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The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

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Abstract and Figures

The National High Blood Pressure Education Program presents the complete Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Like its predecessors, the purpose is to provide an evidence-based approach to the prevention and management of hypertension. The key messages of this report are these: in those older than age 50, systolic blood pressure (BP) of greater than 140 mm Hg is a more important cardiovascular disease (CVD) risk factor than diastolic BP; beginning at 115/75 mm Hg, CVD risk doubles for each increment of 20/10 mm Hg; those who are normotensive at 55 years of age will have a 90% lifetime risk of developing hypertension; prehypertensive individuals (systolic BP 120-139 mm Hg or diastolic BP 80-89 mm Hg) require health-promoting lifestyle modifications to prevent the progressive rise in blood pressure and CVD; for uncomplicated hypertension, thiazide diuretic should be used in drug treatment for most, either alone or combined with drugs from other classes; this report delineates specific high-risk conditions that are compelling indications for the use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers); two or more antihypertensive medications will be required to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg) for patients with diabetes and chronic kidney disease; for patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10 mm Hg above the diastolic BP goal, initiation of therapy using two agents, one of which usually will be a thiazide diuretic, should be considered; regardless of therapy or care, hypertension will be controlled only if patients are motivated to stay on their treatment plan. Positive experiences, trust in the clinician, and empathy improve patient motivation and satisfaction. This report serves as a guide, and the committee continues to recognize that the responsible physician's judgment remains paramount.
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National High Blood Pressure Education Program
Prevention,
Detection,
Evaluation, and
Treatment of
High Blood Pressure
The Seventh Report
of the Joint National
Committee on
JNC 7 Express
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
National Heart, Lung, and Blood Institute
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
National Heart, Lung, and Blood Institute
National High Blood Pressure Education Program
NIH Publication No. 03-5233
December 2003
This work was supported entirely by the
National Heart, Lung, and Blood Institute.
The Executive Committee, writing teams,
and reviewers served as volunteers without
remuneration.
Prevention,
Detection,
Evaluation, and
Treatment of
High Blood Pressure
The Seventh Report
of the Joint National
Committee on
JNC 7 Express
Chair
Aram V. Chobanian, M.D. (Boston University Medical Center, Boston, MA)
Executive Committee
George L. Bakris, M.D. (Rush Presbyterian-St. Luke’s Medical Center,
Chicago, IL); Henry R. Black, M.D. (Rush Presbyterian-St. Luke’s Medical
Center, Chicago, IL); William C. Cushman, M.D. (Veterans Affairs Medical
Center, Memphis, TN); Lee A. Green, M.D., M.P.H. (University of Michigan,
Ann Arbor, MI); Joseph L. Izzo, Jr., M.D. (State University of New York at
Buffalo School of Medicine, Buffalo, NY); Daniel W. Jones, M.D. (University
of Mississippi Medical Center, Jackson, MS); Barry J. Materson, M.D.,
M.B.A. (University of Miami, Miami, FL); Suzanne Oparil, M.D. (University
of Alabama at Birmingham, Birmingham, AL); Jackson T. Wright, Jr., M.D.,
Ph.D. (Case Western Reserve University, Cleveland, OH)
Executive Secretary
Edward J. Roccella, Ph.D., M.P.H. (National Heart, Lung, and Blood
Institute, Bethesda, MD)
National High Blood Pressure Education Program
Coordinating Committee Participants
Claude Lenfant, M.D., Chair (National Heart, Lung, and Blood Institute,
Bethesda, MD); George L. Bakris, M.D. (Rush Presbyterian-St. Luke’s
Medical Center, Chicago, IL); Henry R. Black, M.D. (Rush Presbyterian-
St. Luke’s Medical Center, Chicago, IL); Vicki Burt, Sc.M., R.N. (National
Center for Health Statistics, Hyattsville, MD); Barry L. Carter, Pharm.D.
(University of Iowa, Iowa City, IA); Jerome D. Cohen, M.D. (Saint Louis
University School of Medicine, St. Louis, MO); Pamela J. Colman, D.P.M.
(American Podiatric Medical Association, Bethesda, MD); William C.
Cushman, M.D. (Veterans Affairs Medical Center, Memphis, TN);
Mark J. Cziraky, Pharm.D., F.A.H.A. (Health Core, Inc., Newark, DE);
John J. Davis, P.A.-C. (American Academy of Physician Assistants, Memphis,
TN); Keith Copelin Ferdinand, M.D., F.A.C.C. (Heartbeats Life Center, New
Orleans, LA); Ray W. Gifford, Jr., M.D., M.S. (Cleveland Clinic Foundation,
Fountain Hills, AZ); Michael Glick, D.M.D. (UMDNJ—New Jersey Dental
School, Newark, NJ); Lee A. Green, M.D., M.P.H. (University of Michigan,
Ann Arbor, MI); Stephen Havas, M.D., M.P.H., M.S. (University of Maryland
School of Medicine, Baltimore, MD); Thomas H. Hostetter, M.D. (National
Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD);
Joseph L. Izzo, Jr., M.D. (State University of New York at Buffalo School of
Medicine, Buffalo, NY); Daniel W. Jones, M.D. (University of Mississippi
Medical Center, Jackson, MS); Lynn Kirby, R.N., N.P., C.O.H.N.-S. (Sanofi-
Synthelabo Research, Malvern, PA); Kathryn M. Kolasa, Ph.D., R.D., L.D.N.
iii
(Brody School of Medicine at East Carolina University, Greenville, NC);
Stuart Linas, M.D. (University of Colorado Health Sciences Center, Denver,
CO); William M. Manger, M.D., Ph.D. (New York University Medical
Center, New York, NY); Edwin C. Marshall, O.D., M.S., M.P.H. (Indiana
University School of Optometry, Bloomington, IN); Barry J. Materson, M.D.,
M.B.A. (University of Miami, Miami, FL); Jay Merchant, M.H.A. (Centers
for Medicare & Medicaid Services, Washington, DC); Nancy Houston Miller,
R.N., B.S.N. (Stanford University School of Medicine, Palo Alto, CA);
Marvin Moser, M.D. (Yale University School of Medicine, Scarsdale, NY);
William A. Nickey, D.O. (Philadelphia College of Osteopathic Medicine,
Philadelphia, PA); Suzanne Oparil, M.D. (University of Alabama at
Birmingham, Birmingham, AL); Otelio S. Randall, M.D., F.A.C.C. (Howard
University Hospital, Washington, DC); James W. Reed, M.D., F.A.C.P.,
F.A.C.E. (Morehouse School of Medicine, Atlanta, GA); Edward J. Roccella,
Ph.D., M.P.H. (National Heart, Lung, and Blood Institute, Bethesda, MD);
Lee Shaughnessy (National Stroke Association, Englewood,CO);
Sheldon G. Sheps, M.D. (Mayo Clinic, Rochester, MN); David B. Snyder,
R.Ph., D.D.S. (Health Resources and Services Administration, Rockville,
MD); James R. Sowers, M.D. (SUNY Health Science Center at Brooklyn,
Brooklyn, NY); Leonard M. Steiner, M.S., O.D. (Eye Group, Oakhurst, NJ);
Ronald Stout, M.D., M.P.H. (Procter and Gamble, Mason, OH);
Rita D. Strickland, Ed.D., R.N. (New York Institute of Technology,
Springfield Gardens, NY); Carlos Vallbona, M.D. (Baylor College of
Medicine, Houston, TX); Howard S. Weiss, M.D., M.P.H. (Georgetown
University Medical Center, Washington Hospital Center, Walter Reed Army
Medical Center, Washington, DC); Jack P. Whisnant, M.D. (Mayo Clinic and
Mayo Medical School, Rochester, MN); Laurie Willshire, M.P.H., R.N.
(American Red Cross, Falls Church, VA); Gerald J. Wilson, M.A., M.B.A.
(Citizens for Public Action on High Blood Pressure and Cholesterol, Inc.,
Potomac, MD); Mary Winston, Ed.D., R.D. (American Heart Association,
Dallas, TX); Jackson T. Wright, Jr., M.D., Ph.D., F. A.C.P. (Case Western
Reserve University, Cleveland, OH)
iv
Reviewers
William B. Applegate, M.D., M.P.H. (Wake Forest University School of
Medicine, Winston Salem, NC); Jan N. Basile, M.D., F.A.C.P. (Veterans
Administration Hospital, Charleston, SC); Robert Carey, M.D., (University
of Virginia Health System, Charlottesville, VA); Victor Dzau, M.D. (Brigham
and Women’s Hospital, Boston, MA); Brent M. Egan, M.D. (Medical
University of South Carolina, Charleston, SC); Bonita Falkner, M.D.
(Jefferson Medical College, Philadelphia, PA); John M. Flack, M.D., M.P.H.
(Wayne State University School of Medicine, Detroit, MI); Edward D.
Frohlich, M.D. (Ochsner Clinic Foundation, New Orleans, LA); Haralambos
Gavras, M.D. (Boston University School of Medicine, Boston, MA); Martin
Grais, M.D. (Feinberg School of Medicine, Northwestern University, Chicago,
IL); Willa A. Hsueh, M.D. (David Geffen School of Medicine, UCLA
Department of Medicine, Los Angeles, CA); Kenneth A. Jamerson, M.D.
(University of Michigan Medical Center, Ann Arbor, MI); Norman M.
Kaplan, M.D. (University of Texas Southwestern Medical Center, Dallas, TX);
Theodore A. Kotchen, M.D. (Medical College of Wisconsin, Milwaukee, WI);
Daniel Levy, M.D. (National Heart, Lung, and Blood Institute, Framingham,
MA); Michael A. Moore, M.D. (Dan River Region Cardiovascular Health
Initiative Program, Danville, VA); Thomas J. Moore, M.D. (Boston University
Medical Center, Boston, MA); Vasilios Papademetriou, M.D., F.A.C.P.,
F.A.C.C. (Veterans Affairs Medical Center, Washington, DC); Carl J. Pepine,
M.D. (University of Florida, College of Medicine, Gainesville, FL); Robert A.
