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Hypertension. 2003;42:1206-1252
Published online before print December 1, 2003, doi: 10.1161/01.HYP.0000107251.49515.c2
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(Hypertension. 2003;42:1206.)
© 2003 American Heart Association, Inc.


JNC 7: Complete Report

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

Aram V. Chobanian; George L. Bakris; Henry R. Black; William C. Cushman; Lee A. Green; Joseph L. Izzo, Jr; Daniel W. Jones; Barry J. Materson; Suzanne Oparil; Jackson T. Wright, Jr; Edward J. Roccella; the National High Blood Pressure Education Program Coordinating Committee

From Boston University School of Medicine (A.V.C.), Boston, Mass; Rush University Medical Center (G.L.B., H.R.B.), Chicago, Ill; Veterans Affairs Medical Center (W.C.C.), Memphis, Tenn; University of Michigan (L.A.G.), Ann Arbor, Mich; State University of New York at Buffalo School of Medicine (J.L.I. Jr.), Buffalo, NY; University of Mississippi Medical Center (D.W.J.), Jackson, Miss; University of Miami (B.J.M.), Miami, Fla; University of Alabama at Birmingham (S.O.), Birmingham, Ala; Case Western Reserve University (J.T.W. Jr.), Cleveland, Ohio; National Heart, Lung, and Blood Institute (E.J.R.), Bethesda, Md.

Correspondence to Edward J. Roccella, PhD, Coordinator, National High Blood Pressure Education Program, National Heart, Lung, and Blood Institute, National Institutes of Health, Building 31, Room 4A10, 31 Center Drive MSC 2480, Bethesda, MD 20892. E-mail roccelle{at}nhlbi.nih.gov


*    Abstract
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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.


*    Introduction
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For more than 3 decades, the National Heart, Lung, and Blood Institute (NHLBI) has administered the National High Blood Pressure Education Program (NHBPEP) Coordinating Committee, a coalition of 39 major professional, public, and voluntary organizations and 7 federal agencies. One important function is to issue guidelines and advisories designed to increase awareness, prevention, treatment, and control of hypertension (high blood pressure).

Data from the National Health and Nutrition Examination Survey (NHANES) have indicated that 50 million or more Americans have high blood pressure (BP) warranting some form of treatment.1,2 Worldwide prevalence estimates for hypertension may be as much as 1 billion individuals, and approximately 7.1 million deaths per year may be attributable to hypertension.3 The World Health Organization reports that suboptimal BP (>115 mm Hg SBP) is responsible for 62% of cerebrovascular disease and 49% of ischemic heart disease, with little variation by sex. In addition, suboptimal blood pressure is the number one attributable risk for death throughout the world.3

Considerable success has been achieved in the past in meeting the goals of the program. The awareness of hypertension has improved from a level of 51% of Americans in the period 1976 to 1980 to 70% in 1999 to 2000 (Table 1). The percentage of patients with hypertension receiving treatment has increased from 31% to 59% in the same period, and the percentage of persons with high BP controlled to below 140/90 mm Hg has increased from 10% to 34%. Between 1960 and 1991, median systolic BP (SBP) for individuals 60 to 74 years old declined by approximately 16 mm Hg (Figure 1). These changes have been associated with highly favorable trends in the morbidity and mortality attributed to hypertension. Since 1972, age-adjusted death rates from stroke and coronary heart disease (CHD) have declined by approximately 60% and 50%, respectively (Figures 2 and 3Down). These benefits have occurred independent of gender, age, race, or socioeconomic status. Within the last 2 decades, better treatment of hypertension has been associated with a considerable reduction in the hospital case-fatality rate for heart failure (HF) (Figure 4). This information suggests that there have been substantial improvements.


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TABLE 1. Trends in Awareness, Treatment, and Control of High Blood Pressure 1976–2000



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Figure 1. Smoothed weighted frequency distribution, median, and 90th percentile of SBP for ages 60 to 74 years, United States, 1960 to 1991. Source: Burt et al. Hypertension 1995;26:60–69. Erratum in: Hypertension 1996;27:1192.



