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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: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines

Originally publishedhttps://doi.org/10.1161/CIR.0000000000000597Circulation. 2018;138:e426–e483

    Table of Contents

    • Preamble e428

    • 1. Introduction e429

      • 1.1. Methodology and Evidence Review e430

      • 1.2. Organization of the Writing Committee e431

      • 1.3. Document Review and Approval e431

      • 1.4. Scope of the Guideline e431

      • 1.5. Abbreviations and Acronyms e433

    • 2. BP and CVD Risk e433

      • 2.1. Observational Relationship e433

      • 2.2. BP Components e433

      • 2.3. Population Risk e433

      • 2.4. Coexistence of Hypertension and Related Chronic Conditions e434

    • 3. Classification of BP e434

      • 3.1. Definition of High BP e434

      • 3.2. Lifetime Risk of Hypertension e434

      • 3.3. Prevalence of High BP e434

    • 4. Measurement of BP e435

      • 4.1. Accurate Measurement of BP in the Office e435

      • 4.2. Out-of-Office and Self-Monitoring of BP e435

      • 4.3. Masked and White Coat Hypertension e436

    • 5. Causes of Hypertension e438

      • 5.1. Secondary Forms of Hypertension e438

        • 5.1.1. Drugs and Other Substances With Potential to Impair BP Control e440

        • 5.1.2. Primary Aldosteronism e440

        • 5.1.3. Renal Artery Stenosis e440

        • 5.1.4. Obstructive Sleep Apnea e441

    • 6. Nonpharmacological Interventions e441

    • 7. Patient Evaluation e443

      • 7.1. Laboratory Tests and Other Diagnostic Procedures e443

    • 8. Treatment of High BP e443

      • 8.1. Pharmacological Treatment e443

        • 8.1.1. Initiation of Pharmacological BP Treatment in the Context of Overall CVD Risk e443

        • 8.1.2. BP Treatment Threshold and the Use of CVD Risk Estimation to Guide Drug Treatment of Hypertension e443

        • 8.1.3. Follow-Up After Initial BP Evaluation e444

        • 8.1.4. General Principles of Drug Therapy e445

        • 8.1.5. BP Goal for Patients With Hypertension e447

        • 8.1.6. Choice of Initial Medication e447

      • 8.2. Follow-Up of BP During Antihypertensive Drug Therapy e447

        • 8.2.1. Follow-Up After Initiating Antihypertensive Drug Therapy e447

        • 8.2.2. Monitoring Strategies to Improve Control of BP in Patients on Drug Therapy for High BP e448

    • 9. Hypertension in Patients With Comorbidities e448

      • 9.1. Stable Ischemic Heart Disease e448

      • 9.2. Heart Failure e449

        • 9.2.1. Heart Failure With Reduced Ejection Fraction e449

        • 9.2.2. Heart Failure With Preserved Ejection Fraction e449

      • 9.3. Chronic Kidney Disease e449

        • 9.3.1. Hypertension After Renal Transplantation e449

      • 9.4. Cerebrovascular Disease e450

        • 9.4.1. Acute Intracerebral Hemorrhage e450

        • 9.4.2. Acute Ischemic Stroke e450

        • 9.4.3. Secondary Stroke Prevention e451

      • 9.5. Peripheral Artery Disease e452

      • 9.6. Diabetes Mellitus e452

      • 9.7. Metabolic Syndrome e452

      • 9.8. Atrial Fibrillation e453

      • 9.9. Valvular Heart Disease e453

      • 9.10. Aortic Disease e453

    • 10. Special Patient Groups e453

      • 10.1.1. Racial and Ethnic Differences in Treatment e453

      • 10.2. Sex-Related Issues e453

        • 10.2.1. Women e454

        • 10.2.2. Pregnancy e454

      • 10.3. Age-Related Issues e454

        • 10.3.1. Older Persons e454

    • 11. Other Considerations e455

      • 11.1. Resistant Hypertension e455

      • 11.2. Hypertensive Crises—Emergencies and Urgencies e455

      • 11.3. Cognitive Decline and Dementia e458

      • 11.4. Patients Undergoing Surgical Procedures e458

    • 12. Strategies to Improve Hypertension Treatment and Control e458

      • 12.1. Adherence Strategies for Treatment of Hypertension e458

        • 12.1.1. Antihypertensive Medication Adherence Strategies e458

        • 12.1.2. Strategies to Promote Lifestyle Modification e458

      • 12.2. Structured, Team-Based Care Interventions for Hypertension Control e458

      • 12.3. Health Information Technology–Based Strategies to Promote Hypertension Control e459

        • 12.3.1. EHR and Patient Registries e459

        • 12.3.2. Telehealth Interventions to Improve Hypertension Control e459

      • 12.4. Improving Quality of Care for Patients With Hypertension e459

        • 12.4.1. Performance Measures e459

        • 12.4.2. Quality Improvement Strategies e459

      • 12.5. Financial Incentives e459

    • 13. The Plan of Care for Hypertension e459

      • 13.1. Health Literacy e460

      • 13.2. Access to Health Insurance and Medication Assistance Plans e460

      • 13.3. Social and Community Services e460

    • 14. Summary of BP Thresholds and Goals for Pharmacological Therapy e461

    • References e462

    • Appendix 1. Author Relationships With Industry and Other Entities (Relevant) e475

    • Appendix 2. Reviewer Relationships With Industry and Other Entities (Comprehensive) e477

    Preamble

    Since 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines (guidelines) with recommendations 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 stakeholder 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 guidelines without commercial support, and members of each organization 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 developed 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 presentation and delivery of guidelines are reevaluated and modified 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 recommendations and associated text called the “modular knowledge chunk format.” Each modular “chunk” includes a table of related recommendations, a brief synopsis, recommendation-specific 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 tagging for rapid electronic retrieval of related recommendations on a topic of interest. This evolved approach format was instituted 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 analysis of the value of a drug, device, or intervention may be performed 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 guideline 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 management 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, ethnicities, races, intellectual perspectives/biases, and scopes of clinical practice. The Task Force may also invite organizations and professional societies with related interests 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 comparative 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 writing of a guideline, c) the relevance to a substantial number of patients, and d) the likelihood that the findings can be translated 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 testing, 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 contraindications 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 magnitude 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

    Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care* (Updated August 2015)

    Table 1.

    The reader is encouraged to consult the full-text guidelineP-11 for additional guidance and details about hypertension, since the executive summary contains mainly the recommendations.

    Glenn N. Levine, MD, FACC, FAHA

    Chair, ACC/AHA Task Force on Clinical Practice Guidelines

    1. Introduction

    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.S1-1,S1-2 Accordingly, the ACC and AHA collaborated with the NHLBI and stakeholder 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 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.

    As early as the 1920s, and subsequently in the 1959 Build and Blood Pressure StudyS1-3 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.S1-4 The 1967 and 1970 Veterans Administration Cooperative Study Group reports ushered in the era of effective treatment for high BP.S1-5,S1-6 The first comprehensive guideline for detection, evaluation, and management of high BP was published in 1977, under the sponsorship of the NHLBI.S1-7 In subsequent years, a series of Joint National Committee (JNC) BP guidelines were published to assist the practice community and improve prevention, awareness, treatment, and control of high BP.S1-7–S1-9 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 guideline, was conducted between February and August 2015. Key search words included but were not limited to the following: adherence; aerobic; alcohol intake; ambulatory care; antihypertensive: agents, drug, medication, therapy; beta adrenergic blockers; blood pressure: arterial, control, determination, devices, goal, high, improve, measurement, monitoring, ambulatory; 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; sphygmomanometers; spironolactone; therapy; treatment: adherence, compliance, efficacy, outcome, protocol, regimen; weight. Additional relevant studies published through June 2016, during the guideline writing process, were also considered by the writing committee 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 formulate recommendations.

    As noted in the preamble, an independent ERC was commissioned to perform a formal systematic review of 4 critical 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 process, 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 discussed, and then guideline recommendations were developed. 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,S1-10 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.

    Table 2. Systematic Review Questions on High BP in Adults

    Question NumberQuestionSection Number
    1Is 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
    2What is the optimal target for BP lowering during antihypertensive therapy in adults?8.1.5
    9.3
    9.6
    3In adults with hypertension, do various antihypertensive drug classes differ in their comparative benefits and harms?8.1.6
    8.2
    4In 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.

    1.2. Organization of the Writing Committee

    The writing committee consisted of clinicians, cardiologists, epidemiologists, internists, an endocrinologist, a geriatrician, a nephrologist, a neurologist, a nurse, a pharmacist, a physician assistant, and 2 lay/patient representatives. It 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 governing 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 clinical and public health practice communities. It is designed to be comprehensive but succinct and practical in providing guidance 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).S1-9 It incorporates new information from studies of office-based BP-related risk of CVD, ambulatory blood pressure 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.S1-11,S1-12 In developing 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.

    Table 3. Associated Guidelines and Statements

    TitleOrganizationPublication Year
    Guidelines
     Lower-extremity peripheral artery diseaseAHA/ACC2016S1-13
     Management of primary aldosteronism: case detection, diagnosis, and treatmentEndocrine Society2016S1-14
     Stable ischemic heart diseaseACC/AHA/AATS/PCNA/SCAI/STS2014S1-15* 2012S1-11
     Pheochromocytoma and paragangliomaEndocrine Society2014S1-16
     Atrial fibrillationAHA/ACC/HRS2014S1-17
     Valvular heart diseaseACC/AHA2017S1-18
     Assessment of cardiovascular riskACC/AHA2013S1-19
     Hypertension in pregnancyACOG2013S1-20
     Heart failureACC/AHA2017S1-21
    2013S1-12
     Lifestyle management to reduce cardiovascular riskAHA/ACC2013S1-22
     Management of arterial hypertensionESH/ESC2013S1-23
     Management of overweight and obesity in adultsAHA/ACC/TOS2013S1-24
     ST-elevation myocardial infarctionACC/AHA2013S1-25
     Treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adultsACC/AHA2013S1-26
     Cardiovascular diseases during pregnancyESC2011S1-27
     Effectiveness-based guidelines for the prevention of cardiovascular disease in womenAHA/ACC2011S1-28
     Secondary prevention and risk-reduction therapy for patients with coronary and other atherosclerotic vascular diseaseAHA/ACC2011S1-29
     Assessment of cardiovascular risk in asymptomatic adultsACC/AHA2010S1-30
     Thoracic aortic diseaseACC/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/
    STS/SVM
    2010S1-31
     Diagnosis, evaluation, and treatment of high blood pressure in children and adolescentsNHLBI2004S1-32
    Statements
     Salt sensitivity of blood pressureAHA2016S1-33
     Cardiovascular team-based care and the role of advanced practice providersACC2015S1-34
     Treatment of hypertension in patients with coronary artery diseaseAHA/ACC/ASH2015S1-35
     Ambulatory blood pressure monitoring in children and adolescentsAHA2014S1-36
     An effective approach to high blood pressure controlAHA/ACC/CDC2014S1-37
     Ambulatory blood pressure monitoringESH2013 S1-38
     Performance measures for adults with coronary artery disease and hypertensionACC/AHA/AMA-PCPI2011S1-39
     Interventions to promote physical activity and dietary lifestyle changes for cardiovascular risk factor reduction in adultsAHA2010S1-40
     Resistant hypertension: diagnosis, evaluation, and treatmentAHA2008S1-41

    *The full-text SIHD guideline is from 2012.S1-11 A focused update was published in 2014.S1-15

    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.

    1.5. Abbreviations and Acronyms

    Abbreviation/AcronymMeaning/Phrase
    ABPMambulatory blood pressure monitoring
    ACEangiotensin-converting enzyme
    AFatrial fibrillation
    ARBangiotensin receptor blocker
    BPblood pressure
    CCBcalcium channel blocker
    CHDcoronary heart disease
    CKDchronic kidney disease
    CPAPcontinuous positive airway pressure
    CVDcardiovascular disease
    DBPdiastolic blood pressure
    DMdiabetes mellitus
    ECGelectrocardiogram
    ESRDend-stage renal disease
    GDMTguideline-directed management and therapy
    GFRglomerular filtration rate
    HBPMhome blood pressure monitoring
    EHRelectronic health record
    HFheart failure
    HFpEFheart failure with preserved ejection fraction
    HFrEFheart failure with reduced ejection fraction
    ICHintracerebral hemorrhage
    JNCJoint National Commission
    LVleft ventricular
    LVHleft ventricular hypertrophy
    MImyocardial infarction
    MRImagnetic resonance imaging
    PADperipheral artery disease
    RASrenin-angiotensin system
    RCTrandomized controlled trial
    SBPsystolic blood pressure
    SIHDstable ischemic heart disease
    TIAtransient ischemic attack

    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 >105 mm Hg.S2.1-1 In that analysis, 20 mm Hg higher SBP and 10 mm Hg higher DBP were each associated with a doubling in the risk of death from stroke, heart disease, or other vascular 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 evaluated separately.S2.1-2 An increased risk of CVD associated 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 corresponding 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 CVD risk.S2.2-1,S2.2-2 Higher SBP has consistently been associated 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 consistently 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 trials and because of their ease of measurement in practice settings.S2.2-8–S2.2-11

    Table 4. BP Measurement Definitions

    BP MeasurementDefinition
    SBPFirst Korotkoff sound*
    DBPFifth Korotkoff sound*
    Pulse pressureSBP minus DBP
    Mean arterial pressureDBP plus one third pulse pressure
    Mid-BPSum 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.

    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 follow-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 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 revascularization, stroke, or HF) were attributable to hypertension. In the Northern Manhattan study, the percentage of events attributable 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

    Table 5. CVD Risk Factors Common in Patients With Hypertension

    Modifiable Risk Factors*Relatively Fixed Risk Factors
    Current cigarette smoking, secondhand smokingCKD
    Family history
    Diabetes mellitusIncreased age
    Dyslipidemia/hypercholesterolemiaLow socioeconomic/educational status
    Overweight/obesityMale sex
    Physical inactivity/low fitnessObstructive sleep apnea
    Unhealthy dietPsychosocial 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 apneaS2.4-3), 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.

    3. Classification of BP

    3.1. Definition of High BP

    Table 6. Categories of BP in Adults*

    BP CategorySBPDBP
    Normal<120 mm Hgand<80 mm Hg
    Elevated120–129 mm Hgand<80 mm Hg
    Hypertension
     Stage 1130–139 mm Hgor80–89 mm Hg
     Stage 2≥140 mm Hgor≥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.

    3.2. Lifetime Risk of Hypertension

    Observational studies have documented a relatively high incidence 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 incidence 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 developing 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 developed hypertension during their lifetimes.S3.2-4 All of these estimates 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.

    Table 7. Prevalence of Hypertension Based on 2 SBP/DBP Thresholds*

    SBP/DBP ≥130/80 mm Hg or Self-Reported Antihypertensive MedicationSBP/DBP ≥140/90 mm Hg or Self-Reported Antihypertensive Medication
    Overall, crude46%32%
    Men (n=4717)Women (n=4906)Men (n=4717)Women (n=4906)
    Overall, age-sex adjusted48%43%31%32%
    Age group, y
     20–4430%19%11%10%
     45–5450%44%33%27%
     55–6470%63%53%52%
     65–7477%75%64%63%
     75+79%85%71%78%
    Race-ethnicity§
     Non-Hispanic white47%41%31%30%
     Non-Hispanic black59%56%42%46%
     Non-Hispanic Asian45%36%29%27%
     Hispanic44%42%27%32%

    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.

    3.3. Prevalence of High BP

    4. Measurement of BP

    4.1. Accurate Measurement of BP in the Office

    Table 8. Checklist for Accurate Measurement of BPS4.1-1,S4.1-2

    Key Steps for Proper BP MeasurementsSpecific Instructions
    Step 1: Properly prepare the patient1. Have the patient relax, sitting in a chair (feet 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 technique for BP measurements1. Use a BP measurement device that has been validated, and ensure that the device is 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.S4.1-3,S4.1-4
    Step 3: Take the proper measurements needed for diagnosis and treatment of elevated BP/hypertension1. At the first visit, record BP in both arms. Use the arm that gives the higher reading for subsequent readings.
    2. Separate repeated measurements by 1–2 min.
    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 document accurate BP readings1. Record SBP and DBP. If using the auscultatory technique, record SBP and DBP as onset of 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 readingsUse an average of ≥2 readings obtained on ≥2 occasions to estimate the individual’s level of BP.
    Step 6: Provide BP readings to patientProvide patients the SBP/DBP readings both verbally and in writing.

    *See Section 4.2 for additional guidance.

    Adapted with permission from Mancia et alS4.1-1 (Oxford University Press), Pickering et alS4.1-5 (American Heart Association, Inc.), and Weir et alS4.1-2 (American College of Physicians, Inc.).

