PDF

hyp_0194911X_2018_71_e13

Module 14: Clinical & Applied Pharmacology Evidence Guide

Original source file is included in this package; the embedded viewer and full extracted text are available below.

Original PDF Viewer

This embedded PDF preserves figures, tables, images, and layout.

Searchable Extracted Text

Page 1
Clinical Practice Guideline
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
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##
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; Jose 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 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 the American College of Cardiology (www.acc.org) and the American Heart Association
(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.
(Hypertension. 2018;71:e13-e115. DOI: 10.1161/HYP.0000000000000065.)
(c) 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
e13

Page 2
e14
Hypertension June 2018
Table of Contents
Preamble . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . e15
1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . e16
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
2.1. Observational Relationship . . . . . . . . . . . . . . . . . . e19
2.2. BP Components . . . . . . . . . . . . . . . . . . . . . . . . . . . e20
2.3. Population Risk . . . . . . . . . . . . . . . . . . . . . . . . . . . e20
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. 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
5.1. Genetic Predisposition . . . . . . . . . . . . . . . . . . . . . . e28
5.2. Environmental Risk Factors . . . . . . . . . . . . . . . . . . e28
5.2.1. Overweight and Obesity . . . . . . . . . . . . . . . e28
5.2.2. Sodium Intake. . . . . . . . . . . . . . . . . . . . . . . e29
5.2.3. Potassium . . . . . . . . . . . . . . . . . . . . . . . . . . e29
5.2.4. Physical Fitness. . . . . . . . . . . . . . . . . . . . . . e29
5.2.5. Alcohol . . . . . . . . . . . . . . . . . . . . . . . . . . . . e29
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
5.4.2. Primary Aldosteronism. . . . . . . . . . . . . . . . e32
5.4.3. Renal Artery Stenosis . . . . . . . . . . . . . . . . . e34
5.4.4. Obstructive Sleep Apnea. . . . . . . . . . . . . . . e34
6. Nonpharmacological Interventions . . . . . . . . . . . . . . . . e35
6.1. Strategies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . e35
6.2. Nonpharmacological Interventions . . . . . . . . . . . . e35
7. Patient Evaluation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . e38
7.1. Laboratory Tests and Other
Diagnostic Procedures . . . . . . . . . . . . . . . . . . . . . . e38
7.2. Cardiovascular Target Organ Damage . . . . . . . . . . e38
8. Treatment of High BP. . . . . . . . . . . . . . . . . . . . . . . . . . . e39
8.1. Pharmacological Treatment . . . . . . . . . . . . . . . . . . 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
Hypertension. . . . . . . . . . . . . . . . . . . . . . . . e40
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
Hypertension. . . . . . . . . . . . . . . . . . . . . . . . e43
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. Heart Failure. . . . . . . . . . . . . . . . . . . . . . . . . . . . e50
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
Transplantation . . . . . . . . . . . . . . . . . . . . e53
9.4. Cerebrovascular Disease . . . . . . . . . . . . . . . . . . e53
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
9.6. Diabetes Mellitus . . . . . . . . . . . . . . . . . . . . . . e58
9.7. Metabolic Syndrome. . . . . . . . . . . . . . . . . . . . e59
9.8. Atrial Fibrillation . . . . . . . . . . . . . . . . . . . . . . e59
9.9. Valvular Heart Disease . . . . . . . . . . . . . . . . . . e60
9.10. Aortic Disease. . . . . . . . . . . . . . . . . . . . . . . . . e60
10. Special Patient Groups. . . . . . . . . . . . . . . . . . . . . . . . . e60
10.1. Race and Ethnicity . . . . . . . . . . . . . . . . . . . . . . e60
10.1.1. Racial and Ethnic Differences
in Treatment. . . . . . . . . . . . . . . . . . . . . . e61
10.2. Sex-Related Issues . . . . . . . . . . . . . . . . . . . . . . e61
10.2.1. Women. . . . . . . . . . . . . . . . . . . . . . . . . . e62
10.2.2. Pregnancy . . . . . . . . . . . . . . . . . . . . . . . e62
10.3. Age-Related Issues. . . . . . . . . . . . . . . . . . . . . . . e63
10.3.1. Older Persons . . . . . . . . . . . . . . . . . . . . e63
10.3.2. Children and Adolescents . . . . . . . . . . . e64
11. Other Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . e64
11.1. Resistant Hypertension . . . . . . . . . . . . . . . . . . . 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
Modification . . . . . . . . . . . . . . . . . . . . . e71
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