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Figure 2. Percentage decline in age-adjusted mortality rates for stroke by gender and race: United States, 1970 to 2000. Source: Prepared by T. Thom, National Heart, Lung, and Blood Institute from Vital Statistics of the United States, National Center for Health Statistics. Death rates are age-adjusted to the 2000 US census population.



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Figure 3. Percentage decline in age-adjusted mortality rates for CHD by gender and race: United States, 1970 to 2000. Source: Prepared by T. Thom, National Heart, Lung, and Blood Institute from Vital Statistics of the United States, National Center for Health Statistics. Death rates are age-adjusted to the 2000 US census population.



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Figure 4. Hospital case-fatality rates for congestive heart failure, ages <65 and 65+: United States, 1981 to 2000. Source: National Heart, Lung, and Blood Institute. Morbidity and Mortality: 2002 Chart Book on Cardiovascular, Lung, and Blood Disease. Chart 3–36. Accessed September 2003. http://www.nhlbi.nih.gov/resources/docs/cht-book.htm.

However, these improvements have not been extended to the total population. Current control rates for hypertension in the United States are clearly unacceptable. Approximately 30% of adults are still unaware of their hypertension, more than 40% of individuals with hypertension are not on treatment, and two thirds of hypertensive patients are not being controlled to BP levels less than 140/90 mm Hg (Table 1). Furthermore, the rates of decline of deaths from CHD and stroke have slowed in the past decade. In addition, the prevalence and hospitalization rates of HF, wherein the majority of patients have hypertension before developing heart failure, have continued to increase (Figures 5 and 6Down). Moreover, there is an increasing trend in end-stage renal disease (ESRD) by primary diagnosis. Hypertension is second only to diabetes as the most common antecedent for this condition (Figure 7). Undiagnosed, untreated, and uncontrolled hypertension clearly places a substantial strain on the health care delivery system.



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Figure 5. Prevalence of CHF by race and gender, ages 25 to 74: United States, 1971 to 1974 to 1999 to 2000. Age-adjusted to 2000 US census population. White and African American in 1999 to 2000 excludes Hispanics. Source: National Heart, Lung, and Blood Institute. Morbidity and Mortality: 2002 Chart Book on Cardiovascular, Lung, and Blood Disease. Accessed September 2003. http://www.nhlbi.nih.gov/resources/docs/cht-book.htm and 1999 to 2000 unpublished data computed by M. Wolz and T. Thom, National Heart, Lung, and Blood Institute. June 2003.



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Figure 6. Hospitalization rates for congestive heart failure, ages 45 to 64 and 65+: United States, 1971 to 2000. Source: National Heart, Lung, and Blood Institute. Morbidity and Mortality: 2002 Chart Book on Cardiovascular, Lung, and Blood Disease. Chart 3–35. Accessed September 2003. http://www.nhlbi.nih.gov/resources/docs/cht-book.htm.



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Figure 7. Trends in incident rates of ESRD, by primary diagnosis (adjusted for age, gender, race). Disease categories were treated as being mutually exclusive. Source: United States Renal Data System. 2002. Figure 1.14. Accessed September, 2003. http://www.usrds.org/slides.htm.


*    Methods
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down arrowLifetime Risk of Hypertension
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down arrowClassification of Blood Pressure
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down arrowPrevention of Hypertension:...
down arrowCalibration, Maintenance, and...
down arrowPatient Evaluation
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down arrowGenetics of Hypertension
down arrowTreatment
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The decision to appoint a committee for The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) was based on 4 factors: the publication of many new hypertension observational studies and clinical trials since the last report was published in 19974; the need for a new clear and concise guideline that would be useful to clinicians; the need to simplify the classification of BP; and a clear recognition that the JNC reports did not result in maximum benefit to the public. This JNC report is presented in 2 separate publications. The initial "Express" version, a succinct practical guide, was published in the May 21, 2003, issue of the Journal of the American Medical Association.5 The current, more comprehensive report provides a broader discussion and justification for the recommendations made by the committee. As with prior JNC reports, the committee recognizes that the responsible physician’s judgment is paramount in managing his or her patients.