    BP indicates blood pressure; DBP, diastolic blood pressure; and SBP, systolic blood pressure.

    Table 9. Selection Criteria for BP Cuff Size for Measurement of BP in Adults

    Arm CircumferenceUsual Cuff Size
    22–26 cmSmall adult
    27–34 cmAdult
    35–44 cmLarge adult
    45–52 cmAdult thigh

    Adapted with permission from Pickering et alS4.1-5 (American Heart Association, Inc.).

    BP indicates blood pressure.

    4.2. Out-of-Office and Self-Monitoring of BP

    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.

    Table 11. Corresponding Values of SBP/DBP for Clinic, HBPM, Daytime, Nighttime, and 24-Hour ABPM Measurements

    ClinicHBPMDaytime ABPMNighttime ABPM24-Hour ABPM
    120/80120/80120/80100/65115/75
    130/80130/80130/80110/65125/75
    140/90135/85135/85120/70130/80
    160/100145/90145/90140/85145/90

    ABPM indicates ambulatory blood pressure monitoring; BP, blood pressure; DBP, diastolic blood pressure; HBPM, home blood pressure monitoring; and SBP, systolic blood pressure.

    4.3. Masked and White Coat Hypertension

    Table 12. BP Patterns Based on Office and Out-of-Office Measurements

    Office/Clinic/Healthcare SettingHome/Nonhealthcare/ABPM Setting
    NormotensiveNo hypertensionNo hypertension
    Sustained hypertensionHypertensionHypertension
    Masked hypertensionNo hypertensionHypertension
    White coat hypertensionHypertensionNo hypertension

    ABPM indicates ambulatory blood pressure monitoring; and BP, blood pressure.

    Table 13. Causes of Secondary Hypertension With Clinical Indications and Diagnostic Screening Tests

    PrevalenceClinical IndicationsPhysical ExaminationScreening TestsAdditional/Confirmatory Tests
    Common causes
     Renal parenchymal diseaseS5.1-1,S5.1-21%–2%Urinary tract infections; obstruction, hematuria; urinary frequency and nocturia; analgesic abuse; family history of polycystic kidney disease; elevated serum creatinine; abnormal urinalysisAbdominal mass (polycystic kidney disease); skin pallorRenal ultrasoundTests to evaluate cause of renal disease
     Renovascular diseaseS5.1-35%–34%*Resistant hypertension; hypertension of abrupt onset or worsening or increasingly difficult to control; flash pulmonary edema (atherosclerotic); early-onset hypertension, especially in women (fibromuscular hyperplasia)Abdominal systolic-diastolic bruit; bruits over other arteries (carotid – atherosclerotic or fibromuscular dysplasia), femoralRenal Duplex Doppler ultrasound; MRA; abdominal CTBilateral selective renal intra-arterial angiography
     Primary aldosteronismS5.1-4,S5.1-58%–20%Resistant hypertension; hypertension with hypokalemia (spontaneous or diuretic induced); hypertension and muscle cramps or weakness; hypertension and incidentally discovered adrenal mass; hypertension and obstructive sleep apnea; hypertension and family history of early-onset hypertension or strokeArrhythmias (with hypokalemia); especially atrial fibrillationPlasma aldosterone/renin ratio under standardized conditions (correction of hypokalemia and withdrawal of aldosterone antagonists for 4–6 wk)Oral sodium loading test (with 24-h urine aldosterone) or IV saline infusion test with plasma aldosterone at 4 h of infusion Adrenal CT scan, adrenal vein sampling.
     Obstructive sleep apneaS5.1-625%–50%Resistant hypertension; snoring; fitful sleep; breathing pauses during sleep; daytime sleepinessObesity, Mallampati class III–IV; loss of normal nocturnal BP fallBerlin Questionnaire;S5.1-7 Epworth Sleepiness Score;S5.1-8 overnight oximetryPolysomnography
     Drug or alcohol inducedS5.1-9§2%–4%Sodium-containing antacids; caffeine; nicotine (smoking); alcohol; NSAIDs; oral contraceptives; cyclosporine or tacrolimus; sympathomimetics (decongestants, anorectics); cocaine, amphetamines and other illicit drugs; neuropsychiatric agents; erythropoiesis-stimulating agents; clonidine withdrawal; herbal agents (Ma Huang, ephedra)Fine tremor, tachycardia, sweating (cocaine, ephedrine, MAO inhibitors); acute abdominal pain (cocaine)Urinary drug screen (illicit drugs)Response to withdrawal of suspected agent
    Uncommon causes
     Pheochromocytoma/paragangliomaS5.1-100.1%–0.6%Resistant hypertension; paroxysmal hypertension or crisis superimposed on sustained hypertension; “spells,” BP lability, headache, sweating, palpitations, pallor; positive family history of pheochromocytoma/paraganglioma; adrenal incidentalomaSkin stigmata of neurofibromatosis (café-au-lait spots; neurofibromas);
    Orthostatic hypotension
    24-h urinary fractionated metanephrines or plasma metanephrines under standard conditions (supine position with indwelling IV cannula)CT or MRI scan of abdomen/pelvis
     Cushing’s syndromeS5.1-11<0.1%Rapid weight gain, especially with central distribution; proximal muscle weakness; depression; hyperglycemiaCentral obesity, “moon” face, dorsal and supraclavicular fat pads, wide (1-cm) violaceous striae, hirsutismOvernight 1-mg dexamethasone suppression test24-h urinary free cortisol excretion (preferably multiple); midnight salivary cortisol
     HypothyroidismS5.1-9<1%Dry skin; cold intolerance; constipation; hoarseness; weight gainDelayed ankle reflex; periorbital puffiness; coarse skin; cold skin; slow movement; goiterThyroid-stimulating hormone; free thyroxineNone
     HyperthyroidismS5.1-9<1%Warm, moist skin; heat intolerance; nervousness; tremulousness; insomnia; weight loss; diarrhea; proximal muscle weaknessLid lag; fine tremor of the outstretched hands; warm, moist skinThyroid-stimulating hormone; free thyroxineRadioactive iodine uptake and scan
     Aortic coarctation (undiagnosed or repaired)S5.1-120.1%Young patient with hypertension (<30 y of age)BP higher in upper extremities than in lower extremities; absent femoral pulses; continuous murmur over patient’s back, chest, or abdominal bruit; left thoracotomy scar (postoperative)EchocardiogramThoracic and abdominal CT angiogram or MRA
     Primary hyperparathyroidismS5.1-13RareHypercalcemiaUsually noneSerum calciumSerum parathyroid hormone
     Congenital adrenal hyperplasiaS5.1-14RareHypertension and hypokalemia; virilization (11-beta-hydroxylase deficiency [11-beta-OH]); incomplete masculinization in males and primary amenorrhea in females (17-alpha-hydroxylase deficiency [17-alpha-OH])Signs of virilization (11-beta-OH) or incomplete masculinization (17-alpha-OH)Hypertension and hypokalemia with low or normal aldosterone and renin11-beta-OH: elevated deoxycorticosterone (DOC), 11-deoxycortisol, and androgens17-alpha-OH; decreased androgens and estrogen; elevated deoxycorticosterone and corticosterone
     Mineralocorticoid excess syndromes other than primary aldosteronismS5.1-14RareEarly-onset hypertension; resistant hypertension; hypokalemia or hyperkalemiaArrhythmias (with hypokalemia)Low aldosterone and reninUrinary cortisol metabolites; genetic testing
     AcromegalyS5.1-15RareAcral features, enlarging shoe, glove, or hat size; headache, visual disturbances; diabetes mellitusAcral features; large hands and feet; frontal bossingSerum growth hormone ≥1 ng/mL during oral glucose loadElevated age- and sex-matched IGF-1 level; MRI scan of the pituitary

    *Depending on the clinical situation (hypertension alone, 5%; hypertension starting dialysis, 22%; hypertension and peripheral vascular disease, 28%; hypertension in the elderly with congestive heart failure, 34%).

    †8% in general population with hypertension; up to 20% in patients with resistant hypertension.

    ‡Although obstructive sleep apnea is listed as a cause of secondary hypertension, RCTs on the effects of continuous positive airway pressure on lowering BP in patients with hypertension have produced mixed results (see Section 5.4.4 for details).

    §For a list of frequently used drugs causing hypertension and accompanying evidence, see Table 14.

    BP indicates blood pressure; CT, computed tomography; DOC, 11-deoxycorticosterone; IGF-1, insulin-like growth factor-1; IV, intravenous; MAO, monamine oxidase; MRI, magnetic resonance imaging; MRA, magnetic resonance arteriography; NSAIDs, nonsteroidal anti-inflammatory drugs; OH, hydroxylase; and RCT, randomized clinical trial.

    Table 14. Frequently Used Medications and Other Substances That May Cause Elevated BP*

    AgentPossible Management Strategy
    AlcoholLimit alcohol to ≤1 drink daily for women and ≤2 drinks for menS5.1.1-1
    Amphetamines (eg, amphetamine, methylphenidate dexmethylphenidate, dextroamphetamine)Discontinue or decrease doseS5.1.1-2
    Consider behavioral therapies for ADHDS5.1.1-3
    Antidepressants (eg, MAOIs, SNRIs, TCAs)Consider alternative agents (eg, SSRIs) depending on indication
    Avoid tyramine-containing foods with MAOIs
    Atypical antipsychotics (eg, clozapine, olanzapine)Discontinue or limit use when possible
    Consider behavior therapy where appropriate
    Recommend lifestyle modification (see Section 6.2)
    Consider alternative agents associated with lower risk of weight gain, diabetes mellitus, and dyslipidemia (eg, aripiprazole, ziprasidone)S5.1.1-4,S5.1.1-5
    CaffeineGenerally limit caffeine intake to <300 mg/d
    Avoid use in patients with uncontrolled hypertension
    Coffee use in patients with hypertension is associated with acute increases in BP; long-term use is not associated with increased BP or CVDS5.1.1-6
    Decongestants (eg, phenylephrine, pseudoephedrine)Use for shortest duration possible, and avoid in severe or uncontrolled hypertension
    Consider alternative therapies (eg, nasal saline, intranasal corticosteroids, antihistamines) as appropriate
    Herbal supplements (eg, Ma Huang [ephedra], St. John’s wort [with MAO inhibitors, yohimbine])Avoid use
    Immunosuppressants (eg, cyclosporine)Consider converting to tacrolimus, which may be associated with fewer effects on BPS5.1.1-7–S5.1.1-9
    Oral contraceptivesUse low-dose (eg, 20–30 mcg ethinyl estradiol) agentsS5.1.1-10 or a progestin-only form of contraception, or consider alternative forms of birth control where appropriate (eg, barrier, abstinence, IUD)
    Avoid use in women with uncontrolled hypertensionS5.1.1-10
    NSAIDsAvoid systemic NSAIDs when possible
    Consider alternative analgesics (eg, acetaminophen, tramadol, topical NSAIDs), depending on indication and risk
    Recreational drugs (eg, “bath salts” [MDPV], cocaine, methamphetamine, etc.)Discontinue or avoid use
    Systemic corticosteroids (eg, dexamethasone, fludrocortisone, methylprednisolone, prednisone, prednisolone)Avoid or limit use when possible
    Consider alternative modes of administration (eg, inhaled, topical) when feasible
    Angiogenesis inhibitor (eg, bevacizumab) and tyrosine kinase inhibitors (eg, sunitinib, sorafenib)Initiate or intensify antihypertensive therapy

    *List is not all inclusive.

    ADHD indicates attention-deficit/hyperactivity disorder; BP, blood pressure; CVD, cardiovascular disease; IUD, intra-uterine device; MAOI, monoamine-oxidase inhibitors; MDPV, methylenedioxypyrovalerone; NSAIDs, nonsteroidal anti-inflammatory drugs; SNRI, serotonin norepinephrine reuptake inhibitor; SSRI, selective serotonin reuptake inhibitor; and TCA, tricyclic antidepressant.

    Figure 1.

    Figure 1. Detection of white coat hypertension or masked hypertension in patients not on drug therapy. Colors correspond to Class of Recommendation in Table 1. ABPM indicates ambulatory blood pressure monitoring; BP, blood pressure; and HBPM, home blood pressure monitoring.

    Figure 2.

    Figure 2. Detection of white coat effect or masked uncontrolled hypertension in patients on drug therapy. Colors correspond to Class of Recommendation in Table 1. See Section 8 for treatment options. ABPM indicates ambulatory blood pressure monitoring; BP, blood pressure; CVD, cardiovascular disease; and HBPM, home blood pressure monitoring.

    5. Causes of Hypertension

    5.1. Secondary Forms of Hypertension

    Figure 3.

    Figure 3. Screening for secondary hypertension. Colors correspond to Class of Recommendation in Table 1. TOD indicates target organ damage (eg, cerebrovascular disease, hypertensive retinopathy, left ventricular hypertrophy, left ventricular dysfunction, heart failure, coronary artery disease, chronic kidney disease, albuminuria, peripheral artery disease).

    5.1.1. Drugs and Other Substances With Potential to Impair BP Control
    5.1.2. Primary Aldosteronism
    5.1.3. Renal Artery Stenosis
    5.1.4. Obstructive Sleep Apnea

    6. Nonpharmacological Interventions

    Table 15. Best Proven Nonpharmacological Interventions for Prevention and Treatment of Hypertension*

    Nonpharmacological InterventionDoseApproximate Impact on SBP
    HypertensionNormotensionReference
    Weight lossWeight/body fatBest goal is ideal body weight, but aim for at least a 1-kg reduction in body weight for most adults who are overweight. Expect about 1 mm Hg for every 1-kg reduction in body weight.−5 mm Hg−2/3 mm HgS6-1
    Healthy dietDASH dietary patternConsume a diet rich in fruits, vegetables, whole grains, and low-fat dairy products, with reduced content of saturated and total fat.−11 mm Hg−3 mm HgS6-6,S6-7
    Reduced intake of dietary sodiumDietary sodiumOptimal goal is <1500 mg/d, but aim for at least a 1000-mg/d reduction in most adults.−5/6 mm Hg−2/3 mm HgS6-9,S6-10
    Enhanced intake of dietary potassiumDietary potassiumAim for 3500–5000 mg/d, preferably by consumption of a diet rich in potassium.−4/5 mm Hg−2 mm HgS6-13
    Physical activityAerobic90–150 min/wk
    65%–75% heart rate reserve
    −5/8 mm Hg−2/4 mm HgS6-18,S6-22
    Dynamic resistance90–150 min/wk
    50%–80% 1 rep maximum
    6 exercises, 3 sets/exercise, 10 repetitions/set
    −4 mm Hg−2 mm HgS6-18
    Isometric resistance4 × 2 min (hand grip), 1 min rest between exercises, 30%–40% maximum voluntary contraction, 3 sessions/wk
    8–10 wk
    −5 mm Hg−4 mm HgS6-19,S6-30
    Moderation in alcohol intakeAlcohol consumptionIn individuals who drink alcohol, reduce alcohol to:
    Men: ≤2 drinks daily
    Women: ≤1 drink daily
    −4 mm Hg−3 mm HgS6-22–S6-24

    Resources: Your Guide to Lowering Your Blood Pressure With DASH—How Do I Make the DASH? Available at: https://www.nhlbi.nih.gov/health/resources/heart/hbp-dash-how-to. Accessed September 15, 2017.S6-31

    Top 10 Dash Diet Tips. Available at: http://dashdiet.org/dash_diet_tips.asp. Accessed September 15, 2017.S6-32

    *Type, dose, and expected impact on BP in adults with a normal BP and with hypertension.

    †In the United States, one “standard” drink contains roughly 14 g of pure alcohol, which is typically found in 12 oz of regular beer (usually about 5% alcohol), 5 oz of wine (usually about 12% alcohol), and 1.5 oz of distilled spirits (usually about 40% alcohol).S6-29

    DASH indicates Dietary Approaches to Stop Hypertension; and SBP, systolic blood pressure.

    7. Patient Evaluation

    Table 16. Historical Features Favoring Hypertension Cause

    Primary HypertensionSecondary Hypertension
    Gradual increase in BP, with slow rate of rise in BPBP lability, episodic pallor and dizziness (pheochromocytoma)
    Lifestyle factors that favor higher BP (eg, weight gain, high-sodium diet, decreased physical activity, job change entailing increased travel, excessive consumption of alcohol)Snoring, hypersomnolence (obstructive sleep apnea)
    Prostatism (chronic kidney disease due to post-renal urinary tract obstruction)
    Family history of hypertensionMuscle cramps, weakness (hypokalemia from primary aldosteronism or secondary aldosteronism due to renovascular disease)
    Weight loss, palpitations, heat intolerance (hyperthyroidism)
    Edema, fatigue, frequent urination (kidney disease or failure)
    History of coarctation repair (residual hypertension associated with coarctation)
    Central obesity, facial rounding, easy bruisability (Cushing's syndrome)
    Medication or substance use (eg, alcohol, NSAIDS, cocaine, amphetamines)
    Absence of family history of hypertension

    BP indicates blood pressure; and NSAIDs, nonsteroidal anti-inflammatory drugs.