Phillips, M.D., Ph.D. (New York University, Lenox Hill Hospital, New York,
NY); Thomas G. Pickering, M.D., D.Phil. (Mount Sinai Medical Center,
New York, NY); L. Michael Prisant, M.D., F.A.C.C., F.A.C.P. (Medical
College of Georgia, Augusta, GA); C. Venkata S. Ram, M.D. (University
of Texas Southwestern Medical Center and Texas Blood Pressure Institute,
Dallas, TX); Elijah Saunders, M.D., F.A.C.C., F.A.C.P. (University of
Maryland School of Medicine, Baltimore, MD); Stephen C. Textor, M.D.
(Mayo Clinic, Rochester, MN); Donald G. Vidt, M.D. (Cleveland Clinic
Foundation, Cleveland, OH); Myron H. Weinberger, M.D. (Indiana
University School of Medicine, Indianapolis, IN); Paul K. Whelton, M.D.,
M.Sc. (Tulane University Health Sciences Center, New Orleans, LA)
Staff
Joanne Karimbakas, M.S., R.D. (Prospect Associates, Ltd., now part of
American Institutes for Research Health Program, Silver Spring, MD)
We appreciate the assistance of Carol Creech, M.I.L.S. and Gabrielle Gessner
(Prospect Associates, Ltd., now part of American Institutes for Research
Health Program, Silver Spring, MD).
v
The National High Blood Pressure Education Program (NHBPEP)
Coordinating Committee Member Organizations
American Academy of Family Physicians
American Academy of Neurology
American Academy of Ophthalmology
American Academy of Physician Assistants
American Association of Occupational Health Nurses
American College of Cardiology
American College of Chest Physicians
American College of Occupational and Environmental Medicine
American College of Physicians-American Society of Internal Medicine
American College of Preventive Medicine
American Dental Association
American Diabetes Association
American Dietetic Association
American Heart Association
American Hospital Association
American Medical Association
American Nurses Association
American Optometric Association
American Osteopathic Association
American Pharmaceutical Association
American Podiatric Medical Association
American Public Health Association
American Red Cross
American Society of Health-System Pharmacists
American Society of Hypertension
American Society of Nephrology
Association of Black Cardiologists
Citizens for Public Action on High Blood Pressure and Cholesterol, Inc.
Hypertension Education Foundation, Inc.
International Society on Hypertension in Blacks
National Black Nurses Association, Inc.
National Hypertension Association, Inc.
National Kidney Foundation, Inc.
National Medical Association
National Optometric Association
National Stroke Association
NHLBI Ad Hoc Committee on Minority Populations
Society for Nutrition Education
The Society of Geriatric Cardiology
vi
Federal Agencies:
Agency for Healthcare Research and Quality
Centers for Medicare & Medicaid Services
Department of Veterans Affairs
Health Resources and Services Administration
National Center for Health Statistics
National Heart, Lung, and Blood Institute
National Institute of Diabetes and Digestive and Kidney Diseases
vii
contents
Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xi
Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xiii
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1
Methodology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1
Classification of Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2
Cardiovascular Disease Risk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2
Benefits of Lowering Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3
Blood Pressure Control Rates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .4
Accurate Blood Pressure Measurement in the Office . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .4
Ambulatory Blood Pressure Monitoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .5
Self-Measurement of Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .5
Patient Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .5
Laboratory Tests and Other Diagnostic Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .6
Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7
Goals of Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7
Lifestyle Modifications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7
Pharmacologic Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7
Achieving Blood Pressure Control in Individual Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13
Followup and Monitoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .14
Special Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .14
Compelling Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .14
Ischemic Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .14
Heart Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .15
Diabetic Hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .15
Chronic Kidney Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .16
Cerebrovascular Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .16
ix
x
Other Special Situations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .16
Minorities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .16
Obesity and the metabolic syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .16
Left ventricular hypertrophy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .17
Peripheral arterial disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .17
Hypertension in older persons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .17
Postural hypotension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .17
Dementia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .17
Hypertension in women . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .18
Hypertension in children and adolescents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .18
Hypertensive urgencies and emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .18
Additional Considerations in Antihypertensive Drug Choices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .19
Potential favorable effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .19
Potential unfavorable effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .19
Improving Hypertension Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .19
Adherence to Regimens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .19
Resistant Hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .20
Public Health Challenges and Community Programs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .21
Evidence Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .23
Study Abbreviations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .25
Reference List . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .27
xi
preface
Since the “Sixth Report of the Joint National Committee on the Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure (JNC 6)” was
released in 1997, new knowledge has come to light from a variety of sources.
The National High Blood Pressure Education Program Coordinating
Committee (NHBPEP CC), which represents 46 professional, voluntary, and
Federal organizations, has periodically reviewed the emerging findings during its
biannual meetings. Eventually, a critical mass of information accumulated that
generated much demand for a seventh report. My decision to appoint a JNC 7
Committee was predicated on four reasons: (1) publication of many new hyper-
tension observational studies and clinical trials; (2) need for a new, clear, and
concise guideline that would be useful for clinicians; (3) need to simplify the
classification of blood pressure; and (4) clear recognition that the JNC reports
were not being used to their maximum benefit.
Dr. Aram Chobanian was selected as the JNC 7 chair because, like his predeces-
sors, he is well versed in hypertension, yet independent of these major studies.
The JNC 7 Executive Committee and writing teams were selected entirely from
the NHBPEP CC because they are recognized as experts in their disciplines by
their peers. Dr. Chobanian and his colleagues set—and met—a goal of complet-
ing and publishing this work in 5 months because of the urgency of applying
the new information to improve hypertension prevention and treatment.
This has been a remarkable accomplishment, but the task of NHBPEP CC
numbers is far from over. They and many others are now charged with dissemi-
nating the JNC 7 report, because none of this—neither the research studies nor
the recommendations—will matter, unless the JNC 7 is applied. To facilitate its
application, the JNC 7 will be produced in two versions. A “JNC 7 Express”
has been developed for busy clinicians. A longer version to be published later
will provide for a broader and more detailed review of the recommendations.
Additional professional and patient education tools will support implementation
of the JNC 7 recommendations.
Dr. Chobanian has our deep appreciation for leading the JNC 7 Executive and
Coordinating Committee members in developing this new report. I feel confi-
dent that this represents a landmark document and that its application will
greatly improve our ability to address a very important public health problem.
Claude Lenfant, M.D.
Director
National Heart, Lung, and Blood Institute
Chair
National High Blood Pressure Education
Program
xiii
abstract
The “Seventh Report of the Joint National Committee on Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure” provides a
new guideline for hypertension prevention and management. The following
are the report’s key messages:
In persons older than 50 years, systolic blood pressure greater than
140 mmHg is a much more important cardiovascular disease (CVD) risk
factor than diastolic blood pressure.
The risk of CVD beginning at 115/75 mmHg doubles with each
increment of 20/10 mmHg; individuals who are normotensive at age
55 have a 90 percent lifetime risk for developing hypertension.
Individuals with a systolic blood pressure of 120–139 mmHg or a
diastolic blood pressure of 80–89 mmHg should be considered as
prehypertensive and require health-promoting lifestyle modifications
to prevent CVD.
Thiazide-type diuretics should be used in drug treatment for most
patients with uncomplicated hypertension, either alone or combined with
drugs from other classes. Certain high-risk conditions are compelling
indications for the initial use of other antihypertensive drug classes
(angiotensin converting enzyme inhibitors, angiotensin receptor blockers,
beta-blockers, calcium channel blockers).
Most patients with hypertension will require two or more antihypertensive
medications to achieve goal blood pressure (<140/90 mmHg, or
<130/80 mmHg for patients with diabetes or chronic kidney disease).
If blood pressure is >20/10 mmHg above goal blood pressure, consideration
should be given to initiating therapy with two agents, one of which usually
should be a thiazide-type diuretic.
The most effective therapy prescribed by the most careful clinician will
control hypertension only if patients are motivated. Motivation improves
when patients have positive experiences with, and trust in, the clinician.
Empathy builds trust and is a potent motivator.
In presenting these guidelines, the committee recognizes that the responsible
physician’s judgment remains paramount.
introduction
For more than three decades, the National Heart, Lung, and Blood Institute
(NHLBI) has coordinated the National High Blood Pressure Education Program
(NHBPEP), a coalition of 39 major professional, public, and voluntary organi-
zations and seven Federal Agencies. One important function is to issue guide-
lines and advisories designed to increase awareness, prevention, treatment, and
control of hypertension (high blood pressure (BP)). Since the publication of the
“Sixth Report of the Joint National Committee on the Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure (JNC 6)” released in 1997,1
many large-scale clinical trials have been published. The decision to appoint a
JNC 7 committee was based on four factors: (1) publication of many new
hypertension observational studies and clinical trials; (2) need for a new, clear,
and concise guideline that would be useful for clinicians; (3) need to simplify the
classification of blood pressure; and (4) clear recognition that the JNC reports
were not being used to their maximum benefit. This JNC report is presented in
two separate publications: a current, succinct, practical guide and a more com-
prehensive report to be published separately, which will provide a broader dis-
cussion and justification for the current recommendations. In presenting these
guidelines, the committee recognizes that the responsible physician’s judgment is
paramount in managing patients.
methodology
Since the publication of the JNC 6 report, the NHBPEP Coordinating
Committee (CC), chaired by the director of the NHLBI, has regularly reviewed
and discussed the hypertension clinical trials at its biannual meetings. In many
instances, the principal investigator of the larger studies has presented the
information directly to the CC. The committee’s presentations and reviews are
summarized and posted on the NHLBI Web site.2In agreeing to commission a
new report, the Director requested that the CC members provide in writing a
detailed rationale explaining the necessity to update the guidelines and to
describe the critical issues and concepts to be considered for a new report.