Page 3
Whelton et al
2017 High Blood Pressure Clinical Practice Guideline
e15
12.4. Improving Quality of Care for
Patients With Hypertension . . . . . . . . . . . . . . . . e74
12.4.1. Performance Measures . . . . . . . . . . . . . e74
12.4.2. Quality Improvement Strategies . . . . . . e74
12.5. Financial Incentives . . . . . . . . . . . . . . . . . . . . . . e75
13. The Plan of Care for Hypertension . . . . . . . . . . . . . . . e75
13.1. Health Literacy. . . . . . . . . . . . . . . . . . . . . . . . . . e76
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 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . e79
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. 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. 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
articles.P-7-P-10
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

Page 4
e16
Hypertension June 2018
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.
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
data.P-6-P-9 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. 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
(Table 1).P-6-P-8
Glenn N. Levine, MD, FACC, FAHA
Chair, ACC/AHA Task Force on Clinical Practice
Guidelines
1. Introduction
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
high BP.S1.5-3,S1.5-4 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
BP.S1.5-5-S1.5-7 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. 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. The findings of the ERC and
the writing committee members were formally presented and

Page 5
Whelton et al
2017 High Blood Pressure Clinical Practice Guideline
e17
Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic
Testing in Patient Care* (Updated August 2015)
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

Page 6
e18
Hypertension June 2018
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?
4.2
2
What is the optimal target for BP lowering
during antihypertensive therapy in adults?
8.1.5
9.3
9.6
3
In adults with hypertension, do various
antihypertensive drug classes differ in their
comparative benefits and harms?
8.1.6
8.2
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?
8.1.6.1
BP indicates blood pressure.
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 Medical Association
(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).
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"
(JNC 7).S1.5-7 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. 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

Page 7
Whelton et al
2017 High Blood Pressure Clinical Practice Guideline
e19
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* 2012S1.5-9
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 2013S1.5-10
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
AHA/ACC
2011S1.5-27
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
2010S1.5-29
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
AHA
2010S1.5-38
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.
2. BP and CVD Risk
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
2.1. Observational Relationship
increased in a log-linear fashion from SBP levels <115
Observational studies have demonstrated graded associations
mm Hg to >180 mm Hg and from DBP levels <75 mm Hg to
between higher systolic blood pressure (SBP) and diastolic
>105 mm Hg.S2.1-1 In that analysis, 20 mm Hg higher SBP and

Page 8
e20
Hypertension June 2018
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 t30 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
evaluated separately.S2.1-2 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 (t65 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
CVD risk.S2.2-1,S2.2-2 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
settings.S2.2-8-S2.2-11
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 23 272 US NHANES (National Health and
Nutrition Examination Survey) participants, >50% of deaths
from coronary heart disease (CHD) and stroke occurred
Table 4. BP Measurement Definitions
SBP
First Korotkoff sound*
DBP
Fifth Korotkoff sound*
Pulse pressure
SBP minus DBP
Mean arterial pressure
DBP plus one third pulse pressure
BP Measurement
Definition
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.
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
hypertension.S2.4-1,S2.4-2
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/
min/1.73 m2 and/or urine albumin:creatinine t300 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 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.

Page 9
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
had hypertension.S2.4-5 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
2009 and 2012, 41.7% had a 10-year CHD risk >20%, 40.9%
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
diet.S2.4-8 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
mechanisms.S2.4-9-S2.4-11 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 t3 risk
factors present in 17% of patients.S2.4-1 A meta-analysis
from 18 cohort studies involving 257 384 patients identi
fied a lifetime risk of CVD death, nonfatal MI, and fatal
or nonfatal stroke that was substantially higher in adults
with t2 CVD risk factors than in those with only 1 risk
factor.S2.4-1,S2.4-2
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
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
t140 mm Hg
or
t90 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 t2 careful readings
obtained on t2 occasions, as detailed in Section 4); DBP, diastolic blood
pressure; and SBP, systolic blood pressure.
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. 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
adults.S3.1-1 The prevalence of severe hypertension has been
declining over time, but approximately 12.3% of US adults
with hypertension have an average SBP t160 mm Hg or aver
age DBP t100 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