    7.1. Laboratory Tests and Other Diagnostic Procedures

    Table 17. Basic and Optional Laboratory Tests for Primary Hypertension

    Basic testingFasting blood glucose*
    Complete blood count
    Lipid profile
    Serum creatinine with eGFR*
    Serum sodium, potassium, calcium*
    Thyroid-stimulating hormone
    Urinalysis
    Electrocardiogram
    Optional testingEchocardiogram
    Uric acid
    Urinary albumin to creatinine ratio

    *May be included in a comprehensive metabolic panel.

    eGFR indicates estimated glomerular filtration rate.

    8. Treatment of High BP

    8.1. Pharmacological Treatment

    8.1.1. Initiation of Pharmacological BP Treatment in the Context of Overall CVD Risk

    For any specific difference in BP, the relative risk of CVD is constant across groups that differ in absolute risk of atherosclerotic CVD,S8.1.1-1–S8.1.1-4 albeit with some evidence of lesser relative risk but greater excess risk in older than in younger adults.S8.1.1-5–S8.1.1-8 Thus, there are more potentially preventable CVD events attributable to elevated BP in individuals with higher than with lower risk of CVD and in older than in younger adults. The relative risk reduction for CVD prevention with use of BP-lowering medications is fairly constant for groups that differ in CVD risk across a wide range of estimated absolute risk S8.1.1-9,S8.1.1-10 and across groups defined by sex, age, body mass index, and the presence or absence of DM, AF, and CKD.S8.1.1-5,S8.1.1-11–S8.1.1-21 As a consequence, the absolute CVD risk reduction attributable to BP lowering is greater at greater absolute levels of CVD risk.S8.1.1-9,S8.1.1-10,S8.1.1-12,S8.1.1-15–S8.1.1-19,S8.1.1-22,S8.1.1-23 Put another way, for a given magnitude of BP reduction due to antihypertensive medications, fewer individuals at high CVD risk would need to be treated to prevent a CVD event (ie, lower number needed to treat) than those at low CVD risk.

    8.1.2. BP Treatment Threshold and the Use of CVD Risk Estimation to Guide Drug Treatment of Hypertension
    8.1.3. Follow-Up After Initial BP Evaluation
    8.1.4. General Principles of Drug Therapy

    Table 18. Oral Antihypertensive Drugs

    ClassDrugUsual Dose, Range (mg/d)*Daily FrequencyComments
    Primary agents
     Thiazide or thiazide-type diureticsChlorthalidone12.5–251Chlorthalidone is preferred on the basis of prolonged half-life and proven trial reduction of CVD.
    Monitor for hyponatremia and hypokalemia, uric acid and calcium levels.
    Use with caution in patients with history of acute gout unless patient is on uric acid–lowering therapy.
    Hydrochlorothiazide25–501
    Indapamide1.25–2.51
    Metolazone2.5–51
     ACE inhibitorsBenazepril10–401 or 2Do not use in combination with ARBs or direct renin inhibitor.
    There is an increased risk of hyperkalemia, especially in patients with CKD or in those on K+ supplements or K+-sparing drugs.
    There is a risk of acute renal failure in patients with severe bilateral renal artery stenosis.
    Do not use if patient has history of angioedema with ACE inhibitors.
    Avoid in pregnancy.
    Captopril12.5–1502 or 3
    Enalapril5–401 or 2
    Fosinopril10–401
    Lisinopril10–401
    Moexipril7.5–301 or 2
    Perindopril4–161
    Quinapril10–801 or 2
    Ramipril2.5–201 or 2
    Trandolapril1–41
     ARBsAzilsartan40–801Do not use in combination with ACE inhibitors or direct renin inhibitor.
    There is an increased risk of hyperkalemia in CKD or in those on K+ supplements or K+-sparing drugs.
    There is a risk of acute renal failure in patients with severe bilateral renal artery stenosis.
    Do not use if patient has history of angioedema with ARBs. Patients with a history of angioedema with an ACE inhibitor can receive an ARB beginning 6 weeks after ACE inhibitor is discontinued.
    Avoid in pregnancy.
    Candesartan8–321
    Eprosartan600–8001 or 2
    Irbesartan150–3001
    Losartan50–1001 or 2
    Olmesartan20–401
    Telmisartan20–801
    Valsartan80–3201
     CCB—dihydropyridinesAmlodipine2.5–101Avoid use in patients with HFrEF; amlodipine or felodipine may be used if required.
    They are associated with dose-related pedal edema, which is more common in women than men.
    Felodipine2.5–101
    Isradipine5–102
    Nicardipine SR60–1202
    Nifedipine LA30–901
    Nisoldipine17–341
     CCB—nondihydropyridinesDiltiazem ER120–3601Avoid routine use with beta blockers because of increased risk of bradycardia and heart block.
    Do not use in patients with HFrEF.
    There are drug interactions with diltiazem and verapamil (CYP3A4 major substrate and moderate inhibitor).
    Verapamil IR120-3603
    Verapamil SR120–3601 or 2
    Verapamil-delayed onset ER100–3001 (in the evening)
    Secondary agents
     Diuretics—loopBumetanide0.5–22These are preferred diuretics in patients with symptomatic HF. They are preferred over thiazides in patients with moderate-to-severe CKD (eg, GFR <30 mL/min).
    Furosemide20–802
    Torsemide5–101
     Diuretics—potassium sparingAmiloride5–101 or 2These are monotherapy agents and minimally effective antihypertensive agents.
    Combination therapy of potassium-sparing diuretic with a thiazide can be considered in patients with hypokalemia on thiazide monotherapy.
    Avoid in patients with significant CKD (eg, GFR <45 mL/min).
    Triamterene50–1001 or 2
     Diuretics—aldosterone antagonistsEplerenone50–1001 or 2These are preferred agents in primary aldosteronism and resistant hypertension.
    Spironolactone is associated with greater risk of gynecomastia and impotence as compared with eplerenone.
    This is common add-on therapy in resistant hypertension.
    Avoid use with K+ supplements, other K+-sparing diuretics, or significant renal dysfunction.
    Eplerenone often requires twice-daily dosing for adequate BP lowering.
    Spironolactone25–1001
     Beta blockers—cardioselectiveAtenolol25–1002Beta blockers are not recommended as first-line agents unless the patient has IHD or HF.
    These are preferred in patients with bronchospastic airway disease requiring a beta blocker.
    Bisoprolol and metoprolol succinate are preferred in patients with HFrEF.
    Avoid abrupt cessation.
    Betaxolol5–201
    Bisoprolol2.5–101
    Metoprolol tartrate100–2002
    Metoprolol succinate50–2001
     Beta blockers—cardioselective and vasodilatoryNebivolol5–401Nebivolol induces nitric oxide–induced vasodilation.
    Avoid abrupt cessation.
     Beta blockers—noncardioselectiveNadolol40–1201Avoid in patients with reactive airways disease.
    Avoid abrupt cessation.
    Propranolol IR80–1602
    Propranolol LA80–1601
     Beta blockers—intrinsic sympathomimetic activityAcebutolol200–8002Generally avoid, especially in patients with IHD or HF.
    Avoid abrupt cessation.
    Penbutolol10–401
    Pindolol10–602
     Beta blockers—combined alpha- and beta-receptorCarvedilol12.5–502Carvedilol is preferred in patients with HFrEF.
    Avoid abrupt cessation.
    Carvedilol phosphate20–801
    Labetalol200–8002
     Direct renin inhibitorAliskiren150–3001Do not use in combination with ACE inhibitors or ARBs.
    Aliskiren is very long acting.
    There is an increased risk of hyperkalemia in CKD or in those on K+ supplements or K+-sparing drugs.
    Aliskiren may cause acute renal failure in patients with severe bilateral renal artery stenosis.
    Avoid in pregnancy.
     Alpha-1 blockersDoxazosin1–161These are associated with orthostatic hypotension, especially in older adults.
    They may be considered as second-line agent in patients with concomitant BPH.
    Prazosin2–202 or 3
    Terazosin1–201 or 2
     Central alpha2-agonist and other centrally acting drugsClonidine oral0.1–0.82These are generally reserved as last-line because of significant CNS adverse effects, especially in older adults.
    Avoid abrupt discontinuation of clonidine, which may induce hypertensive crisis; clonidine must be tapered to avoid rebound hypertension.
    Clonidine patch0.1–0.31 weekly
    Methyldopa250–10002
    Guanfacine0.5–21
     Direct vasodilatorsHydralazine100-2002 or 3These are associated with sodium and water retention and reflex tachycardia; use with a diuretic and beta blocker.
    Hydralazine is associated with drug-induced lupus-like syndrome at higher doses.
    Minoxidil is associated with hirsutism and requires a loop diuretic. Minoxidil can induce pericardial effusion.
    Minoxidil5–1001-3

    *Dosages may vary from those listed in the FDA-approved labeling (available at https://dailymed.nlm.nih.gov/dailymed/). From Chobanian et al JNC 7.S8.1.4-4

    ACE indicates angiotensin-converting enzyme; ARB, angiotensin receptor blocker; BP, blood pressure; BPH, benign prostatic hyperplasia; CCB, calcium channel blocker; CKD, chronic kidney disease; CNS, central nervous system; CVD, cardiovascular disease; ER, extended release; GFR, glomerular filtration rate; HF, heart failure; HFrEF, heart failure with reduced ejection fraction; IHD, ischemic heart disease; IR, immediate release; LA, long-acting; and SR, sustained release.

    8.1.5. BP Goal for Patients With Hypertension
    8.1.6. Choice of Initial Medication
    8.1.6.1. Choice of Initial Monotherapy Versus Initial Combination Drug Therapy

    8.2. Follow-Up of BP During Antihypertensive Drug Therapy

    Appropriate follow-up and monitoring enable assessment of adherence (see Section 12.1) and response to therapy, help identify adverse responses to therapy and target organ damage, and allow assessment of progress toward treatment goals. High-quality RCTs have successfully and safely developed strategies for follow-up, monitoring, and reassessment from which recommendations can be made (Figure 4).S8.2-1,S8.2-2 A systematic approach to out-of-office BP assessment is an essential part of follow-up and monitoring of BP, to assess response to therapy; check for evidence of white coat hypertension, white coat effect, masked hypertension, or masked uncontrolled hypertension; and help achieve BP targets (see Sections 4 and 12).

    Figure 4.

    Figure 4. Blood Pressure (BP) thresholds and recommendations for treatment and follow-up. Colors correspond to Class of Recommendation in Table 1. *Using the ACC/AHA Pooled Cohort Equations.S8.1.2-14,S8.1.2-15 Note that patients with DM or CKD are automatically placed in the high-risk category. For initiation of RAS inhibitor or diuretic therapy, assess blood tests for electrolytes and renal function 2 to 4 weeks after initiating therapy. †Consider initiation of pharmacological therapy for stage 2 hypertension with 2 antihypertensive agents of different classes. Patients with stage 2 hypertension and BP ≥160/100 mm Hg should be promptly treated, carefully monitored, and subject to upward medication dose adjustment as necessary to control BP. Reassessment includes BP measurement, detection of orthostatic hypotension in selected patients (eg, older or with postural symptoms), identification of white coat hypertension or a white coat effect, documentation of adherence, monitoring of the response to therapy, reinforcement of the importance of adherence, reinforcement of the importance of treatment, and assistance with treatment to achieve BP target. ACC indicates American College of Cardiology; AHA, American Heart Association; ASCVD, atherosclerotic cardiovascular disease; BP, blood pressure; CKD, chronic kidney disease; DM, diabetes mellitus; and RAS, renin-angiotensin system.

    8.2.1. Follow-Up After Initiating Antihypertensive Drug Therapy
    8.2.2. Monitoring Strategies to Improve Control of BP in Patients on Drug Therapy for High BP

    9. Hypertension in Patients With Comorbidities

    Certain comorbidities may affect clinical decision-making in hypertension. These include ischemic heart disease, HF with reduced ejection fraction (HFrEF), HFpEF, CKD (including renal transplantation), cerebrovascular disease, AF, PAD, DM, and metabolic syndrome.S9-1 As noted in Section 8.1.2, this guideline generally recommends use of BP-lowering medications for secondary prevention of CVD in patients with clinical CVD (CHD, HF, and stroke) and an average BP ≥130/80 mm Hg and for primary prevention of CVD in adults with an estimated 10-year ASCVD risk of ≥10% and an average SBP ≥130 mm Hg or an average DBP ≥80 mm Hg. Although we recommend use of the ACC/AHA Pooled Cohort Equations (http://tools.acc.org/ASCVD-Risk-Estimator/) to estimate 10-year risk of ASCVD to establish the BP threshold for treatment, the vast majority of adults with a co-morbidity are likely to have a 10-year risk of ASCVD that exceeds 10%. In some instances, clinical trial confirmation of treatment in patients with comorbidities is limited to a target BP of 140/90 mm Hg. In addition, the selection of medications for use in treating high BP in patients with CVD is guided by their use for other compelling indications (eg, beta blockers after MI, ACE inhibitors for HFrEF), as discussed in specific guidelines for the clinical condition.S9-2–S9-4 The present guideline does not address the recommendations for treatment of hypertension occurring with acute coronary syndromes.

    9.1. Stable Ischemic Heart Disease

    Figure 5.

    Figure 5. Management of hypertension in patients with SIHD. Colors correspond to Class of Recommendation in Table 1. *GDMT beta blockers for BP control or relief of angina include carvedilol, metoprolol tartrate, metoprolol succinate, nadolol, bisoprolol, propranolol, and timolol. Avoid beta blockers with intrinsic sympathomimetic activity. The beta blocker atenolol should not be used because it is less effective than placebo in reducing cardiovascular events. †If needed for BP control. ACE indicates angiotensin-converting enzyme; ARB, angiotensin receptor blocker; BP, blood pressure; CCB, calcium channel blocker; GDMT, guideline-directed management and therapy; and SIHD, stable ischemic heart disease.

    9.2. Heart Failure

    9.2.1. Heart Failure With Reduced Ejection Fraction
    9.2.2. Heart Failure With Preserved Ejection Fraction

    9.3. Chronic Kidney Disease

    Figure 6.

    Figure 6. Management of hypertension in patients with CKD. Colors correspond to Class of Recommendation in Table 1. *CKD stage 3 or higher or stage 1 or 2 with albuminuria ≥300 mg/d or ≥300 mg/g creatinine. ACE indicates angiotensin-converting enzyme; ARB, angiotensin receptor blocker; BP, blood pressure; and CKD, chronic kidney disease.

    Figure 7.

    Figure 7. Management of hypertension in patients with acute ICH. Colors correspond to Class of Recommendation in Table 1. BP indicates blood pressure; ICH, intracerebral hemorrhage; IV, intravenous; and SBP, systolic blood pressure.

    9.3.1. Hypertension After Renal Transplantation

    9.4. Cerebrovascular Disease

    9.4.1. Acute Intracerebral Hemorrhage
    9.4.2. Acute Ischemic Stroke
    Figure 8.

    Figure 8. Management of hypertension in patients with acute ischemic stroke. Colors correspond to Class of Recommendation in Table 1. BP indicates blood pressure; DBP, diastolic blood pressure; IV, intravenous; and SBP, systolic blood pressure.

    9.4.3. Secondary Stroke Prevention
    Figure 9.

    Figure 9. Management of hypertension in patients with a previous history of stroke (secondary stroke prevention). Colors correspond to Class of Recommendation in Table 1. DBP indicates diastolic blood pressure; SBP, systolic blood pressure; and TIA, transient ischemic attack.

