical evaluation, diagnostic test- ing, and pharmacological and procedural treatments. For these and all recommended drug treatment regimens, the reader should confirm the dosage by reviewing product insert material and evaluate the treatment regimen for contraindica- tions and interactions. The recommendations are limited to drugs, devices, and treatments approved for clinical use in the United States. Class of Recommendation and Level of Evidence The Class of Recommendation (COR) indicates the strength of the recommendation, encompassing the estimated magni- tude and certainty of benefit in proportion to risk. The Level of Evidence (LOE) rates the quality of scientific evidence that supports the intervention on the basis of the type, quantity, and consistency of data from clinical trials and other sources Glenn N. Levine, MD, FACC, FAHA Chair, ACC/AHA Task Force on Clinical Practice Guidelines As early as the 1920s, and subsequently in the 1959 Build and Blood Pressure StudyS1.5-1 of almost 5 million adults insured between 1934 and 1954, a strong direct relationship was noted between level of BP and risk of clinical complications and death.


The Level of Evidence (LOE) rates the quality of scientific evidence that supports the intervention on the basis of the type, quantity, and consistency of data from clinical trials and other sources Glenn N. Levine, MD, FACC, FAHA Chair, ACC/AHA Task Force on Clinical Practice Guidelines As early as the 1920s, and subsequently in the 1959 Build and Blood Pressure StudyS1.5-1 of almost 5 million adults insured between 1934 and 1954, a strong direct relationship was noted between level of BP and risk of clinical complications and death. In the 1960s, these findings were confirmed in a series of reports from the Framingham Heart Study.S1.5-2 The 1967 and 1970 Veterans Administration Cooperative Study Group reports ushered in the era of effective treatment for The first comprehensive guideline for detec- tion, evaluation, and management of high BP was published in 1977, under the sponsorship of the NHLBI.S1.5-5 In subsequent years, a series of Joint National Committee (JNC) BP guide- lines were published to assist the practice community and improve prevention, awareness, treatment, and control of high The present guideline updates prior JNC reports. 1.1. Methodology and Evidence Review An extensive evidence review, which included literature derived from research involving human subjects, published in English, and indexed in MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and other selected databases relevant to this guide- line, was conducted between February and August 2015.


Methodology and Evidence Review An extensive evidence review, which included literature derived from research involving human subjects, published in English, and indexed in MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and other selected databases relevant to this guide- line, was conducted between February and August 2015. Key search words included but were not limited to the following: adherence; aerobic; alcohol intake; ambulatory care; antihy- pertensive: agents, drug, medication, therapy; beta adrener- gic blockers; blood pressure: arterial, control, determination, devices, goal, high, improve, measurement, monitoring, ambu- latory; calcium channel blockers; diet; diuretic agent; drug therapy; heart failure: diastolic, systolic; hypertension: white coat, masked, ambulatory, isolated ambulatory, isolated clinic, diagnosis, reverse white coat, prevention, therapy, treatment, control; intervention; lifestyle: measures, modification; office visits; patient outcome; performance measures; physical activity; potassium intake; protein intake; renin inhibitor; risk reduction: behavior, counseling; screening; sphygmomanom- eters; spironolactone; therapy; treatment: adherence, compli- ance, efficacy, outcome, protocol, regimen; weight. Additional relevant studies published through June 2016, during the guide- line writing process, were also considered by the writing com- mittee and added to the evidence tables when appropriate. The final evidence tables included in the Online Data Supplement summarize the evidence used by the writing committee to for- mulate recommendations. As noted in the preamble, an independent ERC was com- missioned to perform a formal systematic review of 4 criti- cal clinical questions related to hypertension (Table 2), the results of which were considered by the writing committee for incorporation into this guideline. Concurrent with this pro- cess, writing committee members evaluated other published data relevant to the guideline.