Since the publication of the JNC 6 report, the NHBPEP Coordinating Committee, chaired by the director of the NHLBI, has regularly reviewed and discussed studies on hypertension. To conduct this task, the Coordinating Committee is divided into 4 subcommittees: Science Base; Long Range Planning; Professional, Patient, and Public Education; and Program Organization. The subcommittees work together to review the hypertension scientific literature from clinical trials, epidemiology, and behavioral science. In many instances, the principal investigator of the larger studies has presented the information directly to the Coordinating Committee. The committee reviews are summarized and posted on the NHLBI web site.6 This ongoing review process keeps the committee apprised of the current state of the science, and the information is also used to develop program plans for future activities, such as continuing education.

During fall 2002, the NHBPEP Coordinating Committee chair solicited opinions regarding the need to update the JNC 6 report. The entire Coordinating Committee membership provided, in writing, a detailed rationale explaining the necessity for updating JNC 6, outlined critical issues, and provided concepts to be addressed in the new report. Thereafter, the NHBPEP Coordinating Committee chair appointed the JNC 7 chair and an Executive Committee derived from the Coordinating Committee membership. The Coordinating Committee members served on 1 of 5 JNC 7 writing teams, which contributed to the writing and review of the document.

The concepts for the new report identified by the NHBPEP Coordinating Committee membership were used to create the report outline. On the basis of these critical issues and concepts, the Executive Committee developed relevant medical subject headings (MeSH) terms and keywords to further review the 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 evidence were considered, and the classification scheme used in JNC 6 and other NHBPEP clinical guidelines was selected.4,7–10 This scheme classifies studies according to a process adapted from Last and Abramson (see the section Scheme Used for Classification of the Evidence).11

In reviewing the exceptionally large body of research literature in hypertension, the Executive Committee focused its deliberations on evidence pertaining to outcomes of importance to patients and with effects of sufficient magnitude to warrant changes in medical practice ("patient oriented evidence that matters" [POEMs]).12,13 Patient-oriented outcomes include not only mortality but also other outcomes that affect patients’ lives and well-being, such as sexual function, ability to maintain family and social roles, ability to work, and ability to carry out activities of daily living. These outcomes are strongly affected by nonfatal stroke, HF, coronary heart disease, and renal disease; hence, these outcomes were considered along with mortality in the committee’s evidence-based deliberations. Studies of physiological end points (disease-oriented evidence [DOEs]) were used to address questions where POEMs were not available.

The Coordinating Committee began the process of developing the JNC 7 Express report in December 2002, and the report was submitted to the Journal of the American Medical Association in April 2003. It was published in an electronic format on May 14, 2003, and in print on May 21, 2003. During this time, the Executive Committee met on 6 occasions, 2 of which included meetings with the entire Coordinating Committee. The writing teams also met by teleconference and used electronic communications to develop the report. Twenty-four drafts were created and reviewed repeatedly. At its meetings, the Executive Committee used a modified nominal group process14 to identify and resolve issues. The NHBPEP Coordinating Committee 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 Coordinating Committee approved the JNC 7 Express report. To complete the longer JNC 7 version, the Executive Committee members met via teleconferences and in person and circulated sections of the larger document via e-mail. The sections were assembled and edited by the JNC 7 chair and were circulated among the Coordinating Committee members for review and comment. The JNC 7 chair synthesized the comments, and the longer version was submitted to the journal Hypertension in November, 2003.


*    Lifetime Risk of Hypertension
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Hypertension is an increasingly important medical and public health issue. The prevalence of hypertension increases with advancing age to the point where more than half of people aged 60 to 69 years old and approximately three-fourths of those aged 70 years and older are affected.1 The age-related rise in SBP is primarily responsible for an increase in both incidence and prevalence of hypertension with increasing age.15

Whereas the short-term absolute risk for hypertension is conveyed effectively by incidence rates, the long-term risk is best summarized by the lifetime risk statistic, which is the probability of developing hypertension during the remaining years of life (either adjusted or unadjusted for competing causes of death). Framingham Heart Study investigators recently reported the lifetime risk of hypertension to be approximately 90% for men and women who were nonhypertensive at 55 or 65 years old and survived to age 80 to 85 (Figure 8).16 Even after adjusting for competing mortality, the remaining lifetime risks of hypertension were 86 to 90% in women and 81 to 83% in men.