    9.5. Peripheral Artery Disease

    9.6. Diabetes Mellitus

    9.7. Metabolic Syndrome

    Metabolic syndrome is a state of metabolic dysregulation characterized by visceral fat accumulation, insulin resistance, hyperinsulinemia, and hyperlipidemia, as well as predisposition to type 2 DM, hypertension, and atherosclerotic CVD.S9.7-1–S9.7-3 According to data from the NHANES III and NHANES 1999–2006,S9.7-1,S9.7-4 the prevalence of metabolic syndrome in the United States was 34.2% in 2006 and has likely increased substantially since that time. The metabolic syndrome is linked to several other disorders, including nonalcoholic steatohepatitis, polycystic ovary syndrome, certain cancers, CKD, Alzheimer’s disease, Cushing’s syndrome, lipodystrophy, and hyperalimentation.S9.7-5,S9.7-6

    Lifestyle modification, with an emphasis on improving insulin sensitivity by means of dietary modification, weight reduction, and exercise, is the foundation of treatment of the metabolic syndrome. The optimal antihypertensive drug therapy for patients with hypertension in the setting of the metabolic syndrome has not been clearly defined.S9.7-1 Although caution exists with regard to the use of thiazide diuretics in this population because of their ability to increase insulin resistance, dyslipidemia, and hyperuricemia and to accelerate conversion to overt DM, no data are currently available demonstrating deterioration in cardiovascular or renal outcomes in patients treated with these agents.S9.7-1 Indeed, as shown in follow-up of ALLHAT, chlorthalidone use was associated with only a small increase in fasting glucose levels (1.5–4.0 mg/dL), and this increase did not translate into increased CVD risk at a later date.S9.7-7–S9.7-10 In addition, in post hoc analysis of the nearly two thirds of participants in ALLHAT that met criteria for the metabolic syndrome, chlorthalidone was unsurpassed in reducing CVD and renal outcomes compared with lisinopril, amlodipine, or doxazosin.S9.7-9,S9.7-11 Similarly, high-dose ARB therapy reduces arterial stiffness in patients with hypertension with the metabolic syndrome, but no outcomes data are available from patients in which this form of treatment was used.S9.7-12 Use of traditional beta blockers may lead to dyslipidemia or deterioration of glucose tolerance, and ability to lose weight.S9.7-2 In several large clinical trials, the risk of developing DM as a result of traditional beta-blocker therapy was 15% to 29%.S9.7-2 However, the newer vasodilating beta blockers (eg, labetalol, carvedilol, nebivolol) have shown neutral or favorable effects on metabolic profiles compared with the traditional beta blockers.S9.7-13 Trials using vasodilator beta blockers have not been performed to demonstrate effects on CVD outcomes.

    9.8. Atrial Fibrillation

    9.9. Valvular Heart Disease

    9.10. Aortic Disease

    10. Special Patient Groups

    Special attention is needed for specific patient subgroups.

    10.1.1. Racial and Ethnic Differences in Treatment

    10.2. Sex-Related Issues

    The prevalence of hypertension is lower in women than in men until about the fifth decade but is higher later in life.S10.2-1 Other than special recommendations for management of hypertension during pregnancy, there is no evidence that the BP threshold for initiating drug treatment, the treatment target, the choice of initial antihypertensive medication, or the combination of medications for lowering BP differs for women versus men.S10.2-2,S10.2-3

    10.2.1. Women

    A potential limitation of RCTs, including SPRINT, is that they are not specifically powered to determine the value of intensive SBP reduction in subgroups, including women in the case of SPRINT. However, in prespecified analyses, there was no evidence of an interaction between sex and treatment effect. Furthermore, no significant differences in CVD outcomes were observed between men and women in a large meta-analysis that included 31 RCTs with about 100 000 men and 90 000 women with hypertension (1 Some have called for conduct of a SPRINT-like trial with sufficient power to assess the effects of intensive SBP reduction in women {Wenger, 2016 #9131). Some have called for a SPRINT-like trial with sufficient power to assess the effects of intensive SBP reduction in women.S10.2.1-2 In meta-analyses, there was no convincing evidence that different antihypertensive drug classes exerted sex-related differences in BP lowering or provided distinct CVD protection.S10.2.1-1 Calcium antagonists offered slightly greater benefits for stroke prevention than did ACE inhibitors for women than for men, whereas calcium antagonists reduced all-cause deaths compared with placebo in men but not in women. However, these sex-related differences might have been due to chance because of the large number of statistical comparisons that were performed. The Heart Attack Trial and Hypertension Care Computing Project reported that beta blockers were associated with reduced mortality in men but not in women, but this finding was likely due to the low event rates in women.S10.2.1-3 Similarly, in the open-label Second Australian National BP study, a significant reduction in CVD events was demonstrated in men but not in women with ACE inhibitors versus diuretics.S10.2.1-4

    Adverse effects of antihypertensive therapy were noted twice as often in women as in men in the TOMHS study.S10.2.1-5 A higher incidence of ACE inhibitor–induced cough and of edema with calcium antagonists was observed in women than in men.S10.2.1-6 Women were more likely to experience hypokalemia and hyponatremia and less likely to experience gout with diuretics.S10.2.1-7 Hypertension in pregnancy has special requirements (see Section 10.2.2).

    10.2.2. Pregnancy

    10.3. Age-Related Issues

    10.3.1. Older Persons

    11. Other Considerations

    11.1. Resistant Hypertension

    Figure 10.

    Figure 10. Resistant hypertension: diagnosis, evaluation, and treatment. *See additional details in Section 6, Nonpharmacological Intervention. †See Section 5.4.1 and Table 14 for complete list of drugs that elevate BP. ‡See Section 5.4 and Table 13 for secondary hypertension. BP indicates blood pressure; CKD, chronic kidney disease; DBP, diastolic blood pressure; eGFR, estimated glomerular filtration rate; NSAIDs, nonsteroidal anti-inflammatory drugs; and SBP, systolic blood pressure. Adapted with permission from Calhoun et alS11.1-1 (American Heart Association, Inc.).

    11.2. Hypertensive Crises—Emergencies and Urgencies

    Figure 11.

    Figure 11. Diagnosis and management of a hypertensive crisis. Colors correspond to Class of Recommendation in Table 1. *Use drug(s) specified in Table 19. †If other comorbidities are present, select a drug specified in Table 20. BP indicates blood pressure; DBP, diastolic blood pressure; ICU, intensive care unit; and SBP, systolic blood pressure.

    Table 19. Intravenous Antihypertensive Drugs for Treatment of Hypertensive Emergencies

    ClassDrug(s)Usual Dose RangeComments
    CCB—dihydropyridinesNicardipineInitial 5 mg/h, increasing every 5 min by 2.5 mg/h to maximum 15 mg/h.Contraindicated in advanced aortic stenosis; no dose adjustment needed for elderly.
    ClevidipineInitial 1–2 mg/h, doubling every 90 s until BP approaches target, then increasing by less than double every 5–10 min; maximum dose 32 mg/h; maximum duration 72 h.Contraindicated in patients with soybean, soy product, egg, and egg product allergy and in patients with defective lipid metabolism (eg, pathological hyperlipidemia, lipoid nephrosis or acute pancreatitis). Use low-end dose range for elderly patients.
    Vasodilators—Nitric-oxide dependentSodium nitroprussideInitial 0.3–0.5 mcg/kg/min; increase in increments of 0.5 mcg/kg/min to achieve BP target; maximum dose 10 mcg/kg/min; duration of treatment as short as possible. For infusion rates ≥4–10 mcg/kg/min or duration >30 min, thiosulfate can be coadministered to prevent cyanide toxicity.Intra-arterial BP monitoring recommended to prevent “overshoot.” Lower dosing adjustment required for elderly. Tachyphylaxis common with extended use.
    Cyanide toxicity with prolonged use can result in irreversible neurological changes and cardiac arrest.
    NitroglycerinInitial 5 mcg/min; increase in increments of 5 mcg/min every 3–5 min to a maximum of 20 mcg/min.Use only in patients with acute coronary syndrome and/or acute pulmonary edema. Do not use in volume-depleted patients.
    Vasodilators—directHydralazineInitial 10 mg via slow IV infusion (maximum initial dose 20 mg); repeat every 4–6 h as needed.BP begins to decrease within 10–30 min, and the fall lasts 2–4 h. Unpredictability of response and prolonged duration of action do not make hydralazine a desirable first-line agent for acute treatment in most patients.
    Adrenergic blockers—beta1 receptor selective antagonistEsmololLoading dose 500–1000 mcg/kg/min over 1 min followed by a 50-mcg/kg/min infusion. For additional dosing, the bolus dose is repeated and the infusion increased in 50-mcg/kg/min increments as needed to a maximum of 200 mcg/kg/min.Contraindicated in patients with concurrent beta-blocker therapy, bradycardia, or decompensated HF.
    Monitor for bradycardia.
    May worsen HF.
    Higher doses may block beta2 receptors and impact lung function in reactive airway disease.
    Adrenergic blockers—combined alpha1 and nonselective beta receptor antagonistLabetalolInitial 0.3–1.0-mg/kg dose (maximum 20 mg) slow IV injection every 10 min or 0.4–1.0-mg/kg/h IV infusion up to 3 mg/kg/h. Adjust rate up to total cumulative dose of 300 mg. This dose can be repeated every 4–6 h.Contraindicated in reactive airways disease or chronic obstructive pulmonary disease. Especially useful in hyperadrenergic syndromes. May worsen HF and should not be given in patients with second- or third-degree heart block or bradycardia.
    Adrenergic blockers—nonselective alpha receptor antagonistPhentolamineIV bolus dose 5 mg. Additional bolus doses every 10 min as needed to lower BP to target.Used in hypertensive emergencies induced by catecholamine excess (pheochromocytoma, interactions between monamine oxidase inhibitors and other drugs or food, cocaine toxicity, amphetamine overdose, or clonidine withdrawal).
    Dopamine1-receptor selective agonistFenoldopamInitial 0.1–0.3 mcg/kg/min; may be increased in increments of 0.05–0.1 mcg/kg/min every 15 min until target BP is reached. Maximum infusion rate 1.6 mcg/kg/min.Contraindicated in patients at risk of increased intraocular pressure (glaucoma) or intracranial pressure and those with sulfite allergy.
    ACE inhibitorEnalaprilatInitial 1.25 mg over a 5-min period. Doses can be increased up to 5 mg every 6 h as needed to achieve BP target.Contraindicated in pregnancy and should not be used in acute MI or bilateral renal artery stenosis.
    Mainly useful in hypertensive emergencies associated with high plasma renin activity.
    Dose not easily adjusted.
    Relatively slow onset of action (15 min) and unpredictability of BP response.

    BP indicates blood pressure; CCB, calcium channel blocker; HF, heart failure; IV, intravenous; and MI, myocardial infarction.

    Table 20. Intravenous Antihypertensive Drugs for Treatment of Hypertensive Emergencies in Patients With Selected Comorbidities

    ComorbidityPreferred Drug(s)*Comments
    Acute aortic dissectionEsmolol, labetalolRequires rapid lowering of SBP to ≤120 mm Hg.
    Beta blockade should precede vasodilator (eg, nicardipine or nitroprusside) administration, if needed for BP control or to prevent reflex tachycardia or inotropic effect; SBP ≤120 mm Hg should be achieved within 20 min.
    Acute pulmonary edemaClevidipine, nitroglycerin, nitroprussideBeta blockers contraindicated.
    Acute coronary syndromesEsmolol, labetalol, nicardipine, nitroglycerinNitrates given in the presence of PDE-5 inhibitors may induce profound hypotension. Contraindications to beta blockers include moderate-to-severe LV failure with pulmonary edema, bradycardia (<60 bpm), hypotension (SBP <100 mm Hg), poor peripheral perfusion, second- or third-degree heart block, and reactive airways disease.
    Acute renal failureClevidipine, fenoldopam, nicardipineN/A
    Eclampsia or preeclampsiaHydralazine, labetalol, nicardipineRequires rapid BP lowering.
    ACE inhibitors, ARBs, renin inhibitors, and nitroprusside contraindicated.
    Perioperative hypertension (BP ≥160/90 mm Hg or SBP elevation ≥20% of the preoperative value that persists for >15 min)Clevidipine, esmolol, nicardipine, nitroglycerinIntraoperative hypertension is most frequently seen during anesthesia induction and airway manipulation.
    Acute sympathetic discharge or catecholamine excess states (eg, pheochromocytoma, post-carotid endarterectomy status)Clevidipine, nicardipine, phentolamineRequires rapid lowering of BP.
    Acute ICHSection 9.4.1Section 9.4.1
    Acute ischemic strokeSection 9.4.2Section 9.4.2

    *Agents are listed in alphabetical order, not in order of preference.

    †Agent of choice for acute coronary syndromes.

    ACE indicates angiotensin-converting enzyme; ARB, angiotensin receptor blocker; BP, blood pressure; bpm, beats per minute; ICH, intracerebral hemorrhage; LV, left ventricular; PDE-5, phosphodiesterase type-5; and SBP, systolic blood pressure.

    11.3. Cognitive Decline and Dementia

    11.4. Patients Undergoing Surgical Procedures

    12. Strategies to Improve Hypertension Treatment and Control

    12.1. Adherence Strategies for Treatment of Hypertension

    12.1.1. Antihypertensive Medication Adherence Strategies
    12.1.2. Strategies to Promote Lifestyle Modification

    12.2. Structured, Team-Based Care Interventions for Hypertension Control

    12.3. Health Information Technology–Based Strategies to Promote Hypertension Control

    12.3.1. EHR and Patient Registries
    12.3.2. Telehealth Interventions to Improve Hypertension Control

    12.4. Improving Quality of Care for Patients With Hypertension

    12.4.1. Performance Measures
    12.4.2. Quality Improvement Strategies

    12.5. Financial Incentives

    13. The Plan of Care for Hypertension

    Table 21. Clinician’s Sequential Flow Chart for the Management of Hypertension

    Clinician’s Sequential Flow Chart for the Management of Hypertension
    Measure office BP accuratelySection 4
    Detect white coat hypertension or masked hypertension by using ABPM and HBPMSection 4
    Evaluate for secondary hypertensionSection 5
    Identify target organ damageSections 5 and 7
    Introduce lifestyle interventionsSection 6
    Identify and discuss treatment goalsSections 7 and 8
    Use ASCVD risk estimation to guide BP threshold for drug therapySection 8.1.2
    Align treatment options with comorbiditiesSection 9
    Account for age, race, ethnicity, sex, and special circumstances in antihypertensive treatmentSections 10 and 11
    Initiate antihypertensive pharmacological therapySection 8
    Insure appropriate follow-upSection 8
    Use team-based careSection 12
    Connect patient to clinician via telehealthSection 12
    Detect and reverse nonadherenceSection 12
    Detect white coat effect or masked uncontrolled hypertensionSection 4
    Use health information technology for remote monitoring and self-monitoring of BPSection 12

    ABPM indicates ambulatory blood pressure monitoring; ASCVD, atherosclerotic cardiovascular disease; BP, blood pressure; and HBPM, home blood pressure monitoring.

    13.1. Health Literacy

    Communicating alternative behaviors that support self-management of healthy BP in addition to medication adherence is important. This should be done both verbally and in writing. Today, mobile phones have a recording option. For patients with mobile phones, the phone can be used to inform patients and family members of medical instructions after the doctor’s visit as an additional level of communication. Inclusion of a family member or friend that can help interpret and encourage self-management treatment goals is suggested when appropriate. Examples of needed communication for alternative behaviors include a specific regimen relating to physical activity; a specific sodium-reduced meal plan indicating selections for breakfast, lunch, and dinner; lifestyle recommendations relating to sleep, rest, and relaxation; and finally, suggestions and alternatives to environmental barriers, such as barriers that prevent healthy food shopping or limit reliable transportation to and from appointments with health providers and pharmacy visits.

    13.2. Access to Health Insurance and Medication Assistance Plans

    Health insurance and medication plan assistance for patients is especially important to improving access to and affordability of medical care and BP medications. Learning how the patient financially supports and budgets for his or her medical care and medications offers the opportunity to share additional insight relating to cost reductions, including restructured payment plans. Ideally, this would improve the patient’s compliance with medication adherence and treatment goals.

    13.3. Social and Community Services

    Health care can be strengthened through local partnerships. Hypertensive patients, particularly patients with lower incomes, have more opportunity to achieve treatment goals with the assistance of strong local partnerships. In patients with low socioeconomic status or patients who are challenged by social situations, integration of social and community services offers complementary reinforcement of clinically identified treatment goals. Social and community services are helpful when explicitly related to medical care. However, additional financial support and financial services are incredibly beneficial to patients, some of whom may choose to skip a doctor’s appointment to pay a residential utility bill.