The JNC 7 chair was selected, plus a nine-member Executive Committee
appointed entirely from the NHBPEP CC membership. The NHBPEP CC
served as members of five writing teams, each of which was cochaired by two
Executive Committee members. The concepts identified by the NHBPEP CC
membership were used to develop the report outline. A timeline was devel-
oped to complete and publish the work in 5 months. Based on the identified
critical issues and concepts, the Executive Committee identified relevant
Medical Subject Headings (MeSH) terms and keywords to further review the
1
scientific literature. These MeSH terms were used to generate MEDLINE
searches that focused on English language peer-reviewed scientific literature
from January 1997 through April 2003. Various systems of grading the evi-
dence were considered, and the classification scheme used in the JNC 6 report
and other NHBPEP clinical guidelines was selected3,4 which classifies studies in
a process adapted from Last and Abramson.5The Executive Committee met
on six occasions, two of which included meetings with the entire NHBPEP
CC. The writing teams also met by teleconference and used electronic com-
munications to develop the report. Twenty-four drafts were created and
reviewed in a reiterative fashion. At its meetings, the Executive Committee
used a modified nominal group process to identify and resolve issues. The
NHBPEP CC reviewed the penultimate draft and provided written comments
to the Executive Committee. In addition, 33 national hypertension leaders
reviewed and commented on the document. The NHBPEP CC approved the
JNC 7 report.
classification of blood pressure
Table 1 provides a classification of BP for adults ages 18 and older. The classi-
fication is based on the average of two or more properly measured, seated BP
readings on each of two or more office visits. In contrast to the classification
provided in the JNC 6 report, a new category designated prehypertension has
been added, and stages 2 and 3 hypertension have been combined. Patients
with prehypertension are at increased risk for progression to hypertension;
those in the 130–139/80–89 mmHg BP range are at twice the risk to develop
hypertension as those with lower values.6
cardiovascular disease risk
Hypertension affects approximately 50 million individuals in the United States
and approximately 1 billion worldwide. As the population ages, the prevalence
of hypertension will increase even further unless broad and effective preventive
measures are implemented. Recent data from the Framingham Heart Study
suggest that individuals who are normotensive at age 55 have a 90 percent life-
time risk for developing hypertension.7
The relationship between BP and risk of CVD events is continuous, consistent,
and independent of other risk factors. The higher the BP, the greater is the
chance of heart attack, heart failure, stroke, and kidney disease. For individu-
2
als 40–70 years of age, each increment of 20 mmHg in systolic BP (SBP) or
10 mmHg in diastolic BP (DBP) doubles the risk of CVD across the entire BP
range from 115/75 to 185/115 mmHg.8
The classification “prehypertension,” introduced in this report (table 1), recog-
nizes this relationship and signals the need for increased education of health care
professionals and the public to reduce BP levels and prevent the development of
hypertension in the general population.9Hypertension prevention strategies are
available to achieve this goal. (See “Lifestyle Modifications” section.)
benefits of lowering blood pressure
In clinical trials, antihypertensive therapy has been associated with reductions
in stroke incidence averaging 35–40 percent; myocardial infarction, 20–25
percent; and heart failure, more than 50 percent.10 It is estimated that in
patients with stage 1 hypertension (SBP 140–159 mmHg and/or DBP
90–99 mmHg) and additional cardiovascular risk factors, achieving a sus-
tained 12 mmHg reduction in SBP over 10 years will prevent 1 death for
every 11 patients treated. In the presence of CVD or target organ damage,
only 9 patients would require such BP reduction to prevent a death.11
3
Table 1. Classification and management of blood pressure for adults*
SBP*
mmHg
BP
Classification
DBP*
mmHg
Lifestyle
Modification
Without Compelling
Indication
With Compelling
Indications
(See Table 8)
Normal
Prehypertension
Stage 1
Hypertension
Stage 2
Hypertension
<120
120–139
140–159
160
and <80
or 80–89
or 90–99
or ≥100
Encourage
Yes
Yes
Yes
No antihypertensive
drug indicated.
Thiazide-type diuretics
for most. May consider
ACEI, ARB, BB, CCB,
or combination.
Two-drug combination
for most(usually
thiazide-type diuretic
and ACEI or ARB or BB
or CCB).
Drug(s) for compelling
indications.
Drug(s) for the com-
pelling indications.
Other antihypertensive
drugs (diuretics, ACEI,
ARB, BB, CCB)
as needed.
Initial drug therapy
DBP, diastolic blood pressure; SBP, systolic blood pressure.
Drug abbreviations: ACEI, angiotensin converting enzyme inhibitor; ARB, angiotensin receptor blocker; BB, beta-blocker;
CCB, calcium channel blocker.
*Treatment determined by highest BP category.
Initial combined therapy should be used cautiously in those at risk for orthostatic hypotension.
Treat patients with chronic kidney disease or diabetes to BP goal of <130/80 mmHg.
blood pressure control rates
Hypertension is the most common primary diagnosis in America (35 million
office visits as the primary diagnosis).12 Current control rates (SBP <140
mmHg and DBP <90 mmHg), though improved, are still far below the
Healthy People 2010 goal of 50 percent; 30 percent are still unaware they
have hypertension. (See table 2.) In the majority of patients, controlling
systolic hypertension, which is a more important CVD risk factor than DBP
except in patients younger than age 5013 and occurs much more commonly in
older persons, has been considerably more difficult than controlling diastolic
hypertension. Recent clinical trials have demonstrated that effective BP control
can be achieved in most patients who are hypertensive, but the majority will
require two or more antihypertensive drugs.14,15 When clinicians fail to pre-
scribe lifestyle modifications, adequate antihypertensive drug doses, or
appropriate drug combinations, inadequate BP control may result.
accurate blood pressure measurement in the office
The auscultatory method of BP measurement with a properly calibrated and
validated instrument should be used.16 Persons should be seated quietly for
at least 5 minutes in a chair (rather than on an exam table), with feet on the
floor, and arm supported at heart level. Measurement of BP in the standing
position is indicated periodically, especially in those at risk for postural hypoten-
sion. An appropriate-sized cuff (cuff bladder encircling at least 80 percent of the
arm) should be used to ensure accuracy. At least two measurements should be
made. SBP is the point at which the first of two or more sounds is heard
4
Table 2. Trends in awareness, treatment, and control of high blood
pressure in adults ages 18–74*
II
(1976–80)
III (Phase 1
1988–91)
III (Phase 2
1991–94) 1999–2000
National Health and Nutrition Examination Survey, Percent
Awareness
Treatment
Control
51
31
10
73
55
29
68
54
27
70
59
34
*High blood pressure is systolic blood pressure (SBP) 140 mmHg or diastolic blood
pressure (DBP) 90 mmHg or taking antihypertensive medication.
SBP <140 mmHg and DBP <90 mmHg.
Sources: Unpublished data for 1999–2000 computed by M. Wolz, National Heart, Lung,
and Blood Institute; JNC 6.1
(phase 1), and DBP is the point before the disappearance of sounds (phase 5).
Clinicians should provide to patients, verbally and in writing, their specific BP
numbers and BP goals.
ambulatory blood pressure monitoring
Ambulatory blood pressure monitoring (ABPM)17 provides information about
BP during daily activities and sleep. ABPM is warranted for evaluation of
“white-coat” hypertension in the absence of target organ injury. It is also helpful
to assess patients with apparent drug resistance, hypotensive symptoms with
antihypertensive medications, episodic hypertension, and autonomic dysfunction.
The ambulatory BP values are usually lower than clinic readings. Awake, indi-
viduals with hypertension have an average BP of more than 135/85 mmHg and
during sleep, more than 120/75 mmHg. The level of BP measurement by using
ABPM correlates better than office measurements with target organ injury.18
ABPM also provides a measure of the percentage of BP readings that are elevat-
ed, the overall BP load, and the extent of BP reduction during sleep. In most
individuals, BP decreases by 10 to 20 percent during the night; those in whom
such reductions are not present are at increased risk for cardiovascular events.
self-measurement of blood pressure
BP self measurements may benefit patients by providing information on response
to antihypertensive medication, improving patient adherence with therapy,19 and
in evaluating white-coat hypertension. Persons with an average BP more than
135/85 mmHg measured at home are generally considered to be hypertensive.
Home measurement devices should be checked regularly for accuracy.
patient evaluation
Evaluation of patients with documented hypertension has three objectives:
(1) to assess lifestyle and identify other cardiovascular risk factors or con-
comitant disorders that may affect prognosis and guide treatment (table 3);
(2) to reveal identifiable causes of high BP (table 4); and (3) to assess the pres-
ence or absence of target organ damage and CVD. The data needed are
acquired through medical history, physical examination, routine laboratory
tests, and other diagnostic procedures. The physical examination should
5
include an appropriate measurement of BP, with verification in the contralat-
eral arm; examination of the optic fundi; calculation of body mass index
(BMI) (measurement of waist circumference also may be useful); auscultation
for carotid, abdominal, and femoral bruits; palpation of the thyroid gland;
thorough examination of the heart and lungs; examination of the abdomen
for enlarged kidneys, masses, and abnormal aortic pulsation; palpation of the
lower extremities for edema and pulses; and neurological assessment.
Laboratory Tests and Other Diagnostic Procedures
Routine laboratory tests recommended before initiating therapy include an
electrocardiogram; urinalysis; blood glucose and hematocrit; serum potassium,
creatinine (or the corresponding estimated glomerular filtration rate [GFR]),
and calcium;20 and a lipid profile, after 9- to 12-hour fast, that includes high-
density lipoprotein cholesterol and low-density lipoprotein cholesterol, and
triglycerides. Optional tests include measurement of urinary albumin excre-
tion or albumin/creatinine ratio. More extensive testing for identifiable causes
is not indicated generally unless BP control is not achieved.