Concurrent with this pro- cess, writing committee members evaluated other published data relevant to the guideline. The findings of the ERC and the writing committee members were formally presented and Whelton et al 2017 High Blood Pressure Clinical Practice Guideline e17 discussed, and then guideline recommendations were devel- oped. The systematic review report, Systematic Review for the 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults, is published in conjunction with this guideline,S1.5-8 and its respective data supplements are available online. No writing committee member reported a RWI. Drs. Whelton, Wright, and Williamson had leadership roles in SPRINT (Systolic Blood Pressure Intervention Trial). Dr. Carey chaired committee discussions in which the SPRINT results were considered. 1.2. Organization of the Writing Committee The writing committee consisted of clinicians, cardiolo- gists, epidemiologists, internists, an endocrinologist, a geri- atrician, a nephrologist, a neurologist, a nurse, a pharmacist, a physician assistant, and 2 lay/patient representatives. It Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care* (Updated August 2015) included representatives from the ACC, AHA, American Academy of Physician Assistants (AAPA), Association of Black Cardiologists (ABC), American College of Preventive Medicine (ACPM), American Geriatrics Society (AGS), American Pharmacists Association (APhA), American Society of Hypertension (ASH), American Society for Preventive Cardiology (ASPC), National MedicalAssociation (NMA), and Preventive Cardiovascular Nurses Association (PCNA). 1.3. Document Review and Approval This document was reviewed by 2 official reviewers nominated by the ACC and AHA; 1 reviewer each from the AAPA, ABC, ACPM, AGS, APhA, ASH, ASPC, NMA, and PCNA; and 38 individual content reviewers. Reviewers RWI information was distributed to the writing committee and is published in this document (Appendix 2).


Reviewers RWI information was distributed to the writing committee and is published in this document (Appendix 2). This document was approved for publication by the gov- erning bodies of the ACC, AHA, AAPA, ABC, ACPM, AGS, APhA, ASH, ASPC, NMA, and PCNA. 1.4. Scope of the Guideline The present guideline is intended to be a resource for the clini- cal and public health practice communities. It is designed to be comprehensive but succinct and practical in providing guid- ance for prevention, detection, evaluation, and management of high BP. It is an update of the NHLBI publication, The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure It incorporates new information from studies of office-based BP-related risk of CVD, ambulatory blood pres- sure monitoring (ABPM), home blood pressure monitoring (HBPM), telemedicine, and various other areas. This guideline does not address the use of BP-lowering medications for the purposes of prevention of recurrent CVD events in patients with stable ischemic heart disease (SIHD) or chronic heart failure (HF) in the absence of hypertension; these topics are the focus of other ACC/AHA guidelines.S1.5-9,S1.5-10 In develop- ing the present guideline, the writing committee reviewed prior published guidelines, evidence reviews, and related statements. Table 3 contains a list of publications and statements deemed pertinent to this writing effort and is intended for use as a resource, thus obviating the need to repeat existing guideline recommendations. 1.5.


Table 3 contains a list of publications and statements deemed pertinent to this writing effort and is intended for use as a resource, thus obviating the need to repeat existing guideline recommendations. 1.5. Abbreviations and Acronyms Abbreviation/Acronym Meaning/Phrase ABPM ambulatory blood pressure monitoring ACE angiotensin-converting enzyme AF atrial fibrillation ARB angiotensin receptor blocker BP blood pressure CCB calcium channel blocker CHD coronary heart disease CKD chronic kidney disease CPAP continuous positive airway pressure CVD cardiovascular disease DBP diastolic blood pressure DM diabetes mellitus ECG electrocardiogram ESRD end-stage renal disease GDMT guideline-directed management and therapy GFR glomerular filtration rate HBPM home blood pressure monitoring EHR electronic health record HF heart failure HFpEF heart failure with preserved ejection fraction HFrEF heart failure with reduced ejection fraction ICH intracerebral hemorrhage JNC Joint National Commission LV left ventricular LVH left ventricular hypertrophy MI myocardial infarction MRI magnetic resonance imaging PAD peripheral artery disease RAS renin-angiotensin system RCT randomized controlled trial SBP systolic blood pressure SIHD stable ischemic heart disease TIA transient ischemic attack Table 2. Systematic Review Questions on High BP in Adults Question Number Question Section Number 1 Is there evidence that self-directed monitoring of BP and/or ambulatory BP monitoring are superior to office-based measurement of BP by a healthcare worker for 1) preventing adverse outcomes for which high BP is a risk factor and 2) achieving better BP control? 2 What is the optimal target for BP lowering during antihypertensive therapy in adults? 3 In adults with hypertension, do various antihypertensive drug classes differ in their comparative benefits and harms?