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Figure 8. Residual lifetime risk of hypertension in women and men aged 65 years. Cumulative incidence of hypertension in 65-year-old women and men. Data for 65-year-old men in the 1952 to 1975 period are truncated at 15 years since there were few participants in this age category who were followed up beyond this time interval. Source: JAMA 2002;287:1003–1010. Copyright 2002, American Medical Association. All rights reserved.

The impressive increase of BP to hypertensive levels with age is also illustrated by data indicating that the 4-year rates of progression to hypertension are 50% for those 65 years and older with BP in the 130 to 139/85 to 89 mm Hg range and 26% for those with BP in the 120 to 129/80 to 84 mm Hg range.17


*    Blood Pressure and Cardiovascular Risk
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Data from observational studies involving more than 1 million individuals have indicated that death from both ischemic heart disease and stroke increases progressively and linearly from BP levels as low as 115 mm Hg systolic and 75 mm Hg diastolic upward (Figures 9 and 10Down).18 The increased risks are present in all age groups ranging from 40 to 89 years old. For every 20 mm Hg systolic or 10 mm Hg diastolic increase in BP, there is a doubling of mortality from both ischemic heart disease and stroke.



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Figure 9. Ischemic heart disease (IHD) mortality rate in each decade of age versus usual blood pressure at the start of that decade. Source: Reprinted with permission from Elsevier (The Lancet, 2002;360:1903–1913).



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Figure 10. Stroke mortality rate in each decade of age versus usual blood pressure at the start of that decade. Source: Reprinted with permission from Elsevier (The Lancet, 2002;360:1903–1913).

In addition, longitudinal data obtained from the Framingham Heart Study have indicated that BP values in the 130 to 139/85 to 89 mm Hg range are associated with a more than 2-fold increase in relative risk from cardiovascular disease (CVD) compared with those with BP levels below 120/80 mm Hg (Figure 11).19



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Figure 11. Impact of high normal blood pressure on the risk of cardiovascular disease. Cumulative incidence of cardiovascular events in women (A) and men (B) without hypertension, according to blood-pressure category at the baseline examination. Vertical bars indicate 95% confidence intervals. Optimal BP is defined here as a systolic pressure of less than 120 mm Hg and a diastolic pressure of less than 80 mm Hg. Normal BP is a systolic pressure of 120 to 129 mm Hg or a diastolic pressure of 80 to 84 mm Hg. High-normal BP is a systolic pressure of 130 to 139 mm Hg or a diastolic pressure of 85 to 89 mm Hg. If the systolic and diastolic pressure readings for a subject were in different categories, the higher of the two categories was used. Source: N Engl J Med 2001;345:1291–1297. Copyright © 2001, Massachusetts Medical Society. All rights reserved.


*    Basis for Reclassification of Blood Pressure
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Because of the new data on lifetime risk of hypertension and the impressive increase in the risk of cardiovascular complications associated with levels of BP previously considered to be normal, the JNC 7 report has introduced a new classification that includes the term "prehypertension" for those with BPs ranging from 120 to 139 mm Hg systolic and/or 80 to 89 mm Hg diastolic blood pressure (DBP). This new designation is intended to identify those individuals in whom early intervention by adoption of healthy lifestyles could reduce BP, decrease the rate of progression of BP to hypertensive levels with age, or prevent hypertension entirely.

Another change in classification from JNC 6 is the combining of stage 2 and stage 3 hypertension into a single stage 2 category. This revision reflects the fact that the approach to the management of the former two groups is similar (Table 2).



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TABLE 2. Changes in Blood Pressure Classification


*    Classification of Blood Pressure
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Table 3 provides a classification of BP for adults aged 18 and older. The classification is based on the average of 2 or more properly measured, seated BP readings on each of 2 or more office visits.