6
Table 4. Identifiable causes of hypertension
Sleep apnea
Drug-induced or related causes (see table 9)
Chronic kidney disease
Primary aldosteronism
Renovascular disease
Chronic steroid therapy and Cushing’s syndrome
Pheochromocytoma
Coarctation of the aorta
Thyroid or parathyroid disease
Table 3. Cardiovascular risk factors
Major Risk Factors
Target Organ Damage
Hypertension*
Cigarette smoking
Obesity*(body mass index ≥30 kg/m2)
Physical inactivity
Dyslipidemia*
Diabetes mellitus*
Microalbuminuria or estimated GFR <60 mL/min
Age (older than 55 for men, 65 for women)
Family history of premature cardiovascular disease
(men under age 55 or women under age 65)
GFR, glomerular filtration rate.
*Components of the metabolic syndrome.
Heart
Left ventricular hypertrophy
Angina or prior myocardial infarction
Prior coronary revascularization
Heart failure
Brain
Stroke or transient ischemic attack
Chronic kidney disease
Peripheral arterial disease
Retinopathy
treatment
Goals of Therapy
The ultimate public health goal of antihypertensive therapy is the reduction
of cardiovascular and renal morbidity and mortality. Since most persons with
hypertension, especially those age >50 years, will reach the DBP goal once
SBP is at goal, the primary focus should be on achieving the SBP goal.
Treating SBP and DBP to targets that are <140/90 mmHg is associated with
a decrease in CVD complications. In patients with hypertension and diabetes
or renal disease, the BP goal is <130/80 mmHg.21,22
Lifestyle Modifications
Adoption of healthy lifestyles by all persons is critical for the prevention of
high BP and is an indispensable part of the management of those with hyper-
tension. Major lifestyle modifications shown to lower BP include weight
reduction in those individuals who are overweight or obese,23,24 adoption of
the Dietary Approaches to Stop Hypertension (DASH) eating plan25 which is
rich in potassium and calcium,26 dietary sodium reduction,25–27 physical activi-
ty,28,29 and moderation of alcohol consumption. (See table 5.)30 Lifestyle modifi-
cations reduce BP, enhance antihypertensive drug efficacy, and decrease cardio-
vascular risk. For example, a 1,600 mg sodium DASH eating plan has effects
similar to single drug therapy.25 Combinations of two (or more) lifestyle modi-
fications can achieve even better results.
Pharmacologic Treatment
There are excellent clinical outcome trial data proving that lowering BP with
several classes of drugs, including angiotensin converting enzyme inhibitors
(ACEIs), angiotensin receptor blockers (ARBs), beta-blockers (BBs), calcium
channel blockers (CCBs), and thiazide-type diuretics, will all reduce the com-
plications of hypertension.10,31–37 Tables 6 and 7 provide a list of commonly
used antihypertensive agents.
Thiazide-type diuretics have been the basis of antihypertensive therapy in
most outcome trials.37 In these trials, including the recently published
Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial
(ALLHAT),33 diuretics have been virtually unsurpassed in preventing the car-
diovascular complications of hypertension. The exception is the Second
Australian National Blood Pressure trial which reported slightly better out-
comes in White men with a regimen that began with an ACEI compared to
one starting with a diuretic.36 Diuretics enhance the antihypertensive efficacy
7
of multidrug regimens, can be useful in achieving BP control, and are more
affordable than other antihypertensive agents. Despite these findings, diuretics
remain underutilized.39
Thiazide-type diuretics should be used as initial therapy for most patients with
hypertension, either alone or in combination with one of the other classes
(ACEIs, ARBs, BBs, CCBs) demonstrated to be beneficial in randomized con-
trolled outcome trials. The list of compelling indications requiring the use of
other antihypertensive drugs as initial therapy are listed in table 8. If a drug is
not tolerated or is contraindicated, then one of the other classes proven to
reduce cardiovascular events should be used instead.
8
Table 5. Lifestyle modifications to manage hypertension*†
Modification Recommendation
Approximate SBP
Reduction (Range)
Weight reduction Maintain normal body weight 5–20 mmHg/10 kg
(body mass index 18.5–24.9 kg/m2). weight loss23,24
Adopt DASH eating plan Consume a diet rich in fruits, 8–14 mmHg25,26
vegetables, and lowfat dairy
products with a reduced content
of saturated and total fat.
Dietary sodium reduction Reduce dietary sodium intake to 2–8 mmHg25–27
no more than 100 mmol per day
(2.4 g sodium or 6 g sodium chloride).
Physical activity Engage in regular aerobic physical 4–9 mmHg28,29
activity such as brisk walking
(at least 30 min per day, most
days of the week).
Moderation of alcohol Limit consumption to no more than 2–4 mmHg30
consumption 2 drinks (1 oz or 30 mL ethanol;
e.g., 24 oz beer, 10 oz wine,
or 3 oz 80-proof whiskey)
per day in most men and to no
more than 1 drink per day in women
and lighter weight persons.
DASH, Dietary Approaches to Stop Hypertension.
*For overall cardiovascular risk reduction, stop smoking.
The effects of implementing these modifications are dose and time dependent, and could be greater for some
individuals.
9
Table 6. Oral antihypertensive drugs*
Class Drug (Trade Name)
Usual dose range
in mg/day
Usual Daily
Frequency
Thiazide diuretics Chlorothiazide (Diuril) 125-500 1-2
chlorthalidone (generic) 12.5-25 1
hydrochlorothiazide (Microzide, HydroDIURIL)12.5-50 1
polythiazide (Renese) 2-4 1
indapamide (Lozol)1.25-2.5 1
metolazone (Mykrox) 0.5-1.0 1
metolazone (Zaroxolyn) 2.5-5 1
Loop diuretics bumetanide (Bumex)0.5-2 2
furosemide (Lasix)20-80 2
torsemide (Demadex) 2.5-10 1
Potassium-sparing diuretics amiloride (Midamor)5-10 1-2
triamterene (Dyrenium) 50-100 1-2
Aldosterone receptor blockers eplerenone (Inspra) 50-100 1
spironolactone (Aldactone) 25-50 1
BBs atenolol (Tenormin)25-100 1
betaxolol (Kerlone)5-20 1
bisoprolol (Zebeta)2.5-10 1
metoprolol (Lopressor)50-100 1-2
metoprolol extended release (Toprol XL) 50-100 1
nadolol (Corgard)40-120 1
propranolol (Inderal)40-160 2
propranolol long-acting (Inderal LA)60-180 1
timolol (Blocadren)20-40 2
BBs with intrinsic acebutolol (Sectral)200-800 2
sympathomimetic activity
penbutolol (Levatol) 10-40 1
pindolol (generic) 10-40 2
Combined alpha- and BBs carvedilol (Coreg) 12.5-50 2
labetalol (Normodyne, Trandate) 200-800 2
10
Table 6. Oral antihypertensive drugs*(continued)
Class Drug (Trade Name)
ACEIs benazepril (Lotensin)10-40 1
captopril (Capoten)25-100 2
enalapril (Vasotec)5-40 1-2
fosinopril (Monopril) 10-40 1
lisinopril (Prinivil, Zestril)10-40 1
moexipril (Univasc) 7.5-30 1
perindopril (Aceon) 4-8 1
quinapril (Accupril) 10-80 1
ramipril (Altace) 2.5-20 1
trandolapril (Mavik) 1-4 1
Angiotensin II antagonists candesartan (Atacand) 8-32 1
eprosartan (Teveten) 400-800 1-2
irbesartan (Avapro) 150-300 1
losartan (Cozaar) 25-100 1-2
olmesartan (Benicar) 20-40 1
telmisartan (Micardis) 20-80 1
valsartan (Diovan) 80-320 1-2
CCBs—non-Dihydropyridines Diltiazem extended release 180-420 1
(Cardizem CD, Dilacor XR, Tiazac)
diltiazem extended release (Cardizem LA) 120-540 1
verapamil immediate release (Calan, Isoptin)80-320 2
verapamil long acting (Calan SR, Isoptin SR)120-480 1-2
verapamil—Coer, Covera HS, Verelan PM) 120-360 1
CCBs—Dihydropyridines amlodipine (Norvasc) 2.5-10 1
felodipine (Plendil) 2.5-20 1
isradipine (Dynacirc CR) 2.5-10 2
nicardipine sustained release (Cardene SR) 60-120 2
nifedipine long-acting (Adalat CC, Procardia XL) 30-60 1
nisoldipine (Sular) 10-40 1
Usual dose range
in mg/day
Usual Daily
Frequency
11
*In some patients treated once daily, the antihypertensive effect may diminish toward the end of the dosing interval
(trough effect). BP should be measured just prior to dosing to determine if satisfactory BP control is obtained.
Accordingly, an increase in dosage or frequency may need to be considered. These dosages may vary from those listed
in the “Physicians Desk Reference, 57th ed.”
Available now or soon to become available in generic preparations.