3 In adults with hypertension, do various antihypertensive drug classes differ in their comparative benefits and harms? 4 In adults with hypertension, does initiating treatment with antihypertensive pharmacological monotherapy versus initiating treatment with 2 drugs (including fixed-dose combination therapy), either of which may be followed by the addition of sequential drugs, differ in comparative benefits and/or harms on specific health outcomes? BP indicates blood pressure. Whelton et al 2017 High Blood Pressure Clinical Practice Guideline e19 2. BP and CVD Risk 2.1. Observational Relationship Observational studies have demonstrated graded associations between higher systolic blood pressure (SBP) and diastolic blood pressure (DBP) and increased CVD risk.S2.1-1,S2.1-2 In a meta-analysis of 61 prospective studies, the risk of CVD increased in a log-linear fashion from SBP levels <115 mm Hg to >180 mm Hg and from DBP levels <75 mm Hg to In that analysis, 20 mm Hg higher SBP and Table 3.


Observational Relationship Observational studies have demonstrated graded associations between higher systolic blood pressure (SBP) and diastolic blood pressure (DBP) and increased CVD risk.S2.1-1,S2.1-2 In a meta-analysis of 61 prospective studies, the risk of CVD increased in a log-linear fashion from SBP levels <115 mm Hg to >180 mm Hg and from DBP levels <75 mm Hg to In that analysis, 20 mm Hg higher SBP and Table 3. Associated Guidelines and Statements Title Organization Publication Year Guidelines Lower-extremity peripheral artery disease AHA/ACC 2016S1.5-11 Management of primary aldosteronism: case detection, diagnosis, and treatment Endocrine Society 2016S1.5-12 Stable ischemic heart disease ACC/AHA/AATS/PCNA/SCAI/STS 2014S1.5-13* Pheochromocytoma and paraganglioma Endocrine Society 2014S1.5-14 Atrial fibrillation AHA/ACC/HRS 2014S1.5-15 Valvular heart disease ACC/AHA 2017S1.5-16 Assessment of cardiovascular risk ACC/AHA 2013S1.5-17 Hypertension in pregnancy ACOG 2013S1.5-18 Heart failure ACC/AHA 2017S1.5-19 Lifestyle management to reduce cardiovascular risk AHA/ACC 2013S1.5-20 Management of arterial hypertension ESH/ESC 2013S1.5-21 Management of overweight and obesity in adults AHA/ACC/TOS 2013S1.5-22 ST-elevation myocardial infarction ACC/AHA 2013S1.5-23 Treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults ACC/AHA 2013S1.5-24 Cardiovascular diseases during pregnancy ESC 2011S1.5-25 Effectiveness-based guidelines for the prevention of cardiovascular disease in women AHA/ACC 2011S1.5-26 Secondary prevention and risk-reduction therapy for patients with coronary and other atherosclerotic vascular disease Assessment of cardiovascular risk in asymptomatic adults ACC/AHA 2010S1.5-28 Thoracic aortic disease ACC/AHA/AATS/ACR/ASA/SCA/ SCAI/SIR/STS/SVM Diagnosis, evaluation, and treatment of high blood pressure in children and adolescents NHLBI 2004S1.5-30 Statements Salt sensitivity of blood pressure AHA 2016S1.5-31 Cardiovascular team-based care and the role of advanced practice providers ACC 2015S1.5-32 Treatment of hypertension in patients with coronary artery disease AHA/ACC/ASH 2015S1.5-33 Ambulatory blood pressure monitoring in children and adolescents AHA 2014S1.5-34 An effective approach to high blood pressure control AHA/ACC/CDC 2014S1.5-35 Ambulatory blood pressure monitoring ESH 2013S1.5-36 Performance measures for adults with coronary artery disease and hypertension ACC/AHA/AMA-PCPI 2011S1.5-37 Interventions to promote physical activity and dietary lifestyle changes for cardiovascular risk factor reduction in adults Resistant hypertension: diagnosis, evaluation, and treatment AHA 2008S1.5-39 *The full-text SIHD guideline is from 2012.S1.5-9 A focused update was published in 2014.S1.5-13 AATS indicates American Association for Thoracic Surgery; ACC, American College of Cardiology; ACOG, American College of Obstetricians and Gynecologists; ACR, American College of Radiology; AHA, American Heart Association; AMA, American Medical Association; ASA, American Stroke Association; ASH, American Society of Hypertension; CDC, Centers for Disease Control and Prevention; ESC, European Society of Cardiology; ESH, European Society of Hypertension; HRS, Heart Rhythm Society; NHLBI, National Heart, Lung, and Blood Institute; PCNA, Preventive Cardiovascular Nurses Association; PCPI, Physician Consortium for Performance Improvement; SCA, Society of Cardiovascular Anesthesiologists; SCAI, Society for Cardiovascular Angiography and Interventions; SIHD, stable ischemic heart disease; SIR, Society of Interventional Radiology; STS, Society of Thoracic Surgeons; SVM, Society for Vascular Medicine; and TOS, The Obesity Society.