Page 10
e22
Hypertension June 2018
BP and hypertension are associated with increased risk
of CVD, ESRD, subclinical atherosclerosis, and all-cause
death.S3.1-1-S3.1-17 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. Lifetime Risk of Hypertension
Observational studies have documented a relatively high inci
dence of hypertension over periods of 5 to 10 years of follow
up.S3.2-1,S3.2-2 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,
0.3%, 6.5%, and 37% developed hypertension at age 25, 45,
and 65 years, respectively.S3.2-5 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
adults.S3.2-3 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 (t20 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
Table 7. Prevalence of Hypertension Based on 2 SBP/DBP
Thresholds*
SBP/DBP t130/80
mm Hg or Self-Reported
Antihypertensive
Medication
SBP/DBP t140/90
mm Hg or Self-Reported
Antihypertensive
Medication
Overall, crude
46%
32%
Men
(n=4717)
Women
(n=4906)
Men
(n=4717)
Women
(n=4906)
Overall, age-sex
adjusted
48%
43%
31%
32%
Age group, y
20-44
30%
19%
11%
10%
45-54
50%
44%
33%
27%
55-64
70%
63%
53%
52%
65-74
77%
75%
64%
63%
75+
79%
85%
71%
78%
Race-ethnicity
Non-Hispanic white
47%
41%
31%
30%
Non-Hispanic black
59%
56%
42%
46%
Non-Hispanic Asian
45%
36%
29%
27%
Hispanic
44%
42%
27%
32%
The prevalence estimates have been rounded to the nearest full percentage.
*130/80 and 140/90 mm Hg in 9623 participants (t20 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.
in an overestimate of hypertension prevalence compared
with what would be found by using an average of t2 read
ings taken on t2 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 t2 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
lifestyle.S3.3-2,S3.3-6
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

Page 11
Whelton et al
2017 High Blood Pressure Clinical Practice Guideline
e23
have been steadily improving since the 1960s,S3.4-1-S3.4-4 with
NHANES 2009 to 2012 prevalence estimates for men and
women, respectively, being 80.2% and 85.4% for awareness,
70.9% and 80.6% for treatment (88.4% and 94.4% in those
who were aware), 69.5% and 68.5% for control in those being
treated, and 49.3% and 55.2% for overall control in adults
with hypertension.S3.4-5 The NHANES experience may under
estimate awareness, treatment, and control of hypertension
because it is based on BP estimates derived from an aver
age of readings obtained at a single visit, whereas guidelines
recommend use of BP averages of t2 readings obtained
on t2 occasions. In addition, the current definition of con
trol excludes the possibility of control resulting from life
style change or nonpharmacological interventions. NHANES
hypertension control rates have been consistently higher in
women than in men (55.3% versus 38.0% in 2009-2012); in
whites than in blacks and Hispanics (41.3% versus 31.1% and
23.6%, respectively, in men, and 57.2% versus 43.2% and
52.9%, respectively, in women, for 2009-2012); and in older
than in younger adults (50.5% in adults t60 years of age ver
sus 34.4% in patients 18 to 39 years of age for 2011-2012)
up to the seventh decade,S3.4-4,S3.4-5 although control rates
are considerably lower for those t75 years (46%) and only
39.8% for adults t80 years.S3.4-6 In addition, control rates are
higher for persons of higher socioeconomic status (43.2%
for adults with an income >400% above the US government
poverty line versus 30.2% for those below this line in 2003
to 2006).S3.4-5 Research studies have repeatedly demonstrated
that structured, goal-oriented BP treatment initiatives with
feedback and provision of free medication result in a substan
tial improvement in BP control.S3.4-7-S3.4-9 Control rates that are
much higher than noted in the general population have been