Source: Physicians' Desk Reference. 57 ed. Montvale, NJ: Thomson PDR, 2003
Table 6. Oral antihypertensive drugs*(continued)
Class Drug (Trade Name)
Alpha-1 blockers doxazosin (Cardura) 1-16 1
prazosin (Minipress)2-20 2-3
terazosin (Hytrin) 1-20 1-2
Central alpha-2 agonists and clonidine (Catapres)0.1-0.8 2
other centrally acting drugs
clonidine patch (Catapres-TTS) 0.1-0.3 1 wkly
methyldopa (Aldomet)250-1,000 2
reserpine (generic) 0.1-0.25 1
guanfacine (Tenex)0.5-2 1
Direct vasodilators hydralazine (Apresoline)25-100 2
minoxidil (Loniten)2.5-80 1-2
Usual dose range
in mg/day
Usual Daily
Frequency
12
Table 7. Combination drugs for hypertension
Combination Type*Fixed-Dose Combination, mgTrade Name
ACEIs and CCBs Amlodipine-benazepril hydrochloride (2.5/10, 5/10, 5/20, 10/20) Lotrel
Enalapril-felodipine (5/5) Lexxel
Trandolapril-verapamil (2/180, 1/240, 2/240, 4/240) Tarka
ACEIs and diuretics Benazepril-hydrochlorothiazide (5/6.25, 10/12.5, 20/12.5, 20/25) Lotensin HCT
Captopril-hydrochlorothiazide (25/15, 25/25, 50/15, 50/25) Capozide
Enalapril-hydrochlorothiazide (5/12.5, 10/25) Vaseretic
Fosinopril-hydrochlorothiazide (10/12.5, 20/12.5) Monopril/HCT
Lisinopril-hydrochlorothiazide (10/12.5, 20/12.5, 20/25) Prinzide, Zestoretic
Moexipril-hydrochlorothiazide (7.5/12.5, 15/25) Uniretic
Quinapril-hydrochlorothiazide (10/12.5, 20/12.5, 20/25) Accuretic
ARBs and diuretics Candesartan-hydrochlorothiazide (16/12.5, 32/12.5) Atacand HCT
Eprosartan-hydrochlorothiazide (600/12.5, 600/25) Teveten-HCT
Irbesartan-hydrochlorothiazide (150/12.5, 300/12.5) Avalide
Losartan-hydrochlorothiazide (50/12.5, 100/25) Hyzaar
Olmesartan medoxomil-hydrochlorothiazide (20/12.5,40/12.5,40/25) Benicar HCT
Telmisartan-hydrochlorothiazide (40/12.5, 80/12.5) Micardis-HCT
Valsartan-hydrochlorothiazide (80/12.5, 160/12.5, 160/25) Diovan-HCT
BBs and diuretics Atenolol-chlorthalidone (50/25, 100/25) Tenoretic
Bisoprolol-hydrochlorothiazide (2.5/6.25, 5/6.25, 10/6.25) Ziac
Metoprolol-hydrochlorothiazide (50/25, 100/25) Lopressor HCT
Nadolol-bendroflumethiazide (40/5, 80/5) Corzide
Propranolol LA-hydrochlorothiazide (40/25, 80/25) Inderide LA
Timolol-hydrochlorothiazide (10/25) Timolide
Centrally acting drug Methyldopa-hydrochlorothiazide (250/15, 250/25, 500/30, 500/50) Aldoril
and diuretic
Reserpine-chlothalidone (0.125/25, 0.25/50) Demi-Regroton,
Regroton
Reserpine-chlorothiazide (0.125/250, 0.25/500) Diupres
Reserpine-hydrochlorothiazide (0.125/25, 0.125/50) Hydropres
Diuretic and diuretic Amiloride-hydrochlorothiazide (5/50) Moduretic
Spironolactone-hydrochlorothiazide (25/25, 50/50) Aldactazide
Triamterene-hydrochlorothiazide (37.5/25, 75/50) Dyazide, Maxzide
*Drug abbreviations: BB, beta-blocker; ACEI, angiotensin converting enzyme inhibitor; ARB, angiotensin receptor blocker;
CCB, calcium channel blocker.
Some drug combinations are available in multiple fixed doses. Each drug dose is reported in milligrams.
13
Figure 1. Algorithm for treatment of hypertension
Lifestyle Modifications
Not at Goal Blood Pressure (<140/90 mmHg)
(<130/80 mmHg for patients with diabetes or chronic kidney disease)
Initial Drug Choices
Without Compelling
Indications
With Compelling
Indications
Not at Goal Blood Pressure
Stage 1
Hypertension
(SBP 140–159 or DBP
90–99 mmHg)
Thiazide-type diuretics
for most. May consider
ACEI, ARB, BB, CCB,
or combination.
Stage 2
Hypertension
(SBP ≥160 or DBP
≥100 mmHg)
Two-drug combination for
most (usually thiazide-
type diuretic and ACEI,
or ARB, or BB, or CCB).
Drug(s) for the
compelling indications
(See table 8)
Other antihypertensive
drugs (diuretics, ACEI,
ARB, BB, CCB) as needed.
Optimize dosages or add additional drugs until goal blood pressure is
achieved. Consider consultation with hypertension specialist.
Achieving Blood Pressure Control in Individual Patients
Most patients who are hypertensive will require two or more antihypertensive
medications to achieve their BP goals.14,15 Addition of a second drug from a
different class should be initiated when use of a single drug in adequate doses
fails to achieve the BP goal. When BP is more than 20/10 mmHg above goal,
consideration should be given to initiating therapy with two drugs, either as
separate prescriptions or in fixed-dose combinations. (See figure 1.) The initia-
tion of drug therapy with more than one agent may increase the likelihood of
achieving the BP goal in a more timely fashion, but particular caution is
advised in those at risk for orthostatic hypotension, such as patients with dia-
betes, autonomic dysfunction, and some older persons. Use of generic drugs
or combination drugs should be considered to reduce prescription costs.
DBP, diastolic blood pressure; SBP, systolic blood pressure.
Drug abbreviations: ACEI, angiotensin converting enzyme inhibitor; ARB, angiotensin receptor blocker;
BB, beta-blocker; CCB, calcium channel blocker.
14
Followup and Monitoring
Once antihypertensive drug therapy is initiated, most patients should return for
followup and adjustment of medications at approximately monthly intervals
until the BP goal is reached. More frequent visits will be necessary for patients
with stage 2 hypertension or with complicating comorbid conditions. Serum
potassium and creatinine should be monitored at least 1–2 times/year.60 After
BP is at goal and stable, followup visits can usually be at 3- to 6-month inter-
vals. Comorbidities, such as heart failure, associated diseases such as diabetes,
and the need for laboratory tests influence the frequency of visits. Other car-
diovascular risk factors should be treated to their respective goals, and tobacco
avoidance should be promoted vigorously. Low-dose aspirin therapy should be
considered only when BP is controlled, because the risk of hemorrhagic stroke
is increased in patients with uncontrolled hypertension.61
special considerations
The patient with hypertension and certain comorbidities requires special
attention and followup by the clinician.
Compelling Indications
Table 8 describes compelling indications that require certain antihypertensive
drug classes for high-risk conditions. The drug selections for these compelling
indications are based on favorable outcome data from clinical trials. A combi-
nation of agents may be required. Other management considerations include
medications already in use, tolerability, and desired BP targets. In many cases,
specialist consultation may be indicated.
Ischemic Heart Disease
Ischemic heart disease (IHD) is the most common form of target organ damage
associated with hypertension. In patients with hypertension and stable angina
pectoris, the first drug of choice is usually a BB; alternatively, long-acting CCBs
can be used.1In patients with acute coronary syndromes (unstable angina or
myocardial infarction), hypertension should be treated initially with BBs and
ACEIs,49 with addition of other drugs as needed for BP control. In patients
with postmyocardial infarction, ACEIs, BBs, and aldosterone antagonists have
proven to be most beneficial.50,52,53,62 Intensive lipid management and aspirin
therapy are also indicated.
15
Heart Failure
Heart failure (HF), in the form of systolic or diastolic ventricular dysfunction,
results primarily from systolic hypertension and IHD. Fastidious BP and cho-
lesterol control are the primary preventive measures for those at high risk for
HF.40 In asymptomatic individuals with demonstrable ventricular dysfunction,
ACEIs and BBs are recommended.52,62 For those with symptomatic ventricular
dysfunction or end-stage heart disease, ACEIs, BBs, ARBs and aldosterone
blockers are recommended along with loop diuretics.40–48
Diabetic Hypertension
Combinations of two or more drugs are usually needed to achieve the target
goal of <130/80 mmHg.21,22 Thiazide diuretics, BBs, ACEIs, ARBs, and CCBs
are beneficial in reducing CVD and stroke incidence in patients with dia-
betes.33,54,63 ACEI- or ARB-based treatments favorably affect the progression of
diabetic nephropathy and reduce albuminuria,55,56 and ARBs have been shown
to reduce progression to macroalbuminuria.56,57
ACC/AHA Heart Failure Guideline,40
MERIT-HF,41 COPERNICUS,42 CIBIS,43
SOLVD,44 AIRE,45 TRACE,46 ValHEFT,47
RALES48
ACC/AHA Post-MI Guideline,49 BHAT,50
SAVE,51 Capricorn,52 EPHESUS53
ALLHAT,33 HOPE,34 ANBP2,36 LIFE,32
CONVINCE31
NKF-ADA Guideline,21,22 UKPDS,54
ALLHAT33
NFK Guideline,22 Captopril Trial,55
RENAAL,56 IDNT,57 REIN,58 AASK59
PROGRESS35
Table 8. Clinical trial and guideline basis for compelling indications for individual drug classes
Compelling Indication*Clinical Trial Basis
Recommended Drugs
Heart failure
Postmyocardial infarction
High coronary disease risk
Diabetes
Chronic kidney disease
Recurrent stroke prevention
*Compelling indications for antihypertensive drugs are based on benefits from outcome studies or existing clinical
guidelines; the compelling indication is managed in parallel with the BP.
Drug abbreviations: ACEI, angiotensin converting enzyme inhibitor; ARB, angiotensin receptor blocker;
Aldo ANT, aldosterone antagonist; BB, beta-blocker; CCB, calcium channel blocker.
Conditions for which clinical trials demonstrate benefit of specific classes of antihypertensive drugs.