10 mm Hg higher DBP were each associated with a doubling in the risk of death from stroke, heart disease, or other vas- cular disease. In a separate observational study including >1 million adult patients 30 years of age, higher SBP and DBP were associated with increased risk of CVD incidence and angina, myocardial infarction (MI), HF, stroke, peripheral artery disease (PAD), and abdominal aortic aneurysm, each An increased risk of CVD asso- ciated with higher SBP and DBP has been reported across a broad age spectrum, from 30 years to >80 years of age. Although the relative risk of incident CVD associated with higher SBP and DBP is smaller at older ages, the correspond- ing high BP related increase in absolute risk is larger in older persons ( 65 years) given the higher absolute risk of CVD at an older age.S2.1-1 2.2. BP Components Epidemiological studies have evaluated associations of SBP and DBP, as well as derived components of BP measurements (including pulse pressure, mean BP, and mid-BP), with CVD outcomes (Table 4). When considered separately, higher levels of both SBP and DBP have been associated with increased Higher SBP has consistently been associ- ated with increased CVD risk after adjustment for, or within strata of, DBP.S2.2-3 S2.2-5 In contrast, after consideration of SBP through adjustment or stratification, DBP has not been con- sistently associated with CVD risk.S2.2-6,S2.2-7 Although pulse pressure and mid-BP have been associated with increased CVD risk independent of SBP and DBP in some studies, SBP (especially) and DBP are prioritized in the present document because of the robust evidence base for these measures in both observational studies and clinical tri- als and because of their ease of measurement in practice 2.3.


When considered separately, higher levels of both SBP and DBP have been associated with increased Higher SBP has consistently been associ- ated with increased CVD risk after adjustment for, or within strata of, DBP.S2.2-3 S2.2-5 In contrast, after consideration of SBP through adjustment or stratification, DBP has not been con- sistently associated with CVD risk.S2.2-6,S2.2-7 Although pulse pressure and mid-BP have been associated with increased CVD risk independent of SBP and DBP in some studies, SBP (especially) and DBP are prioritized in the present document because of the robust evidence base for these measures in both observational studies and clinical tri- als and because of their ease of measurement in practice 2.3. Population Risk In 2010, high BP was the leading cause of death and disability-adjusted life years worldwide.S2.3-1,S2.3-2 In the United States, hypertension (see Section 3.1 for definition) accounted for more CVD deaths than any other modifiable CVD risk factor and was second only to cigarette smoking as a preventable cause of death for any reason.S2.3-3 In a fol- low-up study of 23272 US NHANES (National Health and Nutrition Examination Survey) participants, >50% of deaths from coronary heart disease (CHD) and stroke occurred among individuals with hypertension.S2.3-4 Because of the high prevalence of hypertension and its associated increased risk of CHD, stroke, and end-stage renal disease (ESRD), the population-attributable risk of these outcomes associated with hypertension is high.S2.3-4,S2.3-5 In the population-based ARIC (Atherosclerosis Risk in Communities) study, 25% of the cardiovascular events (CHD, coronary revasculariza- tion, stroke, or HF) were attributable to hypertension.