    Table 22. Evidence-Based Elements of the Plan of Care for Patients With Hypertension

    Plan of CareAssociated Section(s) of Guideline and Other Reference(s)
    Pharmacological and nonpharmacological treatments
     Medication selection (initial and ongoing)Section 8.1
     Monitoring for adverse effects and adherenceSections 8.3.1, 8.3.2, 12.1.1
     Nonpharmacological interventions
      Diet
      Exercise
      Weight loss if overweight
      Moderate alcohol consumption
    Sections 6, 12.1.2S13-1
    Management of common comorbidities and conditions
     Ischemic heart diseaseSection 9.1S13-2,S13-3
     Heart failure
      Reduced ejection fraction
      Preserved ejection fraction
    Section 9.2S13-4
     Diabetes mellitusSection 9.6S13-5
     Chronic kidney diseaseSection 9.3
     Cerebrovascular diseaseSection 9.4
     Peripheral artery diseaseSection 9.5
     Atrial fibrillationSection 9.8
     Valvular heart diseaseSection 9.9
     Left ventricular hypertrophySection 7.3
     Thoracic aortic diseaseSection 9.10
    Patient and family education
     Achieving BP control and self-monitoringSections 4.2, 8.2
     Risk assessment and prognosisSection 8.1.2
     Sexual activity and dysfunctionSection 11.4
    Special patient groups
     PregnancySection 10.2.2
     Older personsSection 10.3.1
     Children and adolescentsSection 10.3.2
     Metabolic syndromeSection 9.7
     Possible secondary causes of hypertensionSection 5.4
     Resistant hypertensionSection 11.1
     Patients with hypertension undergoing surgerySection 11.5
     Renal transplantationSection 9.3.1
    Psychosocial factors
     Sex-specific issuesSection 10.2
     Culturally sensitive issues (race and ethnicity)Section 10.1
     Resource constraintsSection 12.5
    Clinician follow-up, monitoring, and care coordination
     Follow-up visitsSections 8.1.3, 8.3.1, 8.3.2
     Team-based careSection 12.2
     Electronic health recordSection 12.3.1
     Health information technology tools for remote and self-monitoringSection 12.3.2
    Socioeconomic and cultural factors
     Health literacySection 13.1.3
     Access to health insurance and medication assistance plansSection 13.1.3
     Social servicesSection 13.1.3
     Community servicesSection 13.1.3

    BP indicates blood pressure.

    14. Summary of BP Thresholds and Goals for Pharmacological Therapy

    Table 23. BP Thresholds for and Goals of Pharmacological Therapy in Patients With Hypertension According to Clinical Conditions

    Clinical Condition(s)BP Threshold, mm HgBP Goal, mm Hg
    General
     Clinical CVD or 10-year ASCVD risk ≥10%≥130/80<130/80
     No clinical CVD and 10-year ASCVD risk <10%≥140/90<130/80
     Older persons (≥65 years of age; noninstitu tionalized, ambulatory, community-living adults)≥130 (SBP)<130 (SBP)
    Specific comorbidities
     Diabetes mellitus≥130/80<130/80
     Chronic kidney disease≥130/80<130/80
     Chronic kidney disease after renal transplantation≥130/80<130/80
     Heart failure≥130/80<130/80
     Stable ischemic heart disease≥130/80<130/80
     Secondary stroke prevention≥140/90<130/80
     Peripheral artery disease≥130/80<130/80

    ASCVD indicates atherosclerotic cardiovascular disease; BP, blood pressure; CVD, cardiovascular disease; and SBP, systolic blood pressure.

    ACC/AHA TASK FORCE MEMBERS

    Glenn N. Levine, MD, FACC, FAHA, Chair; Patrick T. O’Gara, MD, FAHA, MACC, 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; José 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

    Presidents and Staff

    American College of Cardiology

    Mary Norine Walsh, MD, MACC, President

    Shalom Jacobovitz, Chief Executive Officer

    William J. Oetgen, MD, MBA, FACC, Executive Vice President, Science, Education, Quality, and Publishing

    MaryAnne Elma, MPH, Senior Director, Science, Education, Quality, and Publishing

    Amelia Scholtz, PhD, Publications Manager, Science, Education, Quality, and Publishing

    American College of Cardiology/American Heart Association

    Katherine A. Sheehan, PhD, Director, Guideline Strategy and Operations

    Abdul R. Abdullah, MD, Science and Medicine Advisor

    Naira Tahir, MPH, Associate Guideline Advisor

    American Heart Association

    John J. Warner, MD, President

    Nancy Brown, Chief Executive Officer

    Rose Marie Robertson, MD, FAHA, Chief Science and Medicine Officer

    Gayle R. Whitman, PhD, RN, FAHA, FAAN, Senior Vice President, Office of Science Operations

    Jody Hundley, Manager, Production and Operations, Scientific Publications, Office of Science Operations

    * Former Task Force member; current member during the writing effort.

    Footnotes

    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: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2018;138:e426–e483. DOI: 10.1161/CIR.0000000000000597.

    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 https://www.ahajournals.org/doi/suppl/10.1161/CIR.0000000000000597.

    The online Data Supplement is available with this article at https://www.ahajournals.org/doi/suppl/10.1161/CIR.0000000000000597.

    This article has been copublished in Hypertension and the Journal of the American College of Cardiology.

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    References

      Preamble

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    • 1. Introduction

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    • 2. BP and CVD Risk

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    • 2.2. BP Components

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    • 2.3. Population Risk

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    • 2.4. Coexistence of Hypertension and Related Chronic Conditions

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    • 3. Classification of BP

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    • 3.2. Lifetime Risk of Hypertension

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    • 4. Measurement of BP

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    • 4.2. Out-of-Office and Self-Monitoring of BP

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    • 4.3. Masked and White Coat Hypertension

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    • 5. Causes of Hypertension

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    • 5.1.1. Drugs and Other Substances With Potential to Impair BP Control

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    • 5.1.2. Primary Aldosteronism

    • S5.1.2-1. Montori VM, Young WF. Use of plasma aldosterone concentration-to-plasma renin activity ratio as a screening test for primary aldosteronism. A systematic review of the literature.Endocrinol Metab Clin North Am. 2002; 31:619–32; xi.CrossrefMedlineGoogle Scholar

    • 5.1.3. Renal Artery Stenosis

    • S5.1.3-1. Cooper CJ, Murphy TP, Cutlip DE, et al. Stenting and medical therapy for atherosclerotic renal-artery stenosis.N Engl J Med. 2014; 370:13–22.CrossrefMedlineGoogle Scholar
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    • 5.1.4. Obstructive Sleep Apnea

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    • 6. Nonpharmacological Interventions

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    • 8. Treatment of High BP

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    • 8.1.2. BP Treatment Threshold and the Use of CVD Risk Estimation to Guide Drug Treatment of Hypertension

    • S8.1.2-1. Law MR, Morris JK, Wald NJ. Use of blood pressure lowering drugs in the prevention of cardiovascular disease: meta-analysis of 147 randomised trials in the context of expectations from prospective epidemiological studies.BMJ. 2009; 338:b1665.CrossrefMedlineGoogle Scholar
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    • 8.1.3. Follow-Up After Initial BP Evaluation

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    • 8.1.4. General Principles of Drug Therapy

    • S8.1.4-1. Yusuf S, Teo KK, Pogue J, et al. Telmisartan, ramipril, or both in patients at high risk for vascular events. ONTARGET Investigators.N Engl J Med. 2008; 358:1547–59.CrossrefMedlineGoogle Scholar
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    • 8.1.5. BP Goal for Patients With Hypertension

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    • 8.1.6. Choice of Initial Medication

    • S8.1.6-1. Reboussin DM, Allen NB, Griswold ME, et al. 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: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines.Circulation. 2018; 138:e595–e616.LinkGoogle Scholar
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    • 8.2. Follow-Up of BP During Antihypertensive Drug Therapy

    • S8.2-1. Ambrosius WT, Sink KM, Foy CG, et al. The design and rationale of a multicenter clinical trial comparing two strategies for control of systolic blood pressure: the Systolic Blood Pressure Intervention Trial (SPRINT).Clin Trials. 2014; 11:532–46.CrossrefMedlineGoogle Scholar
    • S8.2-2. Cushman WC, Grimm RH, Cutler JA, et al. Rationale and design for the blood pressure intervention of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial.Am J Cardiol. 2007; 99:44i–55i.CrossrefMedlineGoogle Scholar

    • 8.2.1. Follow-Up After Initiating Antihypertensive Drug Therapy

    • S8.2.1-1. Ambrosius WT, Sink KM, Foy CG, et al. The design and rationale of a multicenter clinical trial comparing two strategies for control of systolic blood pressure: the Systolic Blood Pressure Intervention Trial (SPRINT).Clin Trials. 2014; 11:532–46.CrossrefMedlineGoogle Scholar
    • S8.2.1-2. Cushman WC, Grimm RH, Cutler JA, et al. Rationale and design for the blood pressure intervention of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial.Am J Cardiol. 2007; 99:44i–55i.CrossrefMedlineGoogle Scholar
    • S8.2.1-3. Xu W, Goldberg SI, Shubina M, et al. Optimal systolic blood pressure target, time to intensification, and time to follow-up in treatment of hypertension: population based retrospective cohort study.BMJ. 2015; 350:h158.CrossrefMedlineGoogle Scholar

    • 8.2.2. Monitoring Strategies to Improve Control of BP in Patients on Drug Therapy for High BP

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    • S8.2.2-3. Bosworth HB, Powers BJ, Olsen MK, et al. Home blood pressure management and improved blood pressure control: results from a randomized controlled trial.Arch Intern Med. 2011; 171:1173–80.CrossrefMedlineGoogle Scholar
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    • 9. Hypertension in Patients With Comorbidities

    • S9-1. Aronow WS, Fleg JL, Pepine CJ, et al. ACCF/AHA 2011 expert consensus document on hypertension in the elderly: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus documents developed in collaboration with the American Academy of Neurology, American Geriatrics Society, American Society for Preventive Cardiology, American Society of Hypertension, American Society of Nephrology, Association of Black Cardiologists, and European Society of Hypertension.Circulation. 2011; 123:2434–506.LinkGoogle Scholar
    • S9-2. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.Circulation. 2013; 128:e240–327.LinkGoogle Scholar
    • S9-3. Fihn SD, Blankenship JC, Alexander KP, et al. 2014 ACC/AHA/AATS/PCNA/SCAI/STS focused update of the guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, and the American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons.Circulation. 2014; 130:1749–67.LinkGoogle Scholar
    • S9-4. Gerhard-Herman MD, Gornik HL, Barrett C, et al. 2016 AHA/ACC guideline on the management of patients with lower extremity peripheral artery disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines.Circulation. 2017; 135:e726–79.LinkGoogle Scholar

    • 9.1. Stable Ischemic Heart Disease

    • S9.1-1. Wright JT, Williamson JD, Whelton PK, et al. A randomized trial of intensive versus standard blood-pressure control. SPRINT Research Group.N Engl J Med. 2015; 373:2103–16.CrossrefMedlineGoogle Scholar
    • S9.1-2. Bundy JD, Li C, Stuchlik P, et al. Systolic blood pressure reduction and risk of cardiovascular disease and mortality: a systematic review and network meta-analysis.JAMA Cardiol. 2017; 2:775–81.CrossrefMedlineGoogle Scholar
    • S9.1-3. Leenen FH, Nwachuku CE, Black HR, et al. Clinical events in high-risk hypertensive patients randomly assigned to calcium channel blocker versus angiotensin-converting enzyme inhibitor in the antihypertensive and lipid-lowering treatment to prevent heart attack trial.Hypertension. 2006; 48:374–84.LinkGoogle Scholar
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    • S9.1-5. Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial Collaborative Research Group. Diuretic versus alpha-blocker as first-step antihypertensive therapy: final results from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).Hypertension. 2003; 42:239–46.LinkGoogle Scholar
    • S9.1-6. Fihn SD, Blankenship JC, Alexander KP, et al. 2014 ACC/AHA/AATS/PCNA/SCAI/STS focused update of the Guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, and the American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons.Circulation. 2014; 130:1749–67.LinkGoogle Scholar
    • S9.1-7. Fox KM. EURopean trial On reduction of cardiac events with Perindopril in stable coronary Artery disease Investigators. Efficacy of perindopril in reduction of cardiovascular events among patients with stable coronary artery disease: randomised, double-blind, placebo-controlled, multicentre trial (the EUROPA study).Lancet. 2003; 362:782–8.CrossrefMedlineGoogle Scholar
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    • S9.1-11. Leon MB, Rosing DR, Bonow RO, et al. Clinical efficacy of verapamil alone and combined with propranolol in treating patients with chronic stable angina pectoris.Am J Cardiol. 1981; 48:131–9.CrossrefMedlineGoogle Scholar
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    • 9.2. Heart Failure

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    • 9.2.1. Heart Failure With Reduced Ejection Fraction

    • S9.2.1-1. Goldstein RE, Boccuzzi SJ, Cruess D, et al. Diltiazem increases late-onset congestive heart failure in postinfarction patients with early reduction in ejection fraction. The Adverse Experience Committee; and the Multicenter Diltiazem Postinfarction Research Group.Circulation. 1991; 83:52–60.LinkGoogle Scholar

    • 9.2.2. Heart Failure With Preserved Ejection Fraction

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    • 9.3. Chronic Kidney Disease

    • S9.3-1. Klahr S, Levey AS, Beck GJ, et al. The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease. Modification of Diet in Renal Disease Study Group.N Engl J Med. 1994; 330:877–84.CrossrefMedlineGoogle Scholar
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    • 9.3.1. Hypertension After Renal Transplantation

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    • 9.4. Cerebrovascular Disease

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    • 9.4.2. Acute Ischemic Stroke

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    • 9.4.3. Secondary Stroke Prevention

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    • 9.5. Peripheral Artery Disease

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    • 9.6. Diabetes Mellitus

    • S9.6-1. Emdin CA, Rahimi K, Neal B, et al. Blood pressure lowering in type 2 diabetes: a systematic review and meta-analysis.JAMA. 2015; 313:603–15.CrossrefMedlineGoogle Scholar
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    • S9.6-5. Margolis KL, O'Connor PJ, Morgan TM, et al. Outcomes of combined cardiovascular risk factor management strategies in type 2 diabetes: the ACCORD randomized trial.Diabetes Care. 2014; 37:1721–8.CrossrefMedlineGoogle Scholar
    • S9.6-6. Soliman EZ, Byington RP, Bigger JT, et al. Effect of intensive blood pressure lowering on left ventricular hypertrophy in patients with diabetes mellitus: Action to Control Cardiovascular Risk in Diabetes Blood Pressure Trial.Hypertension. 2015; 66:1123–9.LinkGoogle Scholar
    • S9.6-7. Lv J, Ehteshami P, Sarnak MJ, et al. Effects of intensive blood pressure lowering on the progression of chronic kidney disease: a systematic review and meta-analysis.CMAJ. 2013; 185:949–57.CrossrefMedlineGoogle Scholar
    • S9.6-8. Bress AP, King JB, Kreider KE, et al. Effect of intensive versus standard blood pressure treatment according to baseline prediabetes status: a post hoc analysis of a randomized trial.Diabetes Care. 2017; 40:1401–8.CrossrefMedlineGoogle Scholar
    • S9.6-9. Turnbull F, Neal B, Algert C, et al. Effects of different blood pressure-lowering regimens on major cardiovascular events in individuals with and without diabetes mellitus: results of prospectively designed overviews of randomized trials.Arch Intern Med. 2005; 165:1410–9.CrossrefMedlineGoogle Scholar
    • S9.6-10. Whelton PK, Barzilay J, Cushman WC, et al. Clinical outcomes in antihypertensive treatment of type 2 diabetes, impaired fasting glucose concentration, and normoglycemia: Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).Arch Intern Med. 2005; 165:1401–9.CrossrefMedlineGoogle Scholar
    • S9.6-11. Palmer SC, Mavridis D, Navarese E, et al. Comparative efficacy and safety of blood pressure-lowering agents in adults with diabetes and kidney disease: a network meta-analysis.Lancet. 2015; 385:2047–56.CrossrefMedlineGoogle Scholar
    • S9.6-12. Schmieder RE, Hilgers KF, Schlaich MP, et al. Renin-angiotensin system and cardiovascular risk.Lancet. 2007; 369:1208–19.CrossrefMedlineGoogle Scholar