reported in care settings where a systems approach (detailed
in Sections 12.2 and 12.3) has been implemented for insured
adults.S3.4-10-S3.4-12
4. Measurement of BP
4.1. Accurate Measurement of BP in the Office
Recommendation for Accurate Measurement of BP in the Office
COR
LOE
Recommendation
I
C-EO
1. For diagnosis and management of high
BP, proper methods are recommended for
accurate measurement and documentation
of BP (Table 8).
Synopsis
Although measurement of BP in office settings is relatively
easy, errors are common and can result in a misleading esti
mation of an individual's true level of BP. There are various
methods for measuring BP in the office. The clinical standard
of auscultatory measures calibrated to a column of mercury
has given way to oscillometric devices (in part because of
toxicological issues with mercury). Oscillometric devices
use a sensor that detects oscillations in pulsatile blood vol
ume during cuff inflation and deflation. BP is indirectly cal
culated from maximum amplitude algorithms that involve
population-based data. For this reason, only devices with a
Table 8. Checklist for Accurate Measurement of BPS4.1-3,S4.1-4
Key Steps for Proper
BP Measurements
Specific Instructions
Step 1: Properly
1. Have the patient relax, sitting in a chair (feet
prepare the patient
on floor, back supported) for >5 min.
2. The patient should avoid caffeine, exercise,
and smoking for at least 30 min before
measurement.
3. Ensure patient has emptied his/her bladder.
4. Neither the patient nor the observer should
talk during the rest period or during the
measurement.
5. Remove all clothing covering the location of
cuff placement.
6. Measurements made while the patient is
sitting or lying on an examining table do not
fulfill these criteria.
Step 2: Use proper
1. Use a BP measurement device that has been
technique for BP
validated, and ensure that the device is
measurements
calibrated periodically.*
2. Support the patient's arm (eg, resting on a
desk).
3. Position the middle of the cuff on the
patient's upper arm at the level of the right
atrium (the midpoint of the sternum).
4. Use the correct cuff size, such that the
bladder encircles 80% of the arm, and note if
a larger- or smaller-than-normal cuff size is
used (Table 9).
5. Either the stethoscope diaphragm or bell may
be used for auscultatory readings.S4.1-5,S4.1-6
Step 3: Take the
1. At the first visit, record BP in both arms. Use
proper measurements
the arm that gives the higher reading for
needed for
subsequent readings.
diagnosis and
2. Separate repeated measurements by
treatment of elevated
1-2 min.
BP/hypertension
3. For auscultatory determinations, use a
palpated estimate of radial pulse obliteration
pressure to estimate SBP. Inflate the cuff 20-
30 mm Hg above this level for an auscultatory
determination of the BP level.
4. For auscultatory readings, deflate the cuff
pressure 2 mm Hg per second, and listen for
Korotkoff sounds.
Step 4: Properly
1. Record SBP and DBP. If using the auscultatory
document accurate
technique, record SBP and DBP as onset of
BP readings
the first Korotkoff sound and disappearance
of all Korotkoff sounds, respectively, using
the nearest even number.
2. Note the time of most recent BP medication
taken before measurements.
Step 5: Average the
readings
Use an average of t2 readings obtained on t2
occasions to estimate the individual's level of BP.
Step 6: Provide BP
readings to patient
Provide patients the SBP/DBP readings both
verbally and in writing.
*See Section 4.2 for additional guidance.
Adapted with permission from Mancia et alS4.1-3 (Oxford University Press),
Pickering et alS4.1-2 (American Heart Association, Inc.), and Weir et alS4.1-4
(American College of Physicians, Inc.).
BP indicates blood pressure; DBP, diastolic blood pressure; and SBP, systolic
blood pressure.