Diuretic
BB
ACEI
ARB
CCB
Aldo ANT
16
Chronic Kidney Disease
In people with chronic kidney disease (CKD), as defined by either (1) reduced
excretory function with an estimated GFR below 60 ml/min per 1.73 m2
(corresponding approximately to a creatinine of >1.5 mg/dL in men or
>1.3 mg/dL in women),20 or (2) the presence of albuminuria (>300 mg/day
or 200 mg albumin/g creatinine), therapeutic goals are to slow deterioration
of renal function and prevent CVD. Hypertension appears in the majority of
these patients, and they should receive aggressive BP management, often with
three or more drugs to reach target BP values of <130/80 mmHg.59,64 ACEIs
and ARBs have demonstrated favorable effects on the progression of diabetic
and nondiabetic renal disease.55–59,64 A limited rise in serum creatinine of as
much as 35 percent above baseline with ACEIs or ARBs is acceptable and is
not a reason to withhold treatment unless hyperkalemia develops.65 With
advanced renal disease (estimated GFR <30 ml/min 1.73 m2, corresponding to
a serum creatinine of 2.5–3 mg/dL), increasing doses of loop diuretics are usu-
ally needed in combination with other drug classes.
Cerebrovascular Disease
The risks and benefits of acute lowering of BP during an acute stroke are still
unclear; control of BP at intermediate levels (approximately 160/100 mmHg) is
appropriate until the condition has stabilized or improved. Recurrent stroke
rates are lowered by the combination of an ACEI and thiazide-type diuretic.35
Other Special Situations
Minorities
BP control rates vary in minority populations and are lowest in Mexican
Americans and Native Americans.1In general, the treatment of hypertension
is similar for all demographic groups, but socioeconomic factors and lifestyle
may be important barriers to BP control in some minority patients. The
prevalence, severity, and impact of hypertension are increased in African
Americans, who also demonstrate somewhat reduced BP responses to
monotherapy with BBs, ACEIs, or ARBs compared to diuretics or CCBs.
These differential responses are largely eliminated by drug combinations that
include adequate doses of a diuretic. ACEI-induced angioedema occurs 2–4
times more frequently in African American patients with hypertension than in
other groups.33
Obesity and the metabolic syndrome
Obesity (BMI >30 kg/m2) is an increasingly prevalent risk factor for the devel-
opment of hypertension and CVD. The Adult Treatment Panel III guideline
17
for cholesterol management defines the metabolic syndrome as the presence of
three or more of the following conditions: abdominal obesity (waist circum-
ference >40 inches in men or >35 inches in women), glucose intolerance (fast-
ing glucose >110 mg/dL), BP >130/85 mmHg, high triglycerides (>150
mg/dL), or low HDL (<40 mg/dL in men or <50 mg/dL in women).66
Intensive lifestyle modification should be pursued in all individuals with the
metabolic syndrome, and appropriate drug therapy should be instituted for
each of its components as indicated.
Left ventricular hypertrophy
Left ventricular hypertrophy (LVH) is an independent risk factor that increases
the risk of subsequent CVD. Regression of LVH occurs with aggressive BP
management, including weight loss, sodium restriction, and treatment with all
classes of antihypertensive agents except the direct vasodilators hydralazine,
and minoxidil.1,67
Peripheral arterial disease
Peripheral arterial disease (PAD) is equivalent in risk to IHD. Any class of
antihypertensive drugs can be used in most PAD patients. Other risk factors
should be managed aggressively, and aspirin should be used.
Hypertension in older persons
Hypertension occurs in more than two-thirds of individuals after age 65.1This
is also the population with the lowest rates of BP control.68 Treatment recom-
mendations for older people with hypertension, including those who have iso-
lated systolic hypertension, should follow the same principles outlined for the
general care of hypertension. In many individuals, lower initial drug doses may
be indicated to avoid symptoms; however, standard doses and multiple drugs
are needed in the majority of older people to reach appropriate BP targets.
Postural hypotension
A decrease in standing SBP >10 mmHg, when associated with dizziness or faint-
ing, is more frequent in older patients with systolic hypertension, diabetes, and
those taking diuretics, venodilators (e.g., nitrates, alpha-blockers, and sildenafil-
like drugs), and some psychotropic drugs. BP in these individuals should also
be monitored in the upright position. Caution should be used to avoid volume
depletion and excessively rapid dose titration of antihypertensive drugs.
Dementia
Dementia and cognitive impairment occur more commonly in people with
hypertension. Reduced progression of cognitive impairment may occur with
effective antihypertensive therapy.69,70
18
Hypertension in women
Oral contraceptives may increase BP, and the risk of hypertension increases
with duration of use. Women taking oral contraceptives should have their BP
checked regularly. Development of hypertension is a reason to consider other
forms of contraception. In contrast, menopausal hormone therapy does not
raise BP.71
Women with hypertension who become pregnant should be followed carefully
because of increased risks to mother and fetus. Methyldopa, BBs, and vasodila-
tors are preferred medications for the safety of the fetus.72 ACEI and ARBs
should not be used during pregnancy because of the potential for fetal
defects and should be avoided in women who are likely to become pregnant.
Preeclampsia, which occurs after the 20th week of pregnancy, is characterized
by new-onset or worsening hypertension, albuminuria, and hyperuricemia,
sometimes with coagulation abnormalities. In some patients, preeclampsia may
develop into a hypertensive urgency or emergency and may require hospitaliza-
tion, intensive monitoring, early fetal delivery, and parenteral antihypertensive
and anticonvulsant therapy.72
Hypertension in children and adolescents
In children and adolescents, hypertension is defined as BP that is, on repeated
measurement, at the 95th percentile or greater adjusted for age, height, and
gender.73 The fifth Korotkoff sound is used to define DBP. Clinicians should
be alert to the possibility of identifiable causes of hypertension in younger
children (i.e., kidney disease, coarctation of the aorta). Lifestyle interventions
are strongly recommended, with pharmacologic therapy instituted for higher
levels of BP or if there is insufficient response to lifestyle modifications.74
Choices of antihypertensive drugs are similar in children and adults, but effec-
tive doses for children are often smaller and should be adjusted carefully.
ACEIs and ARBs should not be used in pregnant or sexually active girls.
Uncomplicated hypertension should not be a reason to restrict children from
participating in physical activities, particularly because long-term exercise may
lower BP. Use of anabolic steroids should be strongly discouraged. Vigorous
interventions also should be conducted for other existing modifiable risk fac-
tors (e.g., smoking).
Hypertensive urgencies and emergencies
Patients with marked BP elevations and acute target-organ damage (e.g.,
encephalopathy, myocardial infarction, unstable angina, pulmonary edema,
eclampsia, stroke, head trauma, life-threatening arterial bleeding, or aortic
dissection) require hospitalization and parenteral drug therapy.1Patients with
markedly elevated BP but without acute target organ damage usually do not
require hospitalization, but they should receive immediate combination oral
19
antihypertensive therapy. They should be carefully evaluated and monitored
for hypertension-induced heart and kidney damage and for identifiable causes
of hypertension. (See table 4.)
Additional Considerations in Antihypertensive Drug Choices
Antihypertensive drugs can have favorable or unfavorable effects on other
comorbidities.
Potential favorable effects
Thiazide-type diuretics are useful in slowing demineralization in osteoporosis.
BBs can be useful in the treatment of atrial tachyarrhythmias/fibrillation,
migraine, thyrotoxicosis (short term), essential tremor, or perioperative hyper-
tension. CCBs may be useful in Raynaud’s syndrome and certain arrhythmias,
and alpha-blockers may be useful in prostatism.
Potential unfavorable effects
Thiazide diuretics should be used cautiously in patients who have gout or
who have a history of significant hyponatremia. BBs should generally be
avoided in individuals who have asthma, reactive airways disease, or second
or third degree heart block. ACEIs and ARBs should not be given to women
likely to become pregnant and are contraindicated in those who are. ACEIs
should not be used in individuals with a history of angioedema. Aldosterone
antagonists and potassium-sparing diuretics can cause hyperkalemia and
should generally be avoided in patients who have serum potassium values
more than 5.0 mEq/L while not taking medications.
improving hypertension control
Adherence to Regimens
Behavioral models suggest that the most effective therapy prescribed by
the most careful clinician will control hypertension only if the patient is
motivated to take the prescribed medication and to establish and maintain a
health-promoting lifestyle. Motivation improves when patients have positive
experiences with and trust in their clinicians. Empathy both builds trust and is
a potent motivator.75
Patient attitudes are greatly influenced by cultural differences, beliefs, and
previous experiences with the health care system.76 These attitudes must be
understood if the clinician is to build trust and increase communication with
patients and families.
20
Failure to titrate or combine medications, despite knowing the patient is not
at goal BP, represents clinical inertia and must be overcome.77 Decision sup-
port systems (i.e., electronic and paper), flow sheets, feedback reminders,
and involvement of nurse clinicians and pharmacists can be helpful.78
The clinician and the patient must agree upon BP goals. A patient-centered
strategy to achieve the goal and an estimation of the time needed to reach
goal are important.79 When BP is above goal, alterations in the plan should
be documented. BP self-monitoring can also be useful.
Patients’ nonadherence to therapy is increased by misunderstanding of the
condition or treatment, denial of illness because of lack of symptoms or per-
ception of drugs as symbols of ill health, lack of patient involvement in the
care plan, or unexpected adverse effects of medications. The patient should
be made to feel comfortable in telling the clinician all concerns and fears of
unexpected or disturbing drug reactions.
The cost of medications and the complexity of care (i.e., transportation,
patient difficulty with polypharmacy, difficulty in scheduling appointments,
and life’s competing demands) are additional barriers that must be overcome
to achieve goal BP.