    • 9.7. Metabolic Syndrome

    • S9.7-1. Lim S, Eckel RH. Pharmacological treatment and therapeutic perspectives of metabolic syndrome.Rev Endocr Metab Disord. 2014; 15:329–41.CrossrefMedlineGoogle Scholar
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    • S9.7-3. Ruderman NB, Shulman GI. Metabolic syndrome.Jameson JL. Endocrinology: Adult & Pediatric. 2015. Elsevier Saunders: Philadelphia, PA:752–9.Google Scholar
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    • S9.7-5. Chen J, Muntner P, Hamm LL, et al. The metabolic syndrome and chronic kidney disease in US adults.Ann Intern Med. 2004; 140:167–74.CrossrefMedlineGoogle Scholar
    • S9.7-6. Chen J, Gu D, Chen C-S, et al. Association between the metabolic syndrome and chronic kidney disease in Chinese adults.Nephrol Dial Transplant. 2007; 22:1100–6.CrossrefMedlineGoogle Scholar
    • S9.7-7. Barzilay JI, Davis BR, Whelton PK. The glycemic effects of antihypertensive medications.Curr Hypertens Rep. 2014; 16:410.CrossrefMedlineGoogle Scholar
    • S9.7-8. Kostis JB, Wilson AC, Freudenberger RS, et al. Long-term effect of diuretic-based therapy on fatal outcomes in subjects with isolated systolic hypertension with and without diabetes.Am J Cardiol. 2005; 95:29–35.CrossrefMedlineGoogle Scholar
    • S9.7-9. Wright JT, Harris-Haywood S, Pressel S, et al. Clinical outcomes by race in hypertensive patients with and without the metabolic syndrome: Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).Arch Intern Med. 2008; 168:207–17.CrossrefMedlineGoogle Scholar
    • S9.7-10. Wright JT, Probstfield JL, Cushman WC, et al. ALLHAT findings revisited in the context of subsequent analyses, other trials, and meta-analyses.Arch Intern Med. 2009; 169:832–42.CrossrefMedlineGoogle Scholar
    • S9.7-11. Black HR, Davis B, Barzilay J, et al. Metabolic and clinical outcomes in nondiabetic individuals with the metabolic syndrome assigned to chlorthalidone, amlodipine, or lisinopril as initial treatment for hypertension: a report from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).Diabetes Care. 2008; 31:353–60.CrossrefMedlineGoogle Scholar
    • S9.7-12. Laurent S, Boutouyrie P. Vascular Mechanism Collaboration. Dose-dependent arterial destiffening and inward remodeling after olmesartan in hypertensives with metabolic syndrome.Hypertension. 2014; 64:709–16.LinkGoogle Scholar
    • S9.7-13. Reisin E, Owen J. Treatment: special conditions. Metabolic syndrome: obesity and the hypertension connection.J Am Soc Hypertens. 2015; 9:156–59.CrossrefMedlineGoogle Scholar

    • 9.8. Atrial Fibrillation

    • S9.8-1. Healey JS, Baranchuk A, Crystal E, et al. Prevention of atrial fibrillation with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: a meta-analysis.J Am Coll Cardiol. 2005; 45:1832–9.CrossrefMedlineGoogle Scholar
    • S9.8-2. Zhao D, Wang Z-M, Wang L-S. Prevention of atrial fibrillation with renin-angiotensin system inhibitors on essential hypertensive patients: a meta-analysis of randomized controlled trials.J Biomed Res. 2015; 29:475–85.CrossrefMedlineGoogle Scholar

    • 9.9. Valvular Heart Disease

    • S9.9-1. Rieck ÅE, Cramariuc D, Boman K, et al. Hypertension in aortic stenosis: implications for left ventricular structure and cardiovascular events.Hypertension. 2012; 60:90–7.LinkGoogle Scholar
    • S9.9-2. Eleid MF, Nishimura RA, Sorajja P, et al. Systemic hypertension in low-gradient severe aortic stenosis with preserved ejection fraction.Circulation. 2013; 128:1349–53.LinkGoogle Scholar
    • S9.9-3. Bull S, Loudon M, Francis JM, et al. A prospective, double-blind, randomized controlled trial of the angiotensin-converting enzyme inhibitor Ramipril In Aortic Stenosis (RIAS trial).Eur Heart J Cardiovasc Imaging. 2015; 16:834–41.CrossrefMedlineGoogle Scholar
    • S9.9-4. Chockalingam A, Venkatesan S, Subramaniam T, et al. Safety and efficacy of angiotensin-converting enzyme inhibitors in symptomatic severe aortic stenosis: Symptomatic Cardiac Obstruction-Pilot Study of Enalapril in Aortic Stenosis (SCOPE-AS).Am Heart J. 2004; 147:E19.CrossrefMedlineGoogle Scholar
    • S9.9-5. Scognamiglio R, Rahimtoola SH, Fasoli G, et al. Nifedipine in asymptomatic patients with severe aortic regurgitation and normal left ventricular function.N Engl J Med. 1994; 331:689–94.CrossrefMedlineGoogle Scholar
    • S9.9-6. Evangelista A, Tornos P, Sambola A, et al. Long-term vasodilator therapy in patients with severe aortic regurgitation.N Engl J Med. 2005; 353:1342–9.CrossrefMedlineGoogle Scholar

    • 9.10. Aortic Disease

    • S9.10-1. Genoni M, Paul M, Jenni R, et al. Chronic beta-blocker therapy improves outcome and reduces treatment costs in chronic type B aortic dissection.Eur J Cardiothorac Surg. 2001; 19:606–10.CrossrefMedlineGoogle Scholar
    • S9.10-2. Suzuki T, Isselbacher EM, Nienaber CA, et al. Type-selective benefits of medications in treatment of acute aortic dissection (from the International Registry of Acute Aortic Dissection [IRAD]).Am J Cardiol. 2012; 109:122–7.CrossrefMedlineGoogle Scholar

    • 10. Special Patient Groups

    • S10.1.1-1. Leenen FH, Nwachuku CE, Black HR, et al. Clinical events in high-risk hypertensive patients randomly assigned to calcium channel blocker versus angiotensin-converting enzyme inhibitor in the antihypertensive and lipid-lowering treatment to prevent heart attack trial.Hypertension. 2006; 48:374–84.LinkGoogle Scholar
    • S10.1.1-2. Wright JT, Probstfield JL, Cushman WC, et al. ALLHAT findings revisited in the context of subsequent analyses, other trials, and meta-analyses.Arch Intern Med. 2009; 169:832–42.CrossrefMedlineGoogle Scholar
    • S10.1.1-3. Wright JT, Dunn JK, Cutler JA, et al. Outcomes in hypertensive black and nonblack patients treated with chlorthalidone, amlodipine, and lisinopril.JAMA. 2005; 293:1595–608.CrossrefMedlineGoogle Scholar
    • S10.1.1-4. Wright JT, Harris-Haywood S, Pressel S, et al. Clinical outcomes by race in hypertensive patients with and without the metabolic syndrome: Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).Arch Intern Med. 2008; 168:207–17.CrossrefMedlineGoogle Scholar
    • S10.1.1-5. ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).JAMA. 2002; 288:2981–97.CrossrefMedlineGoogle Scholar
    • S10.1.1-6. Wright JT, Williamson JD, Whelton PK, et al. A randomized trial of intensive versus standard blood-pressure control. SPRINT Research Group.N Engl J Med. 2015; 373:2103–16.CrossrefMedlineGoogle Scholar
    • S10.1.1-7. Wright JT, Bakris G, Greene T, et al. Effect of blood pressure lowering and antihypertensive drug class on progression of hypertensive kidney disease: results from the AASK trial.JAMA. 2002; 288:2421–31.CrossrefMedlineGoogle Scholar

    • 10.2. Sex-Related Issues

    • S10.2-1. Benjamin EJ, Blaha MJ, Chiuve SE, et al. Heart disease and stroke statistics–2017 update: a report from the American Heart Association.Circulation. 2017; 135:e146–603.LinkGoogle Scholar
    • S10.2-2. Gueyffier F, Boutitie F, Boissel JP, et al. Effect of antihypertensive drug treatment on cardiovascular outcomes in women and men. A meta-analysis of individual patient data from randomized, controlled trials. The INDANA Investigators.Ann Intern Med. 1997; 126:761–7.CrossrefMedlineGoogle Scholar
    • S10.2-3. Turnbull F, Woodward M, Neal B, et al. Do men and women respond differently to blood pressure-lowering treatment? Results of prospectively designed overviews of randomized trials.Eur Heart J. 2008; 29:2669–80.CrossrefMedlineGoogle Scholar

    • 10.2.1. Women

    • S10.2.1-1. Turnbull F, Woodward M, Neal B, et al. Do men and women respond differently to blood pressure-lowering treatment? Results of prospectively designed overviews of randomized trials.Eur Heart J. 2008; 29:2669–80.CrossrefMedlineGoogle Scholar
    • S10.2.1-2. Wenger NK, Ferdinand KC, Bairey Merz CN, et al. Women, hypertension, and the Systolic Blood Pressure Intervention Trial.Am J Med. 2016; 129:1030–6.CrossrefMedlineGoogle Scholar
    • S10.2.1-3. Fletcher A, Beevers DG, Bulpitt C, et al. Beta adrenoceptor blockade is associated with increased survival in male but not female hypertensive patients: a report from the DHSS Hypertension Care Computing Project (DHCCP).J Hum Hypertens. 1988; 2:219–27.MedlineGoogle Scholar
    • S10.2.1-4. Jansen J, Bonner C, McKinn S, et al. General practitioners' use of absolute risk versus individual risk factors in cardiovascular disease prevention: an experimental study.BMJ OPEN. 2014; 4:e004812.CrossrefMedlineGoogle Scholar
    • S10.2.1-5. Lewis CE, Grandits A, Flack J, et al. Efficacy and tolerance of antihypertensive treatment in men and women with stage 1 diastolic hypertension. Results of the Treatment of Mild Hypertension Study.Arch Intern Med. 1996; 156:377–85.CrossrefMedlineGoogle Scholar
    • S10.2.1-6. Kloner RA, Sowers JR, DiBona GF, et al. Sex- and age-related antihypertensive effects of amlodipine. The Amlodipine Cardiovascular Community Trial Study Group.Am J Cardiol. 1996; 77:713–22.CrossrefMedlineGoogle Scholar
    • S10.2.1-7. Igho Pemu P, Ofili E. Hypertension in women: part I.J Clin Hypertens (Greenwich). 2008; 10:406–10.CrossrefMedlineGoogle Scholar

    • 10.2.2. Pregnancy

    • S10.2.2-1. James PR, Nelson-Piercy C. Management of hypertension before, during, and after pregnancy.Heart. 2004; 90:1499–504.CrossrefMedlineGoogle Scholar
    • S10.2.2-2. American College of Obstetricians and Gynecologists Task Force on Hypertension in Pregnancy. Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists' Task Force on Hypertension in Pregnancy.Obstet Gynecol. 2013; 122:1122–31.CrossrefMedlineGoogle Scholar
    • S10.2.2-3. National Clinical Guideline Centre (UK). Hypertension: The Clinical Management of Primary Hypertension in Adults: Update of Clinical Guidelines 18 and 34. London, UK: Royal College of Physicians (UK); 2011.Google Scholar
    • S10.2.2-4. Pucci M, Sarween N, Knox E, et al. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in women of childbearing age: risks versus benefits.Expert Rev Clin Pharmacol. 2015; 8:221–31.CrossrefMedlineGoogle Scholar
    • S10.2.2-5. Moretti ME, Caprara D, Drehuta I, et al. The fetal safety of angiotensin converting enzyme inhibitors and angiotensin ii receptor blockers.Obstet Gynecol Int. 2012; 2012:658310.CrossrefMedlineGoogle Scholar
    • S10.2.2-6. Ferrer RL, Sibai BM, Mulrow CD, et al. Management of mild chronic hypertension during pregnancy: a review.Obstet Gynecol. 2000; 96:849–60.MedlineGoogle Scholar

    • 10.3. Age-Related Issues

    • S10.3.1-1. Williamson JD, Supiano MA, Applegate WB, et al. Intensive vs standard blood pressure control and cardiovascular disease outcomes in adults aged ≥75 years: a randomized clinical trial.JAMA. 2016; 315:2673–82.CrossrefMedlineGoogle Scholar

    • 11. Other Considerations

    • S11.1-1. Calhoun DA, Jones D, Textor S, et al. Resistant hypertension: diagnosis, evaluation, and treatment: a scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research.Hypertension. 2008; 51:1403–19.LinkGoogle Scholar

    • 11.2. Hypertensive Crises—Emergencies and Urgencies

    • S11.2-1. Farias S, Peacock WF, Gonzalez M, et al. Impact of initial blood pressure on antihypertensive response in patients with acute hypertension.Am J Emerg Med. 2014; 32:833–6.CrossrefMedlineGoogle Scholar
    • S11.2-2. Peacock WF, Chandra A, Char D, et al. Clevidipine in acute heart failure: results of the A Study of Blood Pressure Control in Acute Heart Failure–A Pilot Study (PRONTO).Am Heart J. 2014; 167:529–36.CrossrefMedlineGoogle Scholar

    • 11.3. Cognitive Decline and Dementia

    • S11.3-1. Applegate WB, Pressel S, Wittes J, et al. Impact of the treatment of isolated systolic hypertension on behavioral variables. Results from the systolic hypertension in the elderly program.Arch Intern Med. 1994; 154:2154–60.CrossrefMedlineGoogle Scholar
    • S11.3-2. Forette F, Seux ML, Staessen JA, et al. Prevention of dementia in randomised double-blind placebo-controlled Systolic Hypertension in Europe (Syst-Eur) trial.Lancet. 1998; 352:1347–51.CrossrefMedlineGoogle Scholar
    • S11.3-3. Forette F, Seux ML, Staessen JA, et al. The prevention of dementia with antihypertensive treatment: new evidence from the Systolic Hypertension in Europe (Syst-Eur) study.Arch Intern Med. 2002; 162:2046–52.CrossrefMedlineGoogle Scholar
    • S11.3-4. Lithell H, Hansson L, Skoog I, et al. The Study on Cognition and Prognosis in the Elderly (SCOPE): principal results of a randomized double-blind intervention trial.J Hypertens. 2003; 21:875–86.CrossrefMedlineGoogle Scholar
    • S11.3-5. Tzourio C, Anderson C, Chapman N, et al. Effects of blood pressure lowering with perindopril and indapamide therapy on dementia and cognitive decline in patients with cerebrovascular disease.Arch Intern Med. 2003; 163:1069–75.CrossrefMedlineGoogle Scholar
    • S11.3-6. Peters R, Beckett N, Forette F, et al. Incident dementia and blood pressure lowering in the Hypertension in the Very Elderly Trial cognitive function assessment (HYVET-COG): a double-blind, placebo controlled trial.Lancet Neurology. 2008; 7:683–9.CrossrefMedlineGoogle Scholar

    • 11.4. Patients Undergoing Surgical Procedures

    • S11.4-1. Lindenauer PK, Pekow P, Wang K, et al. Perioperative beta-blocker therapy and mortality after major noncardiac surgery.N Engl J Med. 2005; 353:349–61.CrossrefMedlineGoogle Scholar
    • S11.4-2. Shammash JB, Trost JC, Gold JM, et al. Perioperative beta-blocker withdrawal and mortality in vascular surgical patients.Am Heart J. 2001; 141:148–53.CrossrefMedlineGoogle Scholar
    • S11.4-3. Wallace AW, Au S, Cason BA. Association of the pattern of use of perioperative β-blockade and postoperative mortality.Anesthesiology. 2010; 113:794–805.CrossrefMedlineGoogle Scholar
    • S11.4-4. Andersson C, Merie C, Jorgensen M, et al. Association of β-blocker therapy with risks of adverse cardiovascular events and deaths in patients with ischemic heart disease undergoing noncardiac surgery: a Danish nationwide cohort study.JAMA Intern Med. 2014; 174:336–44.CrossrefMedlineGoogle Scholar
    • S11.4-5. Hoeks SE, Scholte Op Reimer WJM, van Urk H, et al. Increase of 1-year mortality after perioperative beta-blocker withdrawal in endovascular and vascular surgery patients.Eur J Vasc Endovasc Surg. 2007; 33:13–9.CrossrefMedlineGoogle Scholar
    • S11.4-6. Barrett TW, Mori M, De Boer D. Association of ambulatory use of statins and beta-blockers with long-term mortality after vascular surgery.J Hosp Med. 2007; 2:241–52.CrossrefMedlineGoogle Scholar
    • S11.4-7. London MJ, Hur K, Schwartz GG, et al. Association of perioperative β-blockade with mortality and cardiovascular morbidity following major noncardiac surgery.JAMA. 2013; 309:1704–13.CrossrefMedlineGoogle Scholar
    • S11.4-8. Turan A, You J, Shiba A, et al. Angiotensin converting enzyme inhibitors are not associated with respiratory complications or mortality after noncardiac surgery.Anesth Analg. 2012; 114:552–60.CrossrefMedlineGoogle Scholar
    • S11.4-9. Rosenman DJ, McDonald FS, Ebbert JO, et al. Clinical consequences of withholding versus administering renin-angiotensin-aldosterone system antagonists in the preoperative period.J Hosp Med. 2008; 3:319–25.CrossrefMedlineGoogle Scholar
    • S11.4-10. Roshanov PS, Rochwerg B, Patel A, et al. Withholding versus continuing angiotensin-converting enzyme inhibitors or angiotensin ii receptor blockers before noncardiac surgery: an analysis of the vascular events in noncardiac Surgery patIents cOhort evaluatioN Prospective Cohort.Anesthesiology. 2017; 126:16–27.CrossrefMedlineGoogle Scholar
    • S11.4-11. Fleisher LA. Preoperative evaluation of the patient with hypertension.JAMA. 2002; 287:2043–6.CrossrefMedlineGoogle Scholar
    • S11.4-12. Howell SJ, Sear JW, Foex P. Hypertension, hypertensive heart disease and perioperative cardiac risk.Br J Anaesth. 2004; 92:570–83.CrossrefMedlineGoogle Scholar
    • S11.4-13. Hart GR, Anderson RJ. Withdrawal syndromes and the cessation of antihypertensive therapy.Arch Intern Med. 1981; 141:1125–27.CrossrefMedlineGoogle Scholar
    • S11.4-14. Devereaux PJ, Yang H, Yusuf S, et al. Effects of extended-release metoprolol succinate in patients undergoing non-cardiac surgery (POISE trial): a randomised controlled trial.Lancet. 2008; 371:1839–47.CrossrefMedlineGoogle Scholar