Page 12
e24
Hypertension June 2018
validated measurement protocol can be recommended for use
(see Section 4.2 for additional details). Many of the newer
oscillometric devices automatically inflate multiple times
(in 1- to 2-minute intervals), allowing patients to be alone
and undisturbed during measurement. Although much of the
available BP-related risk information and antihypertensive
treatment trial experience have been generated by using "tra
ditional" office methods of BP measurement, there is a grow
ing evidence base supporting the use of automated office BP
measurements.S4.1-1
Recommendation-Specific Supportive Text
1. Accurate measurement and recording of BP are essen
tial to categorize level of BP, ascertain BP-related CVD
risk, and guide management of high BP. Most systematic
errors in BP measurement can be avoided by following
the suggestions provided in Table 8, including having
the patient sit quietly for 5 minutes before a reading is
taken, supporting the limb used to measure BP, ensuring
the BP cuff is at heart level, using the correct cuff size
(Table 9), and, for auscultatory readings, deflating the
cuff slowly.S4.1-2 In those who are already taking medica
tion that affects BP, the timing of BP measurements in
relation to ingestion of the patient's medication should
be standardized. Because individual BP measurements
tend to vary in an unpredictable or random fashion, a
single reading is inadequate for clinical decision-mak
ing. An average of 2 to 3 BP measurements obtained on
2 to 3 separate occasions will minimize random error
and provide a more accurate basis for estimation of BP.
In addition to clinicians, other caregivers and patients
who perform BP self-monitoring should be trained to
follow the checklist in Table 8. Common errors in clini
cal practice that can lead to inaccurate estimation of BP
include failure to allow for a rest period and/or talking
with the patient during or immediately before the record
ing, improper patient positioning (eg, sitting or lying on
an examination table), rapid cuff deflation (for ausculta
tory readings), and reliance on BPs measured at a single
occasion.
4.2. Out-of-Office and Self-Monitoring of BP
Recommendation for Out-of-Office and Self-Monitoring of BP
References that support the recommendation are
summarized in Online Data Supplement 3 and Systematic
Review Report.
COR
LOE
Recommendation
I
ASR
1. Out-of-office BP measurements are
recommended to confirm the diagnosis of
hypertension (Table 11) and for titration
of BP-lowering medication, in conjunction
with telehealth counseling or clinical
interventions.S4.2-1-S4.2-4
SR indicates systematic review.
Synopsis
Out-of-office measurement of BP can be helpful for confir
mation and management of hypertension. Self-monitoring
Table 9. Selection Criteria for BP Cuff Size for Measurement
of BP in Adults
Arm Circumference
Usual Cuff Size
22-26 cm
Small adult
27-34 cm
Adult
35-44 cm
Large adult
45-52 cm
Adult thigh
Adapted with permission from Pickering et alS4.1-2 (American Heart
Association, Inc.).
BP indicates blood pressure.
of BP refers to the regular measurement of BP by an indi
vidual at home or elsewhere outside the clinic setting.
Among individuals with hypertension, self-monitoring of
BP, without other interventions, has shown limited evidence
for treatment-related BP reduction and achievement of BP
control.S4.2-1,S4.2-5,S4.2-6 However, with the increased recogni
tion of inconsistencies between office and out-of-office BPs
(see Section 4.4) and greater reduction in BP being recom
mended for hypertension control, increased attention is
being paid to out-of-office BP readings. Although ABPM
is generally accepted as the best out-of-office measurement
method, HBPM is often a more practical approach in clini
cal practice. Recommended procedures for the collection
of HBPM data are provided in Table 10. If self-monitor
ing is used, it is important to ensure that the BP measure
ment device used has been validated with an internationally
accepted protocol and the results have been published in
a peer-reviewed journal.S4.2-7 A guide to the relationship
between HBPM BP readings and corresponding read
ings obtained in the office and by ABPM is presented in
Table 11. The precise relationships between office readings,
ABPM, and HBPM are unsettled, but there is general agree
ment that office BPs are often higher than ABPM or HBPM
BPs, especially at higher BPs.
Recommendation-Specific Supportive Text
1. ABPM is used to obtain out-of-office BP readings at
set intervals, usually over a period of 24 hours. HBPM
is used to obtain a record of out-of-office BP readings
taken by a patient. Both ABPM and HBPM typically
provide BP estimates that are based on multiple mea
surements. A systematic review conducted by the US
Preventive Services Task Force reported that ABPM
provided a better method to predict long-term CVD out
comes than did office BPs. It incorporates new informa
tion from studies of HBPM, ABPM, the relationship of
overall CVD risk to the effectiveness of blood pressure
lowering, clinical outcomes related to different blood
pressure goals, strategies to improve blood pressure con
trol and various other areas. A small body of evidence
suggested, but did not confirm, that HBPM could serve
as a similar predictor of outcomes.S4.2-4 Meta-analyses of
RCTs have identified clinically useful reductions in SBP
and DBP and achievement of BP goals at 6 months and
1 year when self-monitoring of BP has been used in con
junction with other interventions, compared with usual
care. Meta-analyses of RCTs have identified only small