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TABLE 3. Classification of Blood Pressure for Adults

Prehypertension is not a disease category. Rather it is a designation chosen to identify individuals at high risk of developing hypertension, so that both patients and clinicians are alerted to this risk and encouraged to intervene and prevent or delay the disease from developing. Individuals who are prehypertensive are not candidates for drug therapy on the basis of their level of BP and should be firmly and unambiguously advised to practice lifestyle modification in order to reduce their risk of developing hypertension in the future (see the section Lifestyle Modifications). Moreover, individuals with prehypertension who also have diabetes or kidney disease should be considered candidates for appropriate drug therapy if a trial of lifestyle modification fails to reduce their BP to 130/80 mm Hg or less.

This classification does not stratify hypertensives by the presence or absence of risk factors or target organ damage in order to make different treatment recommendations, if either or both are present. JNC 7 suggests that all people with hypertension (Stages 1 and 2) be treated. The treatment goal for individuals with hypertension and no other compelling conditions is <140/90 mm Hg (see the section Compelling Indications). The goal for individuals with prehypertension and no compelling indications is to lower BP to normal with lifestyle changes and prevent the progressive rise in BP using the recommended lifestyle modifications (See the section Lifestyle Modification).

Cardiovascular Disease Risk
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, HF, stroke, and kidney diseases. The presence of each additional risk factor compounds the risk from hypertension, as illustrated in Figure 12. 20 The easy and rapid calculation of a Framingham CHD risk score using published tables21 may assist the clinician and patient in demonstrating the benefits of treatment. Management of these other risk factors is essential and should follow the established guidelines for controlling these coexisting problems that contribute to overall cardiovascular risk.



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Figure 12. Ten-year risk for CHD by SBP and presence of other risk factors. Source: Derived from K.M. Anderson, P.W.F. Wilson, P.M. Odell, W.B. Kannel. An updated coronary risk profile. A statement for health professionals. Circulation 1991;83:356–362.


*    Importance of Systolic Blood Pressure
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Impressive evidence has accumulated to warrant greater attention to the importance of SBP as a major risk factor for CVDs. Changing patterns of BP occur with increasing age. The rise in SBP continues throughout life, in contrast to DBP, which rises until approximately 50 years old, tends to level off over the next decade, and may remain the same or fall later in life (Figure 13).1,15 Diastolic hypertension predominates before 50 years of age, either alone or in combination with SBP elevation. The prevalence of systolic hypertension increases with age, and above the age of 50 years, systolic hypertension represents the most common form of hypertension. DBP is a more potent cardiovascular risk factor than SBP until age 50; thereafter, SBP is more important (Figure 14).22



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Figure 13. Changes in systolic and diastolic blood pressure with age. SBP and DBP by age and race or ethnicity for men and women over 18 years of age in the US population. Data from NHANES III, 1988 to 1991. Source: Burt VL et al. Hypertension 1995;23:305–313.



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Figure 14. Difference in CHD prediction between systolic and diastolic blood pressure as a function of age. The strength of the relationship as a function of age is indicated by an increase in the ß coefficient. Difference in ß coefficients (from Cox proportional-hazards regression) between SBP and DBP is plotted as function of age, obtaining this regression line: ß (SBP)-ß (DBP)=1.4948+0.0290 x age (P=0.008). A ß coefficient level <0.0 indicates a stronger effect of DBP on CHD risk, while levels >0.0 suggest a greater importance of systolic pressure. Source: Circulation 2001;103:1247.

Clinical trials have demonstrated that control of isolated systolic hypertension reduces total mortality, cardiovascular mortality, stroke, and HF events.23–25 Both observational studies and clinical trial data suggest that poor SBP control is largely responsible for the unacceptably low rates of overall BP control.26,27 In the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) and Controlled Onset Verapamil Investigation of Cardiovascular End Points (CONVINCE) trial, DBP control rates exceeded 90%, but SBP control rates were considerably less (60 to 70%).28,29 Poor SBP control is at least in part related to physician attitudes. A survey of primary care physicians indicated that three-fourths of them failed to initiate antihypertensive therapy in older individuals with SBP of 140 to 159 mm Hg, and most primary care physicians did not pursue control to less than 140 mm Hg.30,31 Most physicians have been taught that the diastolic pressure is more important than SBP and thus treat accordingly. Greater emphasis must clearly be placed on managing systolic hypertension. Otherwise, as the US population becomes older, the toll of uncontrolled SBP will cause increased rates of cardiovascular and renal diseases.