    • 12. Strategies to Improve Hypertension Treatment and Control

    • S12.1.1-1. Claxton AJ, Cramer J, Pierce C. A systematic review of the associations between dose regimens and medication compliance.Clin Ther. 2001; 23:1296–310.CrossrefMedlineGoogle Scholar
    • S12.1.1-2. Iskedjian M, Einarson TR, MacKeigan LD, et al. Relationship between daily dose frequency and adherence to antihypertensive pharmacotherapy: evidence from a meta-analysis.Clin Ther. 2002; 24:302–16.CrossrefMedlineGoogle Scholar
    • S12.1.1-3. Schroeder K, Fahey T, Ebrahim S. How can we improve adherence to blood pressure-lowering medication in ambulatory care? Systematic review of randomized controlled trials.Arch Intern Med. 2004; 164:722–32.CrossrefMedlineGoogle Scholar
    • S12.1.1-4. Bangalore S, Kamalakkannan G, Parkar S, et al. Fixed-dose combinations improve medication compliance: a meta-analysis.Am J Med. 2007; 120:713–19.CrossrefMedlineGoogle Scholar
    • S12.1.1-5. Gupta AK, Arshad S, Poulter NR. Compliance, safety, and effectiveness of fixed-dose combinations of antihypertensive agents: a meta-analysis.Hypertension. 2010; 55:399–407.LinkGoogle Scholar
    • S12.1.1-6. Sherrill B, Halpern M, Khan S, et al. Single-pill vs free-equivalent combination therapies for hypertension: a meta-analysis of health care costs and adherence.J Clin Hypertens (Greenwich). 2011; 13:898–909.CrossrefMedlineGoogle Scholar
    • S12.1.1-7. Yang W, Chang J, Kahler KH, et al. Evaluation of compliance and health care utilization in patients treated with single pill vs. free combination antihypertensives.Curr Med Res Opin. 2010; 26:2065–76.CrossrefMedlineGoogle Scholar

    • 12.1.2. Strategies to Promote Lifestyle Modification

    • S12.1.2-1. Artinian NT, Fletcher GF, Mozaffarian D, et al. Interventions to promote physical activity and dietary lifestyle changes for cardiovascular risk factor reduction in adults: a scientific statement from the American Heart Association.Circulation. 2010; 122:406–41.LinkGoogle Scholar
    • S12.1.2-2. Eckel RH, Jakicic JM, Ard JD, et al. 2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.Circulation. 2014; 129(suppl 2):S76–99.LinkGoogle Scholar

    • 12.2. Structured, Team-Based Care Interventions for Hypertension Control

    • S12.2-1. Carter BL, Rogers M, Daly J, et al. The potency of team-based care interventions for hypertension: a meta-analysis.Arch Intern Med. 2009; 169:1748–55.CrossrefMedlineGoogle Scholar
    • S12.2-2. Clark CE, Smith LF, Taylor RS, et al. Nurse led interventions to improve control of blood pressure in people with hypertension: systematic review and meta-analysis.BMJ. 2010; 341:c3995.CrossrefMedlineGoogle Scholar
    • S12.2-3. Proia KK, Thota AB, Njie GJ, et al. Team-based care and improved blood pressure control: a community guide systematic review.Am J Prev Med. 2014; 47:86–99.CrossrefMedlineGoogle Scholar
    • S12.2-4. Santschi V, Chiolero A, Colosimo AL, et al. Improving blood pressure control through pharmacist interventions: a meta-analysis of randomized controlled trials.J Am Heart Assoc. 2014; 3:e000718.LinkGoogle Scholar
    • S12.2-5. Shaw RJ, McDuffie JR, Hendrix CC, et al. Effects of nurse-managed protocols in the outpatient management of adults with chronic conditions: a systematic review and meta-analysis.Ann Intern Med. 2014; 161:113–21.CrossrefMedlineGoogle Scholar
    • S12.2-6. Thomas KL, Shah BR, Elliot-Bynum S, et al. Check it, change it: a community-based, multifaceted intervention to improve blood pressure control.Circ Cardiovasc Qual Outcomes. 2014; 7:828–34.LinkGoogle Scholar
    • S12.2-7. Carter BL, Coffey CS, Ardery G, et al. Cluster-randomized trial of a physician/pharmacist collaborative model to improve blood pressure control.Circ Cardiovasc Qual Outcomes. 2015; 8:235–43.LinkGoogle Scholar

    • 12.3. Health Information Technology–Based Strategies to Promote Hypertension Control

    • S12.3.1-1. Rakotz MK, Ewigman BG, Sarav M, et al. A technology-based quality innovation to identify undiagnosed hypertension among active primary care patients.Ann Fam Med. 2014; 12:352–8.CrossrefMedlineGoogle Scholar
    • S12.3.1-2. Borden WB, Maddox TM, Tang F, et al. Impact of the 2014 expert panel recommendations for management of high blood pressure on contemporary cardiovascular practice: insights from the NCDR PINNACLE registry.J Am Coll Cardiol. 2014; 64:2196–203.CrossrefMedlineGoogle Scholar
    • S12.3.1-3. Jaffe MG, Lee GA, Young JD, et al. Improved blood pressure control associated with a large-scale hypertension program.JAMA. 2013; 310:699–705.CrossrefMedlineGoogle Scholar

    • 12.3.2. Telehealth Interventions to Improve Hypertension Control

    • S12.3.2-1. Omboni S, Gazzola T, Carabelli G, et al. Clinical usefulness and cost effectiveness of home blood pressure telemonitoring: meta-analysis of randomized controlled studies.J Hypertens. 2013; 31:455–67; discussion 467–8.CrossrefMedlineGoogle Scholar
    • S12.3.2-2. Verberk WJ, Kessels AGH, Thien T. Telecare is a valuable tool for hypertension management, a systematic review and meta-analysis.Blood Press Monit. 2011; 16:149–155.CrossrefMedlineGoogle Scholar
    • S12.3.2-3. Agarwal R, Bills JE, Hecht TJW, et al. Role of home blood pressure monitoring in overcoming therapeutic inertia and improving hypertension control: a systematic review and meta-analysis.Hypertension. 2011; 57:29–38.LinkGoogle Scholar
    • S12.3.2-4. Liu S, Dunford SD, Leung YW, et al. Reducing blood pressure with Internet-based interventions: a meta-analysis.Can J Cardiol. 2013; 29:613–21.CrossrefMedlineGoogle Scholar
    • S12.3.2-5. Burke LE, Ma J, Azar KMJ, et al. Current science on consumer use of mobile health for cardiovascular disease prevention: a scientific statement from the American Heart Association.Circulation. 2015; 132:1157–213.LinkGoogle Scholar

    • 12.4. Improving Quality of Care for Patients With Hypertension

    • S12.4.1-1. Svetkey LP, Pollak KI, Yancy WS, et al. Hypertension improvement project: randomized trial of quality improvement for physicians and lifestyle modification for patients.Hypertension. 2009; 54:1226–33.LinkGoogle Scholar
    • S12.4.1-2. de Lusignan S, Gallagher H, Jones S, et al. Audit-based education lowers systolic blood pressure in chronic kidney disease: the Quality Improvement in CKD (QICKD) trial results.Kidney Int. 2013; 84:609–20.CrossrefMedlineGoogle Scholar
    • S12.4.1-3. Jaffe MG, Lee GA, Young JD, et al. Improved blood pressure control associated with a large-scale hypertension program.JAMA. 2013; 310:699–705.CrossrefMedlineGoogle Scholar

    • 12.4.2. Quality Improvement Strategies

    • S12.4.2-1. Walsh JME, McDonald KM, Shojania KG, et al. Quality improvement strategies for hypertension management: a systematic review.Med Care. 2006; 44:646–57.CrossrefMedlineGoogle Scholar
    • S12.4.2-2. Carter BL, Rogers M, Daly J, et al. The potency of team-based care interventions for hypertension: a meta-analysis.Arch Intern Med. 2009; 169:1748–55.CrossrefMedlineGoogle Scholar
    • S12.4.2-3. Glynn LG, Murphy AW, Smith SM, et al. Interventions used to improve control of blood pressure in patients with hypertension.Cochrane Database Syst Rev. 2010:CD005182.MedlineGoogle Scholar
    • S12.4.2-4. Proia KK, Thota AB, Njie GJ, et al. Team-based care and improved blood pressure control: a community guide systematic review.Am J Prev Med. 2014; 47:86–99.CrossrefMedlineGoogle Scholar
    • S12.4.2-5. Anchala R, Pinto MP, Shroufi A, et al. The role of Decision Support System (DSS) in prevention of cardiovascular disease: a systematic review and meta-analysis.PLoS ONE. 2012; 7:e47064.CrossrefMedlineGoogle Scholar
    • S12.4.2-6. Thomas KL, Shah BR, Elliot-Bynum S, et al. Check it, change it: a community-based, multifaceted intervention to improve blood pressure control.Circ Cardiovasc Qual Outcomes. 2014; 7:828–34.LinkGoogle Scholar
    • S12.4.2-7. Jaffe MG, Lee GA, Young JD, et al. Improved blood pressure control associated with a large-scale hypertension program.JAMA. 2013; 310:699–705.CrossrefMedlineGoogle Scholar
    • S12.4.2-8. Agarwal R, Bills JE, Hecht TJW, et al. Role of home blood pressure monitoring in overcoming therapeutic inertia and improving hypertension control: a systematic review and meta-analysis.Hypertension. 2011; 57:29–38.LinkGoogle Scholar

    • 12.5. Financial Incentives

    • S12.5-1. Hysong SJ, Simpson K, Pietz K, et al. Financial incentives and physician commitment to guideline-recommended hypertension management.Am J Manag Care. 2012; 18:e378–91.MedlineGoogle Scholar
    • S12.5-2. Petersen LA, Simpson K, Pietz K, et al. Effects of individual physician-level and practice-level financial incentives on hypertension care: a randomized trial.JAMA. 2013; 310:1042–50.CrossrefMedlineGoogle Scholar
    • S12.5-3. Karunaratne K, Stevens P, Irving J, et al. The impact of pay for performance on the control of blood pressure in people with chronic kidney disease stage 3-5.Nephrol Dial Transplant. 2013; 28:2107–16.CrossrefMedlineGoogle Scholar
    • S12.5-4. Maimaris W, Paty J, Perel P, et al. The influence of health systems on hypertension awareness, treatment, and control: a systematic literature review.PLoS Med. 2013; 10:e1001490.CrossrefMedlineGoogle Scholar

    • 13. The Plan of Care for Hypertension

    • S13-1. Smith SC, Benjamin EJ, Bonow RO, et al. AHA/ACCF secondary prevention and risk reduction therapy for patients with coronary and other atherosclerotic vascular disease: 2011 update: a guideline from the American Heart Association and American College of Cardiology Foundation.Circulation. 2011; 124:2458–73.LinkGoogle Scholar
    • S13-2. Fihn SD, Blankenship JC, Alexander KP, et al. 2014 ACC/AHA/AATS/PCNA/SCAI/STS focused update of the guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, and the American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons.Circulation. 2014; 130:1749–67.LinkGoogle Scholar
    • S13-3. Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons.Circulation. 2012; 126:e354–471.LinkGoogle Scholar
    • S13-4. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.Circulation. 2013; 128:e240–327.LinkGoogle Scholar
    • S13-5. Standards of Medical Care in Diabetes–2016: Summary of Revisions.Diabetes Care. 2016; 39(suppl 1):S4–5.CrossrefMedlineGoogle Scholar

    Appendix 1. Author Relationships With Industry and Other Entities (Relevant)—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 (October 2017)

    Committee MemberEmploymentConsultantSpeakers BureauOwnership/Partnership/PrincipalPersonal ResearchInstitutional, Organizational, or Other Financial BenefitExpert WitnessSalary
    Paul K. Whelton, ChairTulane University School of Hygiene and Tropical Medicine—Show Chwan Professor of Global Public HealthNoneNoneNoneNoneNoneNoneNone
    Robert M. Carey, Vice ChairUniversity of Virginia School of Medicine—Dean, Emeritus, and Professor of MedicineNoneNoneNone• Daiichi Sankyo IncNoneNoneNone
    Wilbert S. AronowWestchester Medical Center and New York Medical College—Professor of MedicineNoneNoneNoneNoneNoneNoneNone
    Donald E. Casey, JrThomas Jefferson College of Population Health—Adjunct Faculty; Alvarez & Marsal Ipo4health—Principal and FounderNoneNoneNoneNoneNoneNoneNone
    Karen J. CollinsCollins Collaboration—PresidentNoneNoneNoneNoneNoneNoneNone
    Cheryl Dennison HimmelfarbJohn Hopkins University—Professor of Nursing and Medicine, Institute for Clinical and Translational ResearchNoneNoneNoneNoneNoneNoneNone
    Sondra M. DePalmaPinnacleHealth CardioVascular Institute—Physician Assistant; American Academy of PAs—Director, Regulatory and Professional PracticeNoneNoneNoneNoneNoneNoneNone
    Samuel GiddingAlfred I. Dupont Hospital for Children—Chief, Division of Pediatric Cardiology, Nemours Cardiac CenterNoneNoneNoneNoneNoneNoneNone
    David C. Goff, Jr*Colorado School of Public Health—Professor and Dean, Department of EpidemiologyNoneNoneNoneNoneNoneNoneNone
    Kenneth A. JamersonUniversity of Michigan Health System—Professor of Internal Medicine and Frederick G.L. Huetwell Collegiate Professor of Cardiovascular MedicineNoneNoneNoneNoneNoneNoneNone
    Daniel W. JonesUniversity of Mississippi Medical Center—Professor of Medicine and Physiology; Metabolic Diseases and Nutrition—University Sanderson Chair in Obesity Mississippi Center for Obesity Research—Director, Clinical and Population ScienceNoneNoneNoneNoneNoneNoneNone
    Eric J. MacLaughlinTexas Tech University Health Sciences Center—Professor and Chair, Department of Pharmacy Practice, School of PharmacyNoneNoneNoneNoneNoneNoneNone
    Paul MuntnerUniversity of Alabama at Birmingham—Professor, Department of EpidemiologyNoneNoneNoneNoneNoneNoneNone
    Bruce OvbiageleMedical University of South Carolina—Pihl Professor and Chairman of NeurologyNone• Boehringer Ingelheim Korea LtdNoneNoneNoneNoneNone
    Sidney C. Smith, JrUniversity of North Carolina at Chapel Hill—Professor of Medicine; Center for Cardiovascular Science and Medicine—DirectorNoneNoneNoneNoneNoneNoneNone
    Crystal C. SpencerSpencer Law, PA—Attorney at LawNoneNoneNoneNoneNoneNoneNone
    Randall S. StaffordStanford Prevention Research Center—Professor of Medicine; Program on Prevention Outcomes—DirectorNoneNoneNoneNoneNoneNoneNone
    Sandra J. TalerMayo Clinic—Professor of Medicine, College of MedicineNoneNoneNoneNoneNoneNoneNone
    Randal J. ThomasMayo Clinic—Medical Director, Cardiac Rehabilitation ProgramNoneNoneNoneNoneNoneNoneNone
    Kim A. Williams, SrRush University Medical Center—James B. Herrick Professor; Division of Cardiology—ChiefNoneNoneNoneNoneNoneNoneNone
    Jeff D. WilliamsonWake Forest Baptist Medical Center—Professor of Internal Medicine; Section on Gerontology and Geriatric Medicine—ChiefNoneNoneNoneNoneNoneNoneNone
    Jackson T. Wright, JrCase Western Reserve University—Professor of Medicine; William T. Dahms MD Clinical Research Unit—Program Director; University Hospitals Case Medical Center—Director, Clinical Hypertension ProgramNone•AmgenNoneNoneNoneNoneNone

    This table represents the relationships of committee members with industry and other entities that were determined to be relevant to this document. These relationships were reviewed and updated in conjunction with all meetings and/or conference calls of the writing committee during the document development process. The table does not necessarily reflect relationships with industry at the time of publication. A person is deemed to have a significant interest in a business if the interest represents ownership of ≥5% of the voting stock or share of the business entity, or ownership of ≥$5000 of the fair market value of the business entity; or if funds received by the person from the business entity exceed 5% of the person’s gross income for the previous year. Relationships that exist with no financial benefit are also included for the purpose of transparency. Relationships in this table are modest unless otherwise noted.