Population Risk In 2010, high BP was the leading cause of death and disability-adjusted life years worldwide.S2.3-1,S2.3-2 In the United States, hypertension (see Section 3.1 for definition) accounted for more CVD deaths than any other modifiable CVD risk factor and was second only to cigarette smoking as a preventable cause of death for any reason.S2.3-3 In a fol- low-up study of 23272 US NHANES (National Health and Nutrition Examination Survey) participants, >50% of deaths from coronary heart disease (CHD) and stroke occurred among individuals with hypertension.S2.3-4 Because of the high prevalence of hypertension and its associated increased risk of CHD, stroke, and end-stage renal disease (ESRD), the population-attributable risk of these outcomes associated with hypertension is high.S2.3-4,S2.3-5 In the population-based ARIC (Atherosclerosis Risk in Communities) study, 25% of the cardiovascular events (CHD, coronary revasculariza- tion, stroke, or HF) were attributable to hypertension. In the Northern Manhattan study, the percentage of events attribut- able to hypertension was higher in women (32%) than in men (19%) and higher in blacks (36%) than in whites (21%).S2.3-6 In 2012, hypertension was the second leading assigned cause of ESRD, behind diabetes mellitus (DM), and accounted for 34% of incident ESRD cases in the US population.S2.3-7 2.4. Coexistence of Hypertension and Related Chronic Conditions Recommendation for Coexistence of Hypertension and Related Chronic Conditions References that support the recommendation are summarized in Online Data Supplement 1. COR LOE Recommendation I B-NR 1. Screening for and management of other modifiable CVD risk factors are recommended in adults with Synopsis Many adult patients with hypertension have other CVD risk factors; a list of such modifiable and relatively fixed risk factors is provided in Table 5.


Screening for and management of other modifiable CVD risk factors are recommended in adults with Synopsis Many adult patients with hypertension have other CVD risk factors; a list of such modifiable and relatively fixed risk factors is provided in Table 5. Among US adults with hyper- tension between 2009 and 2012, 15.5% were current smok- ers, 49.5% were obese, 63.2% had hypercholesterolemia, 27.2% had DM, and 15.8% had chronic kidney disease (CKD; defined as estimated glomerular filtration rate [eGFR] <60 mL/ and/or urine albumin:creatinine 300 mg/g).S2.4-3 Not only are CVD risk factors common among adults with hypertension, a higher percentage of adults with CVD risk Table 4. BP Measurement Definitions BP Measurement Definition SBP First Korotkoff sound* DBP Fifth Korotkoff sound* Pulse pressure SBP minus DBP Mean arterial pressure DBP plus one third pulse pressure Mid-BP Sum of SBP and DBP, divided by 2 *See Section 4 for a description of Korotkoff sounds. Calculation assumes normal heart rate. BP indicates blood pressure; DBP, diastolic blood pressure; and SBP, systolic blood pressure. Table 5. CVD Risk Factors Common in Patients With Hypertension Modifiable Risk Factors* Relatively Fixed Risk Factors Current cigarette smoking, secondhand smoking CKD Family history Diabetes mellitus Increased age Dyslipidemia/hypercholesterolemia Low socioeconomic/educational status Overweight/obesity Male sex Physical inactivity/low fitness Obstructive sleep apnea Unhealthy diet Psychosocial stress *Factors that can be changed and, if changed, may reduce CVD risk. Factors that are difficult to change (CKD, low socioeconomic/educational status, obstructive sleep apneaS2.4-12 ), cannot be changed (family history, increased age, male sex), or, if changed through the use of current intervention techniques, may not reduce CVD risk (psychosocial stress). CKD indicates chronic kidney disease; and CVD, cardiovascular disease. Whelton et al 2017 High Blood Pressure Clinical Practice Guideline e21 factors have hypertension.