*    Prevention of Hypertension: Public Health Challenges
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The prevention and management of hypertension are major public health challenges for the United States. If the rise in BP with age could be prevented or diminished, much of hypertension, cardiovascular and renal disease, and stroke might be prevented. A number of important causal factors for hypertension have been identified, including excess body weight; excess dietary sodium intake; reduced physical activity; inadequate intake of fruits, vegetables, and potassium; and excess alcohol intake.10,32 The prevalence of these characteristics is high. One hundred twenty-two million Americans are overweight or obese.33 Mean sodium intake is approximately 4100 mg per day for men and 2750 mg per day for women, 75% of which comes from processed foods.34,35 Fewer than 20% of Americans engage in regular physical activity,36 and fewer than 25% consume 5 or more servings of fruits and vegetables daily.37

Because the lifetime risk of developing hypertension is very high (Figure 8), a public health strategy that complements the hypertension treatment strategy is warranted. In order to prevent BP levels from rising, primary prevention measures should be introduced to reduce or minimize these causal factors in the population, particularly in individuals with prehypertension. A population approach that decreases the BP level in the general population by even modest amounts has the potential to substantially reduce morbidity and mortality or at least delay the onset of hypertension. For example, it has been estimated that a 5 mm Hg reduction of SBP in the population would result in a 14% overall reduction in mortality due to stroke, a 9% reduction in mortality due to CHD, and a 7% decrease in all-cause mortality (Figure 15).10,38



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Figure 15. Systolic blood pressure distributions. Source: Whelton PK et al. JAMA 2002;288:1884.

Barriers to prevention include cultural norms; insufficient attention to health education by health care practitioners; lack of reimbursement for health education services; lack of access to places to engage in physical activity; larger servings of food in restaurants; lack of availability of healthy food choices in many schools, worksites, and restaurants; lack of exercise programs in schools; large amounts of sodium added to foods by the food industry and restaurants; and the higher cost of food products that are lower in sodium and calories.10 Overcoming the barriers will require a multipronged approach directed not only to high-risk populations but also to communities, schools, worksites, and the food industry. The recent recommendations by the American Public Health Association and the NHBPEP Coordinating Committee that the food industry, including manufacturers and restaurants, reduce sodium in the food supply by 50% over the next decade is the type of approach that, if implemented, would reduce BP in the population.39,40

Community Programs
Healthy People 2010 has identified the community as a significant partner and vital point of intervention for attaining healthy goals and outcomes.41 Partnerships with community groups such as civic, philanthropic, religious, and senior citizen organizations provide locally focused orientation to the health needs of diverse populations. The probability of success increases as interventional strategies more aptly address the diversity of racial, ethnic, cultural, linguistic, religious, and social factors in the delivery of medical services. Community service organizations can promote the prevention of hypertension by providing culturally sensitive educational messages and lifestyle support services and by establishing cardiovascular risk factor screening and referral programs. Community-based strategies and programs have been addressed in prior NHLBI publications and other documents (Facts About the DASH Eating Plan,42 Your Guide to Lowering High Blood Pressure,43 National High Blood Pressure Education Month,44 The Heart Truth: A National Awareness Campaign for Women About Heart Disease,45 Mobilizing African American Communities To Address Disparities in Cardiovascular Health: The Baltimore City Health Partnership Strategy Development Workshop Summary Report,46 NHLBI Healthy People 2010 Gateway,47 Cardiovascular Disease Enhanced Dissemination and Utilization Centers [EDUCs] Awardees,48 Hearts N’ Parks,49 Healthbeat Radio Network,50 Salud para su Corazón [For the Health of Your Heart]).51


*    Calibration, Maintenance, and Use of Blood Pressure Devices
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowLifetime Risk of Hypertension
up arrowBlood Pressure and...
up arrowBasis for Reclassification of...
up arrowClassification of Blood Pressure
up arrowImportance of Systolic Blood...
up arrowPrevention of Hypertension:...
*Calibration, Maintenance, and...
down arrowPatient Evaluation
down arrowIdentifiable Causes of...
down arrowGenetics of Hypertension
down arrowTreatment
down arrowSpecial Situations in...
down arrowDrugs and Other Agents...
down arrowImproving Hypertension Control
down arrowScheme Used for Classification...
down arrowAppendix
down arrowReferences
 