    According to the ACC/AHA, a person has a relevant relationship IF: a) the relationship or interest relates to the same or similar subject matter, intellectual property or asset, topic, or issue addressed in the document; or b) the company/entity (with whom the relationship exists) makes a drug, drug class, or device addressed in the document, or makes a competing drug or device addressed in the document; or c) the person or a member of the person’s household, has a reasonable potential for financial, professional or other personal gain or loss as a result of the issues/content addressed in the document.

    We gratefully acknowledge the contributions of Dr. Lawrence Appel, who served as a member of the Writing Committee from November 2014 to September 2015.

    *Dr. David C. Goff resigned from the writing committee in December 2016 because of a change in employment before the recommendations were balloted. The writing committee thanks him for his contributions, which were extremely beneficial to the development of the draft.

    †Significant relationship.

    AAPA indicates American Academy of Physician Assistants; ACC, American College of Cardiology; ACPM, American College of Preventive Medicine; AGS, American Geriatrics Society; AHA, American Heart Association; APhA, American Pharmacists Association; ASH, American Society of Hypertension; ASPC, American Society for Preventive Cardiology; ABC, Association of Black Cardiologists; NMA, National Medical Association; and PCNA, Preventive Cardiovascular Nurses Association.

    Appendix 2. Reviewer Relationships With Industry and Other Entities (Comprehensive)—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 (October 2017)

    ReviewerRepresentationEmploymentConsultantSpeakers BureauOwnership/Partnership/PrincipalPersonal ResearchInstitutional, Organizational, or Other Financial BenefitExpert WitnessSalary
    Kim K. BirtcherOfficial Reviewer—TFPG Lead ReviewerUniversity of Houston College of Pharmacy—Clinical Professor, Department of Pharmacy Practice and Translational Research• Jones & Bartlett LearningNoneNoneNone• Accreditation Council for Clinical LipidologyNone• Walgreens*
    Roger BlumenthalOfficial Reviewer—Prevention SubcommitteeJohns Hopkins Hospital—Kenneth Jay Pollin Professor of Cardiology; Ciccarone Center for the Prevention of Heart Disease—DirectorNoneNoneNoneNoneNoneNoneNone
    Anna DominiczakOfficial Reviewer—AHAUniversity of Glasgow—Regius Professor of Medicine; Vice-Principal and Head of College of Medical, Veterinary and Life SciencesNoneNoneNoneNoneNoneNoneNone
    Carlos M. FerrarioOfficial Reviewer—AHAWake Forest School of Medicine—Professor, of Physiology and Pharmacology; Hypertension and Vascular Disease Center—DirectorNoneNoneNoneNoneNoneNoneNone
    Eugene YangOfficial Reviewer—ACC-BOGUniversity of Washington School of Medicine—Associate Clinical Professor of Medicine; UW Medicine Eastside Specialty Center—Medical Director• RubiconMD*
    • Regeneron*
    NoneNone• Amgen Inc.*
    • Gilead Sciences, Inc. (DSMB)*
    None• Third party, CAD, 2016*None
    Robert Jay AmrienOrganizational Reviewer—AAPAMassachusetts General Hospital—Clinical Physician Assistant, Chelsea Health Center; Bryant University—Physician Assistant ProgramNoneNoneNoneNoneNone• Defendant, aortic dissection, 2016*None
    Greg HolzmanOrganizational Reviewer—ACPMMontana Department of Public Health and Human Services—State Medical OfficerNoneNoneNoneNone• American Academy of Family Medicine
    • American College of Preventive Medicine
    NoneNone
    Martha GulatiOrganizational Reviewer—ASPCUniversity of Arizona College of Medicine—Professor of Medicine; Chief, Division of Cardiology; University Medicine Cardiovascular Institute in Phoenix—Physician Executive Director, BannerNoneNoneNoneNone• REATA (spouse)*NoneNone
    Wallace JohnsonOrganizational Reviewer—NMAUniversity of Maryland Medical Center—Assistant Professor of MedicineNoneNoneNoneAmgenNoneNoneNone
    Nancy Houston MillerOrganizational Reviewer—PCNAThe Lifecare Company—Associate Director• Moving Analytics*NoneNoneNoneNoneNoneNone
    Aldo J. PeixotoOrganizational Reviewer—ASHYale University School of Medicine—Professor of Medicine (Nephrology); Associate Chair for Ambulatory Services Operations and Quality, Department of Internal Medicine; Clinical Chief, Section of Nephrology• Lundbeck Inc.NoneNone• Bayer Healthcare Pharmaceuticals• Bayer Healthcare PharmaceuticalsNoneNone
    Carlos RodriguezOrganizational Reviewer—ABCWake Forest University—Professor, Epidemiology and Prevention• Amgen Inc.NoneNoneNoneNoneNoneNone
    Joseph SaseenOrganizational Reviewer—APhAUniversity of Colorado Anschutz Medical Campus—Vice-Chair, Department of Clinical Pharmacy, Skaggs School of Pharmacy and Pharmaceutical SciencesNoneNoneNoneNone• National Lipid Association• Defendant, statin use, 2016None
    Mark SupianoOrganizational Reviewer—AGSUniversity of Utah School of Medicine—D. Keith Barnes, MD, and Dottie Barnes Presidential Endowed Chair in Medicine; Chief, Division of Geriatrics; VA Salt Lake City Geriatric Research—Director, Education, and Clinical Center; University of Utah Center on Aging Executive—DirectorNoneNoneNoneNone• American Geriatrics Society
    • Division Chief
    • McGraw-Hill Medical
    NoneNone
    Sana M. Al-KhatibContent Reviewer—ACC/AHA Task Force on Clinical Practice GuidelinesDuke Clinical Research Institute—Professor of MedicineNoneNoneNone• AHRQ*
    • FDA*
    • PCORI*
    • VA Health System (DSMB)
    • Elsevier*
    • NIH, NHLBI
    • Third party, implantable cardioverter defibrillators, 2017None
    George BakrisContent ReviewerUniversity of Chicago Medicine—Professor of Medicine; Director, Hypertensive Diseases UnitNoneNoneNone• AbbVie, Inc.
    • Janssen, Bayer, Relypsa
    NoneNoneNone
    Jan BasileContent ReviewerMedical University of South Carolina—Professor of Medicine, Seinsheimer Cardiovascular Health Program; Ralph H Johnson VA Medical Center—InternistNone• Amgen Inc.
    • Arbor
    • Janssen Pharmaceuticals, Inc
    None• Eli Lilly and Company
    • NHLBI
    NoneNoneNone
    Joshua A. BeckmanContent Reviewer—ACC/AHA Task Force on Clinical Practice GuidelinesVanderbilt University Medical Center: Director, Cardiovascular Fellowship Program• AstraZeneca*
    • Merck*
    • SANOFI*
    None• EMX
    • JanaCare
    • Bristol Myers Squibb*• Vascular Interventional Advances*None• 2015 Defendant; Venous thromboembolism*
    John BisognanoContent ReviewerUniversity of Rochester Medical Center—Cardiologist• CVRxNoneNone• CVRx*
    • NIH*
    NoneNoneNone
    Biykem BozkurtContent Reviewer—ACC/AHA Task Force on Clinical Practice GuidelinesBaylor College of Medicine—Medical Care Line Executive, Cardiology Chief, Gordon Cain Chair, Professor of Medicine, DebakeyNoneNoneNone• Novartis CorporationNoneNoneNone
    David CalhounContent ReviewerUniversity of Alabama, Birmingham School of Medicine—Professor, Department of Cardiovascular Disease• Novartis
    • Valencia Technologies*
    NoneNone• MEDTRONIC*
    • ReCor Medical*
    NoneNoneNone
    Joaquin E. CigarroaContent Reviewer—ACC/AHA Task Force on Clinical Practice GuidelinesOregon Health and Science University—Clinical Professor of MedicineNoneNoneNone• NIH• ACC/AHA Taskforce on Clinical Practice Guidelines
    • AHA, Board of Directors, Western Affiliate
    • American Stroke Association, Cryptogenic Stroke Initiative Advisory Committee
    • Catheterization and Cardiovascular Intervention
    • SCAI Quality Interventional Council
    • Defendant, CAD, 2011
    • Defendant, sudden death/CAD, 2010
    None
    William CushmanContent ReviewerMemphis VA Medical Center—Chief, Preventive Medicine Section; University of Tennessee College of Medicine—Professor, Medicine, Preventive Medicine, and PhysiologyNoneNoneNone• Lilly• Novartis Corporation
    • Takeda
    NoneNone
    Anita DeswalContent Reviewer—ACC/AHA Task Force on Clinical Practice GuidelinesBaylor College of Medicine—Associate Professor of MedicineNoneNoneNone• NIH*• bAurora Health Care Inc.
    • American Heart Association
    • AHA Committee on Heart Failure and Transplantation – Chair
    • Heart Failure Society of America
    NoneNone
    Dave DixonContent Reviewer—Cardiovascular TeamVirginia Commonwealth University School of Pharmacy—Associate ProfessorNoneNoneNoneNoneNoneNoneNone
    Ross FeldmanContent ReviewerWinnipeg Regional Health Authority—Medical Director, Cardiac Sciences Program; University of Manitoba—Professor of Medicine• GSK*
    • Servier*
    • Valeant Pharmaceuticals International*
    NoneNoneNoneNoneNoneNone
    Keith FerdinandContent ReviewerTulane University School of Medicine—Professor of Clinical Medicine• Amgen Inc.*
    • Boehringer Ingelheim*
    • Eli Lilly*
    • Sanofi-Aventis*
    • Novartis
    • Quantum Genomics
    • Sanofi-Aventis*
    NoneNoneNone• NovartisNoneNone
    Stephan FihnContent ReviewerUniversity of Washington—Professor of Medicine, Heath Services; Division Head, General Internal Medicine; Director, Office of Analytics and Business Intelligence for the Veterans Health Administration; VA Puget Sound Health Care System—General InternistNoneNoneNoneNone• University of WashingtonNoneNone
    Lawrence FineContent ReviewerNational Heart, Lung and Blood Institute—Chief, Clinical Applications and Prevention Branch, Division of Prevention and Population SciencesNoneNoneNoneNone• NIH*NoneNone
    John FlackContent ReviewerSouthern Illinois University School of Medicine—Chair and Professor Department of Internal Medicine; Chief, Hypertension Specialty Services• Regeneron*
    • NuSirt
    NoneNone• Bayer Healthcare Pharmaceuticals
    • GSK
    • American Journal of Hypertension*
    • CardioRenal Medicine
    • International Journal of Hypertension
    • Southern Illinois University Department of Medicine*
    NoneNone
    Joseph FlynnContent ReviewerSeattle Children's Hospital—Chief of the Division of Nephrology; University of Washington School of Medicine—Professor of Pediatrics• Ultragenyx, Inc. (DSMB)NoneNoneNone• UpToDate, Springer*NoneNone
    Federico GentileContent Reviewer—ACC/AHA Task Force on Clinical Practice GuidelinesCentro CardiologicoNoneNoneNoneNoneNoneNoneNone
    Joel HandlerContent ReviewerKaiser Permanente—Physician; National Kaiser Permanente Hypertension—Clinical LeaderNoneNoneNoneNoneNoneNoneNone
    Hani JneidContent Reviewer—ACC/AHA Task Force on Clinical Data StandardsBaylor College of Medicine—Associate Professor of Medicine, MEDVAMCNoneNoneNoneNoneNoneNoneNone
    José A. JoglarContent Reviewer—ACC/AHA Task Force on Clinical Practice GuidelinesUT Southwestern Medical Center—Professor of Internal Medicine; Cardiovascular Clinical Research Center—DirectorNoneNoneNoneNoneNoneNoneNone
    Amit KheraContent ReviewerUniversity of Texas Southwestern Medical Center—Assistant Professor of MedicineNoneNoneNoneNoneNoneNoneNone
    Glenn N. LevineContent Reviewer—ACC/AHA Task Force on Clinical Practice GuidelinesBaylor College of Medicine—Professor of Medicine; Director, Cardiac Care UnitNoneNoneNoneNoneNone• Defendant, catheterization laboratory procedure, 2016
    • Defendant, interpretation of ECG of a patient, 2014
    • Defendant, interpretation of angiogram (non-ACS), 2014
    • Defendant, out-of-hospital death, 2016
    None
    Giuseppe ManciaContent ReviewerUniversity of Milan-Bicocca—Professor of Medicine; Chairman, Department of Clinical Medicine, Prevention and Applied Biotechnologies• Boehringer Ingelheim*
    • CVRx
    • Ferrer
    • MEDTRONIC
    • Menarini International*
    • Recordati
    • Servier International*
    • Actavis
    NoneNoneNone• Novartis*NoneNone
    Andrew MillerContent Reviewer—Geriatric Cardiology SectionCardiovascular Associates—CardiologistNoneNoneNone• Novartis Corporation
    • Pfizer Inc
    • Bristol-Myers Squibb Company
    • Janssen Pharmaceuticals, Inc.
    • NIH
    NoneNone
    Pamela MorrisContent Reviewer—Prevention Council, ChairSeinsheimer Cardiovascular Health Program—Director; Women's Heart Care Medical University of South Carolina—Co-Director• Amgen Inc.
    • AstraZeneca
    • Sanofi Regeneron
    NoneNone• Amgen Inc.NoneNoneNone
    Martin MyersContent ReviewerSunnybrook Health Sciences Centre—Affiliate Scientist; University of Toronto—Professor, Cardiology• Ideal Life Inc*NoneNoneNoneNoneNoneNone
    Rick NishimuraContent ReviewerMayo Clinic College of Medicine—Judd and Mary Morris Leighton Professor of Medicine; Mayo Clinic—Division of Cardiovascular DiseasesNoneNoneNoneNoneNoneNoneNone
    Patrick T. O'GaraContent Reviewer—ACC/AHA Task Force on Clinical Practice GuidelinesHarvard Medical School—Professor of Medicine; Brigham and Women's Hospital—Director, Strategic Planning, Cardiovascular DivisionNoneNoneNoneNone• MEDTRONIC
    • NIH*
    NoneNone
    Suzanne OparilContent ReviewerUniversity of Alabama at Birmingham—Distinguished Professor of Medicine; Professor of Cell, Developmental and Integrative Biology, Division of Cardiology• Actelion
    • Lundbeck
    • Novo Nordisk, Inc.
    NoneNone• AstraZeneca (Duke University)*
    • Bayer Healthcare Pharmaceuticals, Inc.*
    • Novartis*
    • NIH*
    • NIH/NHLBI,
    • Takeda WHF/ESH/EPH
    NoneNone
    Carl PepineContent Reviewer—CV Disease in Women CommitteeShands Hospital at University of Florida—Professor of Medicine, Chief of Cardiovascular MedicineNoneNoneNone• Capricor, Inc.
    • NIH
    • Cytori Therapeutics, Inc.
    • Sanofi-Aventis
    • InVentive Health Clinical. LLC
    NoneNoneNone
    Mahboob RahmanContent ReviewerCase Western Reserve University School of Medicine—Professor of MedicineNoneNoneNoneNoneNoneNoneNone
    Vankata RamContent ReviewerUT Southwestern Medical Center; Apollo Institute for Blood Pressure ClinicsNoneNoneNoneNoneNoneNoneNone
    Barbara RiegelContent Reviewer—ACC/AHA Task Force on Clinical Practice GuidelinesUniversity of Pennsylvania School of Nursing- ProfessorNoneNoneNone• Co-Investigator- mentor
    • Co-investigator NIH
    • NIH grant
    • PCORI
    • Novartis CorpNoneNone
    Edward RoccellaContent ReviewerNational Heart, Lung, and Blood Institute—Coordinator, National High Blood Pressure Education Program• Medical University of South CarolinaNoneNoneNone• American Society of Hypertension
    • Consortium for Southeast Hypertension Control
    • Consortium Southeast Hypertension Control
    • Inter American Society of Hypertension
    NoneNone
    Ernesto SchiffrinContent ReviewerJewish General Hospital—Physician-in-Chief, Chief of the Department of Medicine and Director of the Cardiovascular Prevention Centre; McGill University—Professor, Department of Medicine, Division of Experimental Medicine• Novartis
    • Servier
    • NovartisNone• Servier*
    • Canadian Institutes for Health Research*
    • CME Medical Grand RoundsNoneNone
    Raymond TownsendContent ReviewerUniversity of Pennsylvania School of Medicine—Professor of Medicine; Director, Hypertension Section, Department of Internal Medicine/Renal; Institute for Translational Medicine and Therapeutics—Member• MEDTRONICNoneNone• NIH*• ASN
    • UpToDate
    NoneNone
    Michael Weber