Whelton et al 2017 High Blood Pressure Clinical Practice Guideline e21 factors have hypertension. For example, 71% of US adults with diagnosed DM have hypertension.S2.4-4 In the Chronic Renal Insufficiency Cohort (CRIC), 86% of the participants Also, 28.1% of adults with hyperten- sion and CKD in the population-based REGARDS (Reasons for Geographic and Racial Differences in Stroke) study had apparent resistant hypertension.S2.4-6 In NHANES 1999 2010, 35.7% of obese individuals had hypertension.S2.4-7 The presence of multiple CVD risk factors in individuals with hypertension results in high absolute risks for CHD and stroke in this popula- tion. For example, among US adults with hypertension between had a risk of 10% to 20%, and only 18.4% had a risk <10%.S2.4-3 Modifiable risk factors for CVD that are common among adults with hypertension include cigarette smok- ing/tobacco smoke exposure, DM, dyslipidemia (includ- ing high levels of low-density lipoprotein cholesterol or hypercholesterolemia, high levels of triglycerides, and low levels of high-density lipoprotein cholesterol), overweight/ obesity, physical inactivity/low fitness level, and unhealthy The relationship between hypertension and other modifiable risk factors is complex and interdependent, with several sharing mechanisms of action and pathophysiol- ogy. CVD risk factors affect BP through over activation of the renin-angiotensin-aldosterone system, activation of the sympathetic nervous system, inhibition of the cardiac natri- uretic peptide system, endothelial dysfunction, and other Treating some of the other modifi- able risk factors may reduce BP through modification of shared pathology, and CVD risk may be reduced by treating global risk factor burden. Recommendation-Specific Supportive Text 1.


CVD risk factors affect BP through over activation of the renin-angiotensin-aldosterone system, activation of the sympathetic nervous system, inhibition of the cardiac natri- uretic peptide system, endothelial dysfunction, and other Treating some of the other modifi- able risk factors may reduce BP through modification of shared pathology, and CVD risk may be reduced by treating global risk factor burden. Recommendation-Specific Supportive Text 1. Observational studies have demonstrated that CVD risk factors frequently occur in combination, with 3 risk factors present in 17% of patients.S2.4-1 A meta-analysis from 18 cohort studies involving 257384 patients identi- fied a lifetime risk of CVD death, nonfatal MI, and fatal or nonfatal stroke that was substantially higher in adults with 2 CVD risk factors than in those with only 1 risk 3. Classification of BP 3.1. Definition of High BP Recommendation for Definition of High BP References that support the recommendation are summarized in Online Data Supplement 2. COR LOE Recommendation I B-NR 1. BP should be categorized as normal, elevated, or stage 1 or 2 hypertension to prevent and treat high BP (Table 6).S3.1-1 S3.1-20 Synopsis Although a continuous association exists between higher BP and increased CVD risk (see Section 2.1), it is useful to categorize BP levels for clinical and public health decision making. In the present document, BP is categorized into 4 levels on the basis of average BP measured in a healthcare setting (office pressures): normal, elevated, and stage 1 or 2 hypertension (Table 6). Online Data Supplement C illustrates schematically the SBP and DBP categories defining normal BP, elevated BP, and stages 1 and 2 hypertension.