The potential of mercury spillage contaminating the environment has led to the decreased use or elimination of mercury in sphygmomanometers as well as in thermometers52 However, concerns regarding the accuracy of nonmercury sphygmomanometers have created new challenges for accurate BP determination.53,54 When mercury sphygmomanometers are replaced, the new equipment, including all home BP measurement devices, must be appropriately validated and checked regularly for accuracy.55

Accurate Blood Pressure Measurement in the Office
The accurate measurement of BP is the sine qua non for successful management. The equipment, whether aneroid, mercury, or electronic, should be regularly inspected and validated. The operator should be trained and regularly retrained in the standardized technique, and the patient must be properly prepared and positioned.4,56,57 The auscultatory method of BP measurement should be used.58 Persons should be seated quietly for at least 5 minutes in a chair (rather than on an examination table), with feet on the floor, and arm supported at heart level. Caffeine, exercise, and smoking should be avoided for at least 30 minutes prior to measurement. Measurement of BP in the standing position is indicated periodically, especially in those at risk for postural hypotension, prior to necessary drug dose or adding a drug, and in those who report symptoms consistent with reduced BP on standing. An appropriately sized cuff (cuff bladder encircling at least 80% of the arm) should be used to ensure accuracy. At least two measurements should be made and the average recorded. For manual determinations, palpated radial pulse obliteration pressure should be used to estimate SBP; the cuff should then be inflated 20 to 30 mm Hg above this level for the auscultatory determinations; the cuff deflation rate for auscultatory readings should be 2 mm Hg per second. SBP is the point at which the first of two or more Korotkoff sounds is heard (onset of phase 1), and the disappearance of Korotkoff sound (onset of phase 5) is used to define DBP. Clinicians should provide to patients, verbally and in writing, their specific BP numbers and the BP goal of their treatment.

Follow-up of patients with various stages of hypertension is recommended as shown in Table 4.


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TABLE 4. Recommendations for Follow-Up Based on Initial Blood Pressure Measurements for Adults Without Acute End Organ Damage

Ambulatory Blood Pressure Monitoring
Ambulatory blood pressure monitoring (ABPM) provides information about BP during daily activities and sleep.59 BP has a reproducible circadian profile, with higher values while awake and mentally and physically active, much lower values during rest and sleep, and early morning increases for 3 or more hours during the transition of sleep to wakefulness.60 These devices use either a microphone to measure Korotkoff sounds or a cuff that senses arterial waves using oscillometric techniques. Twenty-four-hour BP monitoring provides multiple readings during all of a patient’s activities. While office BP values have been used in the numerous studies that have established the risks associated with an elevated BP and the benefits of lowering BP, office measurements have some shortcomings. For example, a white-coat effect (increase in BP primarily in the medical care environment) is noted in as many as 20 to 35% of patients diagnosed with hypertension.61

Ambulatory BP values are usually lower than clinic readings. Awake hypertensive individuals have an average BP of >135/85 mm Hg and during sleep, >120/75 mm Hg. The level of BP measurement using ABPM correlates better than office measurements with target organ injury.15 ABPM also provides a measure of the percentage of BP readings that are elevated, the overall BP load, and the extent of BP fall during sleep. In most people, BP drops by 10 to 20% during the night; those in whom such reductions are not present appear to be at increased risk for cardiovascular events. In addition, it was reported recently that ABPM patients whose 24-hour BP exceeded 135/85 mm Hg were nearly twice as likely to have a cardiovascular event as those with 24-hour mean BPs less than 135/85 mm Hg, irrespective of the level of the office BP.62,63

Indications for the use of ABPM are listed in Table 5. Medicare reimbursement for ABPM is now provided to assess patients with suspected white-coat hypertension.