All members of the health care team (e.g., physicians, nurse case managers,
and other nurses, physician assistants, pharmacists, dentists, registered dieti-
tians, optometrists, and podiatrists) must work together to influence and rein-
force instructions to improve patients’ lifestyles and BP control.80
Resistant Hypertension
Resistant hypertension is the failure to reach goal BP in patients who are
adhering to full doses of an appropriate three-drug regimen that includes a
diuretic. After excluding potential identifiable hypertension (see table 4), clini-
cians should carefully explore reasons why the patient is not at goal BP. (See
table 9.) Particular attention should be paid to diuretic type and dose in rela-
tion to renal function. (See “Chronic Kidney Disease” section.) Consultation
with a hypertension specialist should be considered if goal BP cannot be
achieved.
21
public health challenges and community programs
Public health approaches, such as reducing calories, saturated fat, and salt in
processed foods and increasing community/school opportunities for physical
activity, can achieve a downward shift in the distribution of a population’s BP,
thus potentially reducing morbidity, mortality, and the lifetime risk of an indi-
vidual’s becoming hypertensive. This becomes especially critical as the increase
in BMI of Americans has reached epidemic levels. Now, 122 million adults
are overweight or obese, which contributes to the rise in BP and related con-
ditions.81 The JNC 7 endorses the American Public Health Association resolu-
tion that the food manufacturers and restaurants reduce sodium in the food
supply by 50 percent over the next decade. When public health intervention
strategies address the diversity of racial, ethnic, cultural, linguistic, religious,
and social factors in the delivery of their services, the likelihood of their
acceptance by the community increases. These public health approaches can
provide an attractive opportunity to interrupt and prevent the continuing
costly cycle of managing hypertension and its complications.
Drug-Induced or Other Causes
Nonadherence
Inadequate doses
Inappropriate combinations
Nonsteroidal anti-inflammatory drugs; cyclooxygenase 2 inhibitors
Cocaine, amphetamines, other illicit drugs
Sympathomimetics (decongestants, anorectics)
Oral contraceptives
Adrenal steroids
Cyclosporine and tacrolimus
Erythropoietin
Licorice (including some chewing tobacco)
Selected over-the-counter dietary supplements and medicines
(e.g., ephedra, ma haung, bitter orange)
Table 9. Causes of resisitant hypertension
Improper BP Measurement
Identifiable Causes of Hypertension. (See table 4.)
Volume Overload and Pseudotolerance
Excess sodium intake
Volume retention from kidney disease
Inadequate diuretic therapy
Associated Conditions
Obesity
Excess alcohol intake
23
evidence classification
The studies that provided evidence supporting the recommendations of this
report were classified and reviewed by the staff and the Executive Committee.
The classification scheme is from the JNC 6 report.2
MMeta-analysis; use of statistical methods to combine the results from
clinical trials
RA Randomized controlled trials; also known as experimental studies
RE Retrospective analyses; also known as case-control studies
FProspective study; also known as cohort studies, including historical
or prospective followup studies.
XCross-sectional survey; also known as prevalence studies
PR Previous review or position statements
CClinical interventions (nonrandomized)
25
study abbreviations
AASK African American Study of Kidney Disease
and Hypertension
ACC/AHA American College of Cardiology/American Heart
Association
AIRE Acute Infarction Ramipril Efficacy
ALLHAT Antihypertensive and Lipid-Lowering Treatment To Prevent
Heart Attack Trial
ANBP2 Second Australian National Blood Pressure Study
BHAT β-Blocker Heart Attack Trial
CIBIS Cardiac Insufficiency Bisoprolol Study
CONVINCE Controlled Onset Verapamil Investigation
of Cardiovascular End Points
COPERNICUS Carvedilol Prospective Randomized Cumulative
Survival Study
EPHESUS Eplerenone Post-Acute Myocardial Infarction Heart Failure
Efficacy and Survival Study
HOPE Heart Outcomes Prevention Evaluation Study
IDNT Irbesartan Diabetic Nephropathy Trial
LIFE Losartan Intervention For Endpoint Reduction
in Hypertension Study
MERIT-HF Metoprolol CR/XL Randomized Intervention Trial
in Congestive Heart Failure
NKF-ADA National Kidney Foundation-American Diabetes
Association
PROGRESS Perindopril Protection Against Recurrent Stroke Study
RALES Randomized Aldactone Evaluation Study
REIN Ramipril Efficacy in Nephropathy Study
RENAAL Reduction of Endpoints in Non Insulin Dependent
Diabetes Mellitus With the Angiotensin II Antagonist
Losartan Study
SAVE Survival and Ventricular Enlargement Study
SOLVD Studies of Left Ventricular Dysfunction
TRACE Trandolapril Cardiac Evaluation Study
UKPDS United Kingdom Prospective Diabetes Study
ValHEFT Valsartan Heart Failure Trial
27
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... Researchers consulted with bell & brass metal workers to know whether they suffer any health problems, including respiratory trouble, musculoskeletal pain, common cold or vision disorder. Resting blood pressure of the workers was also measured and precisely categorized (Chobanian et al., 2003). ...
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... Hypertension was defined as the individual's systolic BP (SBP) of ≥140 mmHg and/or the individual's diastolic BP (DBP) of ≥ 90 mmHg and/or history of HTN and/or current or past use of antihypertensives [31]. The age considered at risk for HTN was 45 years or older for men and 55 years or older for women [32]. ...
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Several studies have reported that pravastatin can mitigate the progression of kidney disease, but limited evidence exists regarding its effects on kidney function in Asian patients. This multicenter prospective observational study aimed to assess the effect of pravastatin on kidney function in Korean patients with dyslipidemia and type 2 diabetes mellitus (T2DM) in clinical practice. This 48-week prospective multicenter study included 2604 of 2997 eligible patients with dyslipidemia and T2DM who had available estimated glomerular filtration rate (eGFR) measurements. The primary endpoint was eGFR percent change at week 24 from baseline. We also assessed secondary endpoints, which included percent changes in eGFR at weeks 12 and 48 from baseline, as well as changes in eGFR, metabolic profiles (lipid and glycemic levels) at 12, 24, and 48 weeks from baseline, and safety. We noted a significant improvement in eGFR, with mean percent changes of 2.5%, 2.5%, and 3.0% at 12, 24, and 48 weeks, respectively (all adjusted p < 0.05). The eGFR percent changes significantly increased in subgroups with baseline eGFR 30–90 mL/min/1.73 m2, glycated hemoglobin (HbA1c) ≥ 7 at baseline, no hypertension history, T2DM duration > 5 years, or previous statin therapy. Lipid profiles were improved and remained stable throughout the study, and interestingly, fasting glucose and HbA1c were improved at 24 weeks. Our findings suggest that pravastatin may have potential benefits for improving eGFR in Korean patients with dyslipidemia and T2DM. This could make it a preferable treatment option for patients with reduced kidney function. NCT05107063 submitted October 27, 2021.
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Background Hypertension is a serious public health issue in the general population, with a considerable proportion of cases inadequately being treated. Methods This hospital-based prospective study was carried out at our tertiary care teaching hospital between November 2019 and November 2021. One hundred patients who were recently diagnosed to have hypertension were studied. Results The age of the subjects ranged from 31 to 78 years with a mean age of 49 years. Of these, 40% were in the 40–49 years’ age group; there were 68 males. The body mass index (BMI, Kg/m ² ) distribution of the study subjects showed 22% with normal weight, 62% in overweight and 16% in obese category. Microalbuminuria was evident in 28% of newly diagnosed hypertensives. The sex-wise distribution of microalbuminuria revealed that 17 of 68 males (25%) and 11 of 32 females (34.4%) had microalbuminuria. Conclusions The chronicity of hypertension, age and BMI were the main factors determining microalbuminuria.
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Blood pressure (BP) control rates around the world are suboptimal. Part 2 of the National Health and Nutrition Educational Survey (NHANES) III indicates that only 27.4% of hypertensive Americans aged 18 to 74 years have a BP of <140/90 mm Hg. We wanted to assess BP control during the first 2 years and to describe the baseline characteristics of patients enrolled in the Controlled ONset Verapamil INvestigation of Cardiovascular Endpoints (CONVINCE) Study, an international clinical trial that compares outcomes in hypertensive patients randomized to initial treatment with either controlled-onset extended-release verapamil or the investigator’s choice of atenolol or hydrochlorothiazide. At randomization, BP was <140/90 mm Hg in only 20.3% of the 16 602 subjects (average±SD age 65.6±7.4 years; 56% women, 84% white/7% black/7% Hispanic). The average BP at enrollment was 148/85 mm Hg for patients taking BP medications (n=13 879) and 161/94 mm Hg for previously untreated patients (n=2723). After medication titration, with a transtelephonic computer that recommended an increase in the dose or number of antihypertensive agents whenever the BP was 140/90 mm Hg, 84.8% of the subjects attained the goal BP. During 2 years of treatment, BP control was maintained in 67% to 69% of the subjects (69% to 71% for systolic BP of <140 mm Hg and 90% for diastolic BP of <90 mm Hg). These data suggest that the control of systolic BP is more difficult than the control of diastolic BP. The US national goal of having 50% of hypertensives with a BP of <140/90 mm Hg may be achievable if a forced titration strategy is used. Interested investigators, free care and medications, and well-educated subjects may make the attainment of such a goal easier in the CONVINCE study than in the general population.