Online Data Supplement C illustrates schematically the SBP and DBP categories defining normal BP, elevated BP, and stages 1 and 2 hypertension. This cat- egorization differs from that previously recommended in the JNC 7 report, with stage 1 hypertension now defined as an SBP of 130 139 or a DBP of 80 89 mm Hg, and with stage 2 hypertension in the present document corresponding to stages 1 and 2 in the JNC 7 report.S3.1-21 The rationale for this categorization is based on observational data related to the association between SBP/DBP and CVD risk, RCTs of life- style modification to lower BP, and RCTs of treatment with antihypertensive medication to prevent CVD. The increased risk of CVD among adults with stage 2 hypertension is well established. An increasing number of individual studies and meta-analyses of observational data have reported a gradient of progressively higher CVD risk going from normal BP to elevated BP and stage 1 hypertension.S3.1-4 S3.1-10,S3.1-12,S3.1-13,S3.1-16 In many of these meta-analyses, the hazard ratios for CHD and stroke were between 1.1 and 1.5 for the comparison of SBP/DBP of 120 129/80 84 mm Hg versus <120/80 mm Hg and between 1.5 and 2.0 for the comparison of SBP/DBP of 130 139/85 89 mm Hg versus <120/80 mm Hg. This risk gradient was consistent across subgroups defined by sex and race/ethnicity. The relative increase in CVD risk associated with higher BP was attenuated but still present among older The prevalence of severe hypertension has been declining over time, but approximately 12.3% of US adults with hypertension have an average SBP 160 mm Hg or aver- age DBP 100 mm Hg.S3.1-22 Lifestyle modification and phar- macological antihypertensive treatment recommendations for individuals with elevated BP and stages 1 and 2 hypertension are provided in Sections 6 and 8, respectively.


The relative increase in CVD risk associated with higher BP was attenuated but still present among older The prevalence of severe hypertension has been declining over time, but approximately 12.3% of US adults with hypertension have an average SBP 160 mm Hg or aver- age DBP 100 mm Hg.S3.1-22 Lifestyle modification and phar- macological antihypertensive treatment recommendations for individuals with elevated BP and stages 1 and 2 hypertension are provided in Sections 6 and 8, respectively. The relation- ship of this classification schema with measurements obtained by ambulatory BP recording and home BP measurements is discussed in Section 4.2. Recommendation-Specific Supportive Text 1. As was the case in previous BP classification systems, the choice and the naming of the categories were based on a pragmatic interpretation of BP-related CVD risk and benefit of BP reduction in clinical trials. Meta-analyses of observational studies have demonstrated that elevated Table 6. Categories of BP in Adults* BP Category SBP DBP Normal <120 mm Hg and <80 mm Hg Elevated 120 129 mm Hg and <80 mm Hg Hypertension Stage 1 130 139 mm Hg or 80 89 mm Hg Stage 2 140 mm Hg or 90 mm Hg *Individuals with SBP and DBP in 2 categories should be designated to the higher BP category. BP indicates blood pressure (based on an average of 2 careful readings obtained on 2 occasions, as detailed in Section 4); DBP, diastolic blood pressure; and SBP, systolic blood pressure. BP and hypertension are associated with increased risk of CVD, ESRD, subclinical atherosclerosis, and all-cause The recommended BP classification sys- tem is most valuable in untreated adults as an aid in deci- sions about prevention or treatment of high BP. However, it is also useful in assessing the success of interventions to reduce BP. 3.2.


However, it is also useful in assessing the success of interventions to reduce BP. 3.2. Lifetime Risk of Hypertension Observational studies have documented a relatively high inci- dence of hypertension over periods of 5 to 10 years of follow- Thus, there is a much higher long-term population burden of hypertension as BP progressively increases with age. Several studies have estimated the long-term cumulative inci- dence of developing hypertension.S3.2-3,S3.2-4 In an analysis of 1132 white male medical students (mean age: approximately 23 years at baseline) in the Johns Hopkins Precursors study, In MESA (Multi-Ethnic Study of Atherosclerosis), the percentage of the population develop- ing hypertension over their lifetimes was higher for African Americans and Hispanics than for whites and Asians.S3.2-3 For adults 45 years of age without hypertension, the 40-year risk of developing hypertension was 93% for African-American, 92% for Hispanic, 86% for white, and 84% for Chinese In the Framingham Heart Study, approximately 90% of adults free of hypertension at age 55 or 65 years devel- oped hypertension during their lifetimes.S3.2-4 All of these esti- mates were based on use of the 140/90 mm Hg cutpoint for recognition of hypertension and would have been higher had the 130/80 mm Hg cutpoint been used. 3.3. Prevalence of High BP Prevalence estimates are greatly influenced by the choice of cutpoints to categorize high BP, the methods used to estab- lish the diagnosis, and the population studied.S3.3-1,S3.3-2 Most general population prevalence estimates are derived from national surveys. Table 7 provides estimates for prevalence of hypertension in the US general adult population ( 20 years of age) that are based on the definitions of hypertension rec- ommended in the present guideline and in the JNC 7 report.