Page 13
Whelton et al
2017 High Blood Pressure Clinical Practice Guideline
e25
Table 10. Procedures for Use of HBPMS4.2-5-S4.2-7
Patient training should occur under medical supervision, including:
Information about hypertension
Selection of equipment
Acknowledgment that individual BP readings may vary substantially
Interpretation of results
Devices:
Verify use of automated validated devices. Use of auscultatory devices
(mercury, aneroid, or other) is not generally useful for HBPM because
patients rarely master the technique required for measurement of BP with
auscultatory devices.
Monitors with provision for storage of readings in memory are preferred.
Verify use of appropriate cuff size to fit the arm (Table 9).
Verify that left/right inter-arm differences are insignificant. If differences
are significant, instruct patient to measure BPs in the arm with higher
readings.
Instructions on HBPM procedures:
Remain still:
Avoid smoking, caffeinated beverages, or exercise within 30 min before
BP measurements.
Ensure >=5 min of quiet rest before BP measurements.
Sit correctly:
Sit with back straight and supported (on a straight-backed dining chair,
for example, rather than a sofa).
Sit with feet flat on the floor and legs uncrossed.
Keep arm supported on a flat surface (such as a table), with the upper
arm at heart level.
Bottom of the cuff should be placed directly above the antecubital fossa
(bend of the elbow).
Take multiple readings:
Take at least 2 readings 1 min apart in morning before taking medications
and in evening before supper. Optimally, measure and record BP daily.
Ideally, obtain weekly BP readings beginning 2 weeks after a change in
the treatment regimen and during the week before a clinic visit.
Record all readings accurately:
Monitors with built-in memory should be brought to all clinic
appointments.
BP should be based on an average of readings on >=2 occasions for
clinical decision making.
The information above may be reinforced with videos available online.
See Table 11 for HBPM targets.
BP indicates blood pressure; and HBPM, home blood pressure monitoring.
net reductions in SBP and DBP at 6 months and 1 year
for use of self-monitoring of BP on its own, as compared
with usual care.S4.2-1,S4.2-5,S4.2-6 See Section 4.4 for addi
tional details of diagnostic classification and Section 12
for additional details of telehealth and out-of-office BP
measurement for management of high BP.
4.3. Ambulatory BP Monitoring
All of the major RCTs have been based on use of clinic BP
readings. However, ABPM is often used to supplement BP
Table 11. Corresponding Values of SBP/DBP for Clinic, HBPM,
Daytime, Nighttime, and 24-Hour ABPM Measurements
Clinic
120/80
130/80
140/90
160/100
HBPM
Daytime
ABPM
Nighttime
ABPM
24-Hour
ABPM
120/80
100/65
115/75
130/80
110/65
125/75
135/85
120/70
130/80
145/90
140/85
145/90
120/80
130/80
135/85
145/90
ABPM indicates ambulatory blood pressure monitoring; BP, blood pressure;
DBP, diastolic blood pressure; HBPM, home blood pressure monitoring; and
SBP, systolic blood pressure.
readings obtained in office settings.S4.3-1 The monitors are
usually programmed to obtain readings every 15 to 30 min
utes throughout the day and every 15 minutes to 1 hour
during the night. ABPM is conducted while individuals go
about their normal daily activities. ABPM can a) provide
estimates of mean BP over the entire monitoring period
and separately during nighttime and daytime, b) determine
the daytime-to-nighttime BP ratio to identify the extent of
nocturnal "dipping," c) identify the early-morning BP surge
pattern, d) estimate BP variability, and e) allow for recog
nition of symptomatic hypotension. The US Centers for
Medicaid & Medicare Services and other agencies provide
reimbursement for ABPM in patients with suspected white
coat hypertension.S4.3-2 Medicare claims for ABPM between
2007 and 2010 were reimbursed at a median of $52 and were
submitted for <1% of beneficiaries.S4.3-3,S4.3-4 A list of devices
validated for ABPM is available.S4.3-5,S4.3-6
ABPM and HBPM definitions of high BP use different BP
thresholds than those used by the previously mentioned office-
based approach to categorize high BP identified in Section
3.1. Table 11 provides best estimates for corresponding
home, daytime, nighttime, and 24-hour ambulatory levels of
BP, including the values recommended for identification of
hypertension with office measurements. Typically, a clinic BP
of 140/90 mm Hg corresponds to home BP values of 135/85
mm Hg and to ABPM values defined as a daytime SBP/DBP of
135/85 mm Hg, a nighttime SBP/DBP of 120/70 mm Hg, and
a 24-hour SBP/DBP of 130/80 mm Hg.S4.3-7,S4.3-8 These thresh
olds are based on data from European, Australian, and Asian
populations, with few data available for establishing appropri
ate thresholds for US populations.S4.3-9-S4.3-13 They are provided
as a guide but should be interpreted with caution. Higher day
time SBP measurements from ABPM can be associated with
an increased risk of CVD and all-cause death independent
of clinic-measured BP.S4.3-14 A meta-analysis of observational
studies that included 13 844 individuals suggested nighttime
BP is a stronger risk factor for CHD and stroke than either
clinic or daytime BP.S4.3-15
Methodological issues complicate the interpretation of
data from studies that report office and out-of-office BP read
ings. Definitions and diagnostic methods for identifying white
coat hypertension and masked hypertension (see Section 4.4)
have not been standardized. The available studies have dif
fered with regard to number of office readings obtained, use of
24-hour ABPM, use of daytime-only ABPM, inclusion of day
time and nighttime BP readings as separate categories, HBPM