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Context. Hypertensive patients are often given a calcium antagonist to reduce cardio-vascular disease risk, but the benefit compared with other drug classes is controversial. Objective. To determine whether initial therapy with controlled-onset extended- release (COER) verapamil is equivalent to a physician’s choice of atenolol or hydrochlorothiazide in preventing cardiovascular disease. Design, Setting, and Participants. Double-blind, randomized clinical trial conducted at 661 centers in 15 countries. A total of 16602 participants diagnosed as having hypertension and who had 1 or more additional risk factors for cardiovascular disease were enrolled between September 1996 and December 1998 and followed up until December 31, 2000. After a mean of 3 years of follow-up, the sponsor closed the study before unblinding the results. Intervention. Initially, 8241 participants received 180 mg of COER verapamil and 8361 received either 50 mg of atenolol or 12.5 mg of hydrochlorothiazide. Other drugs (eg, diuretic, beta-blocker, or an angiotensin-converting enzyme inhibitor) could be added in specified sequence if needed. Main Outcome Measures. First occurrence of stroke, myocardial infarction, or cardiovascular disease–related death. Results. Systolic and diastolic blood pressure were reduced by 13.6 mm Hg and 7.8mm Hg for participants assigned to the COER verapamil group and by 13.5 and 7.1 nomm Hg for partcipants assigned to the atenolol or hydrochlorothiazide group. There were 364 primary cardiovascular disease–related events that occurred in the COER verapamil group vs 365 in atenolol or hydrochlorothiazide group (hazard ratio [HR], 1.02; 95% confidence interval [CI], 0.88-1.18; P=.77). For fatal or nonfatal stroke, the HR was 1.15 (95% CI, 0.90-1.48); for fatal or nonfatal myocardial infarction, 0.82 (95% CI, 0.65-1.03); and for cardiovascular disease–related death, 1.09 (95% CI, 0.87-1.37). The HR was 1.05 (95% CI, 0.95-1.16) for any prespecified cardiovascular disease–related event and 1.08 (95% CI, 0.93-1.26) for all-cause mortality. Non-stroke hemorrhage was more common with participants in the COER-verapamil group (n=118) compared with the atenolol or hydrochlorothiazide group (n=79) (HR, 1.54[95% CI, 1.16-2.04]; P=.003). More cardiovascular disease–related events occurred between 6 AM and noon in both the COER verapamil (99/277) and atenolol or hydrochlorothiazide (88/274) groups; HR, 1.15 (95% CI, 0.86-1.53). Conclusions. The CONVINCE trial did not demonstrate equivalence of a COER verapamil–based antihypertensive regimen compared with a regimen beginning with a diuretic or beta-blocker. When considered in the context of other trials of calcium antagonists, these data indicate that the effectiveness of calcium-channel therapy in reducing cardiovascular disease is similar but not better than diuretic or �beta-blocker treatment.
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Background Despite treatment, there is often a higher incidence of cardiovascular complications in patients with hypertension than in normotensive individuals. Inadequate reduction of their blood pressure is a likely cause, but the optimum target blood pressure is not known. The impact of acetylsalicylic acid (aspirin) has never been investigated in patients with hypertension. We aimed to assess the optimum target diastolic blood pressure and the potential benefit of a low dose of acetylsalicylic acid in the treatment of hypertension. Methods 18 790 patients, from 26 countries, aged 50–80 years (mean 61·5 years) with hypertension and diastolic blood pressure between 100 mm Hg and 115 mm Hg (mean 105 mm Hg) were randomly assigned a target diastolic blood pressure. 6264 patients were allocated to the target pressure ⩽90 mm Hg, 6264 to ⩽85 mm Hg, and 6262 to ⩽80 mm Hg. Felodipine was given as baseline therapy with the addition of other agents, according to a five-step regimen. In addition, 9399 patients were randomly assigned 75 mg/day acetylsalicylic acid (Bamycor, Astra) and 9391 patients were assigned placebo. Findings Diastolic blood pressure was reduced by 20·3 mm Hg, 22·3 mm Hg, and 24·3 mm Hg, in the ⩽90 mm Hg, ⩽85 mm Hg, and ⩽80 mm Hg target groups, respectively. The lowest incidence of major cardiovascular events occurred at a mean achieved diastolic blood pressure of 82·6 mm Hg; the lowest risk of cardiovascular mortality occurred at 86·5 mm Hg. Further reduction below these blood pressures was safe. In patients with diabetes mellitus there was a 51% reduction in major cardiovascular events in target group ⩽80 mm Hg compared with target group ⩽90 mm Hg (p for trend=0·005). Acetylsalicylic acid reduced major cardiovascular events by 15% (p=0·03) and all myocardial infarction by 36% (p=0·002), with no effect on stroke. There were seven fatal bleeds in the acetylsalicylic acid group and eight in the placebo group, and 129 versus 70 non-fatal major bleeds in the two groups, respectively (p<0·001). Interpretation Intensive lowering of blood pressure in patients with hypertension was associated with a low rate of cardiovascular events. The HOT Study shows the benefits of lowering the diastolic blood pressure down to 82·6 mm Hg. Acetylsalicylic acid significantly reduced major cardiovascular events with the greatest benefit seen in all myocardial infarction. There was no effect on the incidence of stroke or fatal bleeds, but non-fatal major bleeds were twice as common.
Article
The age-specific relevance of blood pressure to cause-specific mortality is best assessed by collaborative meta-analysis of individual participant data from the separate prospective studies. Methods Information was obtained on each of one million adults with no previous vascular disease recorded at baseline in 61 prospective observational studies of blood pressure and mortality. During 12.7 million person-years at risk, there were about 56 000 vascular deaths (12 000 stroke, 34000 ischaemic heart disease [IHD], 10000 other vascular) and 66 000 other deaths at ages 40-89 years. Meta-analyses, involving "time-dependent" correction for regression dilution, related mortality during each decade of age at death to the estimated usual blood pressure at the start of that decade. Findings Within each decade of age at death, the proportional difference in the risk of vascular death associated with a given absolute difference in usual blood pressure is about the same down to at least 115 mm Hg usual systolic blood pressure (SBP) and 75 mm Hg usual diastolic blood pressure (DBP), below which there is little evidence. At ages 40-69 years, each difference of 20 mm Hg usual SBP (or, approximately equivalently, 10 mm Hg usual DBP) is associated with more than a twofold difference in the stroke death rate, and with twofold differences in the death rates from IHD and from other vascular causes. All of these proportional differences in vascular mortality are about half as extreme at ages 80-89 years as at,ages 40-49 years, but the annual absolute differences in risk are greater in old age. The age-specific associations are similar for men and women, and for cerebral haemorrhage and cerebral ischaemia. For predicting vascular mortality from a single blood pressure measurement, the average of SBP and DBP is slightly more informative than either alone, and pulse pressure is much less informative. Interpretation Throughout middle and old age, usual blood pressure is strongly and directly related to vascular (and overall) mortality, without any evidence of a threshold down to at least 115/75 mm Hg.
Article
Background: Functional benefit in heart failure due to idiopathic dilated cardiomyopathy has been observed after beta-blockade, but improvement in survival has not been established in a large-scale randomized trial. This was the main objective of the Cardiac Insufficiency Bisoprolol Study (CIBIS). Methods and results: Six hundred forty-one patients with chronic heart failure of various etiologies and a left ventricular ejection fraction of < 40% entered this placebo-controlled, randomized, double-blind study. Patients were in New York Heart Association functional class III (95%) or IV (5%) at inclusion. All received background diuretic and vasodilator therapy (an angiotensin-converting enzyme inhibitor in 90% of cases). A total of 320 patients was randomized to bisoprolol and 321 to placebo. Mean follow-up was 1.9 years. Bisoprolol was well tolerated without between group difference in premature treatment withdrawals (82 on placebo, 75 on bisoprolol; NS). The observed difference in mortality between groups did not reach statistical significance: 67 patients died on placebo, 53 on bisoprolol (P = .22; relative risk, 0.80; 95% confidence interval, 0.56 to 1.15). No significant difference was observed in sudden death rate (17 on placebo, 15 on bisoprolol) or death related to documented ventricular tachycardia or fibrillation (7 on placebo, 4 on bisoprolol). Bisoprolol significantly improved the functional status of the patients; fewer patients in the bisoprolol group required hospitalization for cardiac decompensation (90 on placebo versus 61 on bisoprolol, P < .01), and more patients improved by at least one New York Heart Association functional class (48 on placebo versus 68 on bisoprolol, P = .04) by the end of follow-up period. Conclusions: These results confirm previous trials evidence that a progressively increasing dose of beta-blocker in severe heart failure confers functional benefit. Subgroup analysis suggested that benefit from beta-blockade therapy was greater for those with nonischemic cardiomyopathy. However, improvement in survival while on beta-blockade remains to be demonstrated.
Article
The β-Blocker Heart Attack Trial (BHAT) was a National Heart, Lung, and Blood Institute-sponsored, multicenter, randomized, double-blind, and placebo-controlled trial designed to test whether the regular administration of propranolol hydrochloride to men and women who had experienced at least one myocardial infarction would result in a significant reduction in total mortality during a two- to four-year period. During a 27-month interval, 3,837 persons between the ages of 30 and 69 years were randomized to either propranolol (1,916 persons) or placebo (1,921 persons), five to 21 days after the infarction. Depending on serum drug levels, the prescribed maintenance dose of propranolol hydrochloride was either 180 or 240 mg/day. The trial was stopped nine months ahead of schedule. Total mortality during the average 25-month follow-up period was 7.2% in the propranolol group and 9.8% in the placebo group. Arteriosclerotic heart disease (ASHD) mortality was 6.2% in the propranolol group and 8.5% in the placebo group. Sudden cardiac death, a subset of ASHD mortality, was 3.3% among the propranolol patients and 4.6% among the placebo patients. Serious side effects were uncommon. Hypotension, gastrointestinal problems, tiredness, bronchospasm, and cold hands and feet occurred more frequently in the propranolol group. Based on the BHAT results, the use of propranolol in patients with no contraindications to β-blockade who have had a recent myocardial infarction is recommended for at least three years. (JAMA 1982;247:1707-1714).