Table 7 provides estimates for prevalence of hypertension in the US general adult population ( 20 years of age) that are based on the definitions of hypertension rec- ommended in the present guideline and in the JNC 7 report. The prevalence of hypertension among US adults is substan- tially higher when the definition in the present guideline is used versus the JNC 7 definition (46% versus 32%). However, as described in Section 8.1, nonpharmacological treatment (not antihypertensive medication) is recommended for most US adults who have hypertension as defined in the present guideline but who would not meet the JNC 7 definition for hypertension. As a consequence, the new definition results in only a small increase in the percentage of US adults for whom antihypertensive medication is recommended in conjunction with lifestyle modification. The prevalence of hypertension rises dramatically with increasing age and is higher in blacks than in whites, Asians, and Hispanic Americans. NHANES estimates of JNC 7 defined hypertension prevalence have remained fairly stable since the early 2000s.S3.3-1 Most contemporary population sur- veys, including NHANES, rely on an average of BP measure- ments obtained at a single visit,S3.3-2 which is likely to result in an overestimate of hypertension prevalence compared with what would be found by using an average of 2 read- ings taken on 2 visits,S3.3-1 as recommended in current and previous BP guidelines.S3.3-3 S3.3-5 The extent to which guide- line recommendations for use of BP averages from 2 occa- sions is followed in practice is unclear. Adding self-report of previously diagnosed hypertension yields a 5% to 10% higher estimate of prevalence.S3.3-1,S3.3-6,S3.3-7 Most individuals who were added by use of this expanded definition have been diagnosed as having hypertension by a health professional on >1 occasion, and many have been advised to change their 3.4.


Adding self-report of previously diagnosed hypertension yields a 5% to 10% higher estimate of prevalence.S3.3-1,S3.3-6,S3.3-7 Most individuals who were added by use of this expanded definition have been diagnosed as having hypertension by a health professional on >1 occasion, and many have been advised to change their 3.4. Awareness, Treatment, and Control Prevalence estimates for awareness, treatment, and con- trol of hypertension are usually based on self-reports of the hypertension diagnosis (awareness), use of BP-lowering medications in those with hypertension (treatment), and achievement of a satisfactory SBP/DBP during treatment of hypertension (control). Before the present publication, awareness and treatment in adults were based on the SBP/ DBP cutpoints of 140/90 mm Hg, and control was based on an SBP/DBP <140/90 mm Hg. In the US general adult population, hypertension awareness, treatment, and control Table 7. Prevalence of Hypertension Based on 2 SBP/DBP Thresholds* mm Hg or Self-Reported Antihypertensive Medication mm Hg or Self-Reported Antihypertensive Medication Men Women Men Women Overall, age-sex adjusted Age group, y Race-ethnicity The prevalence estimates have been rounded to the nearest full percentage. *130/80 and 140/90 mm Hg in 9623 participants ( 20 years of age) in NHANES 2011 2014. BP cutpoints for definition of hypertension in the present guideline. BP cutpoints for definition of hypertension in JNC 7. Adjusted to the 2010 age-sex distribution of the US adult population. BP indicates blood pressure; DBP, diastolic blood pressure; NHANES, National Health and Nutrition Examination Survey; and SBP, systolic blood pressure.