| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 2004;44:398.)
© 2004 American Heart Association, Inc.
Scientific Contributions |
From the Office of the Secretarys Office of Public Health and Science (L.E.F.), U.S. Department of Health and Human Services, Washington, DC; the Cardiovascular Division (L.E.F.), Department of Medicine, Washington University School of Medicine, St. Louis, Mo; National Center for Health Statistics (V.L.B.), Centers for Disease Control and Prevention, US Department of Health and Human Services, Hyattsville, Md; National Heart, Lung, and Blood Institute (J.A.C., E.J.R., P.S.), National Institutes of Health, US Department of Health and Human Services, Bethesda, Md; and The Orkand Corporation (J.H.), Falls Church, Va.
Correspondence to Larry E. Fields, MD, MBA, FACC, Senior Executive Advisor to the Assistant Secretary for Health, US Department of Health and Human Services, 200 Independence Avenue, Washington, DC 20201. E-mail lefields{at}osophs.dhhs.gov
| Abstract |
|---|
|
|
|---|
30% for 1999 to 2000 compared with at least 50 million for 1988 to 1994. The 50 million value was based on a rate of 23.4% for adults with elevated blood pressure or using antihypertensive medications and 5.5% for adults classified as hypertensive by medical history alone (28.9% total; P<0.001). The
30% increase in the total number of adults with hypertension was almost 4-times greater than the 8.3% increase in total prevalence rate. These trends were associated with increased obesity and an aging and growing population. Approximately 35 million women and 30 million men had hypertension. At least 48 million non-Hispanic white adults,
9 million non-Hispanic black adults, 3 million Mexican American, and 5 million other adults had hypertension in 1999 to 2000.
Key Words: hypertension, detection and control blood pressure
| Introduction |
|---|
|
|
|---|
The estimated number of persons with hypertension living in the United States (US) is essential epidemiological data that are widely used for education, estimation of societal impact, cost-effectiveness analysis, strategic resource allocation, prevention, and control.48 At least 50 million US adults were estimated to have hypertension during 1988 to 1994, using the National Health and Nutrition Examination Survey (NHANES) III data set.3 Recent articles refer to this value for the estimated magnitude of the hypertension problem in the US.1,2,48 A recent analysis of NHANES data from 1999 to 2000 reported a 3.7-percentage point increase in the hypertension prevalence rate.6
In this study, data from NHANES and the US Census Bureau are used to estimate hypertension numbers (burden), prevalence rates, and trends relative to 1988 to 1994 for US adults in 1999 to 2000.911
| Methods |
|---|
|
|
|---|
Age-specific crude rates are used to estimate hypertension burden and overall prevalence for 1999 to 2000. Age-specific US resident population estimates were obtained from a bridged-race intercensal file (icen1999) and July 1, 2000 adult population estimates (NA-EST2002-ASRO-01).9,10 For the 1999 estimates, interpolated weights were used to adjust the number of persons 20 years of age and older to the number estimated to be 18 years of age and older. Age adjustment is to the standard for year 2000.14
The 1999 and 2000 adult population estimates were averaged, and the percentage of persons in each age-specific group relative to the total adult population was calculated. The total percent hypertension prevalence was computed using the age-specific hypertension prevalence proportions and US averaged adult population data. In the absence of information on hypertension for the total US resident population, rates based on nonpregnant and noninstitutionalized US resident civilians were applied to resident population values to generate an estimate of the total hypertension burden. The 1990 civilian, noninstitutionalized US population is
2% smaller than the resident US population for the same time period. Sex-specific burdens of hypertension were estimated for both sexes by age.