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TABLE 5. Clinical Situations in Which Ambulatory Blood Pressure Monitoring May Be Helpful

Self-Measurement
Self-monitoring of BP at home and work is a practical approach to assess differences between office and out-of-office BP prior to consideration of ambulatory monitoring. For those whose out-of-office BPs are consistently <130/80 mm Hg despite an elevated office BP and who lack evidence of target organ disease, 24-hour monitoring or drug therapy can be avoided.

Self-measurement or ambulatory monitoring may be particularly helpful in assessing BP in smokers. Smoking raises BP acutely, and the level returns to baseline in about 15 minutes after stopping.


*    Patient Evaluation
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowLifetime Risk of Hypertension
up arrowBlood Pressure and...
up arrowBasis for Reclassification of...
up arrowClassification of Blood Pressure
up arrowImportance of Systolic Blood...
up arrowPrevention of Hypertension:...
up arrowCalibration, Maintenance, and...
*Patient Evaluation
down arrowIdentifiable Causes of...
down arrowGenetics of Hypertension
down arrowTreatment
down arrowSpecial Situations in...
down arrowDrugs and Other Agents...
down arrowImproving Hypertension Control
down arrowScheme Used for Classification...
down arrowAppendix
down arrowReferences
 
Evaluation of hypertensive patients has three objectives: (1) to assess lifestyle and identify other cardiovascular risk factors or concomitant disorders that may affect prognosis and guide treatment (Table 6); (2) to reveal identifiable causes of high BP (Table 7); and (3) to assess the presence or absence of target organ damage and CVD.


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TABLE 6. Cardiovascular Risk Factors


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TABLE 7. Identifiable Causes of Hypertension


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TABLE 18. Causes of Resistant Hypertension

Patient evaluation is made through medical history, physical examination, routine laboratory tests, and other diagnostic procedures. The physical examination should include an appropriate measurement of BP, with verification in the contralateral arm; examination of the optic fundi; calculation of body mass index (BMI) (measurement of waist circumference is also very 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, distended urinary bladder, and abnormal aortic pulsation; palpation of the lower extremities for edema and pulses; and neurological assessment.

Data from epidemiological studies and clinical trials have demonstrated that elevations in resting heart rate and reduced heart rate variability are associated with higher cardiovascular risk. In the Framingham Heart Study, an average resting heart rate of 83 beats per minute was associated with a substantially higher risk of death from a CV event than those at lower heart rate levels.64 Moreover, reduced heart rate variability was also associated with an increase in CV mortality.65 No clinical trials have prospectively evaluated the impact of reducing heart rate on CV outcomes.

Laboratory Tests and Other Diagnostic Procedures
Routine laboratory tests recommended before initiating therapy include a 12-lead ECG; urinalysis; blood glucose and hematocrit; serum potassium, creatinine (or the corresponding estimated glomerular filtration rate [eGFR]), and calcium66; and a lipoprotein profile (after 9- to 12-hour fast) that includes HDL and LDL cholesterol (HDL-C and LDL-C) and triglycerides (TGs). Optional tests include measurement of urinary albumin excretion or albumin/creatinine ratio (ACR), except for those with diabetes or kidney disease, for whom annual measurements should be made. More extensive testing for identifiable causes is not indicated generally unless BP control is not achieved or the clinical and routine laboratory evaluation strongly suggests an identifiable secondary cause (ie, vascular bruits, symptoms of catecholamine excess, unprovoked hypokalemia). See the section Identifiable Causes of Hypertension for a more thorough discussion.

The presence of decreased GFR or albuminuria has prognostic implications as well. Studies reveal a strong relationship between decreases in GFR and increases in cardiovascular morbidity and mortality.67,68 Even small decreases in GFR increase cardiovascular risk.67 Serum creatinine may overestimate glomerular filtration. The optimal tests to determine GFR are debated, but calculating GFR from the recent modifications of the Cockcroft and Gault equations is useful.69

The presence of albuminuria, including microalbuminuria, even in the setting of normal GFR, is also associated with an increase in cardiovascular risk.70–72 Urinary albumin excretion should be quantitated and monitored on an annual basis in high-risk groups, such as those with diabetes or renal disease.

Additionally, three emerging risk factors—(1) high-sensitivity C-reactive protein (HS-C