The average of 1999 and 2000 population estimates for the non-Hispanic white and black populations, Mexican American, and all others are based on: (1) a bridged-race intercensal file (icen1999); (2) the 2000 Census estimate of the proportion of the Hispanic population that is Mexican American (0.5846; Table DP-1); and (3) July 1, 2000 adult population estimates (NA-EST2002-ASRO-02 and NA-EST2002-ASRO-03).9,10 A 2-step process was used to estimate the number of adults with hypertension by sex, race, and ethnicity. First, crude prevalence rates generated from the 1999 to 2000 NHANES sample population were applied to 1999 to 2000 US population estimates to compute weights for each sex, race, and ethnicity category. Second, computed weights were applied to Table 1 hypertension totals for both sexes.
|
Percent, number, and standard error are reported. Prevalence data were generated using SAS version 8.2 and SUDAAN release 8.0, with the exception of the total adult prevalence estimate described. Independent group t tests between means and 1-way factorial analysis of variance were used to determine significance of differences. A more detailed summary of methods is contained in an online supplement available at http://www.hypertensionaha.org.
| Results |
|---|
|
|
|---|
30% higher in 1999 to 2000 compared with 1988 to 1994 (Figure 1; P<0.001).3 Total hypertension burden comprises at least 59 million adults classified as hypertensive by elevated systolic or diastolic BP or use of antihypertensive medication and 6 million men and women who otherwise reported being told at least twice by a physician or other health provider that they had high BP. The estimated total prevalence rate for US adults with hypertension was 8.3% higher in 1999 to 2000 compared with 1988 to 1994 (Table 2; P=0.01). The larger percentage increase in total hypertension burden (
30%) compared with the percentage increase in total prevalence rate (
8%) is associated with an increase in the size of the US resident population from the 1988 to 1994 period to 1999 to 2000. Approximately 81% of US adults with hypertension were aged 45 years or older in 1999 to 2000. The same age group represents
46% of the US population. The number per age group of US adults with hypertension increased with age up to and including 45 to 54 years (Table 1, Figure 2A). Thereafter, hypertension prevalence numbers per age group changed very little (
13 to 14 million per age group). Traditionally defined adult hypertension prevalence rates increased significantly with age (Table 1, Figure 2B).
|
|
|
Almost 30 million men had hypertension (Tables 1 and 3
). More than 10 million US men aged 65 years and older had hypertension in 1999 to 2000. The number of adult males with hypertension increased with age and peaked at 45 to 54 years of age in 1999 to 2000 (Figure 2A). The number of men with hypertension then decreased progressively. The percentage of men with traditionally defined hypertension increased progressively with age (Figure 2B).
|
More than 35 million women had hypertension,
5 million more than men (19.8%; Tables 1 and 3
). At least 17 million women 65 years of age and older had hypertension (
74% higher than for men). The number of women with hypertension increased progressively with age (Figure 2A). The progressive increase in the number of women with hypertension differs significantly from the progressive decline of hypertension numbers observed in men after 45 to 54 years of age. The percent of women with hypertension also increased with age (Figure 2B). Women younger than age 35 years had a lower traditionally defined hypertension prevalence rate compared with men (P<0.001). Women had higher values relative to men after age 54 years, reaching statistical significance for persons at least 75 years of age (P<0.001).
Non-Hispanic white adults constituted the largest component of the total hypertension burden for 1999 to 2000 (at least 48 million; 73.7%; Table 3, Figure 3). More non-Hispanic white females than males had hypertension (26 and 22 million; 39.4% and 34.4%, respectively). The number of non-Hispanic white adults as a percentage of the US hypertension burden was similar to the value that would be predicted by the percentage of non-Hispanic white adults in the general US population (72.9% total; 35.1% male; and 37.8% female).
|
Non-Hispanic black adults constituted the second largest component of the total hypertension burden (
9 million; 13.7%; Table 3, Figure 3). More non-Hispanic black females than males had hypertension (5 and 4 million; 7.7% and 6.0%, respectively). The number of non-Hispanic black adults as a percentage of the US hypertension burden was 21.2% higher than would be expected based on the percentage of non-Hispanic black adults in the general US population (11.3% total; 5.3% males; and 6.0% female).
Mexican American adults constituted a smaller component of the total hypertension burden (
3 million; 4.5%). A similar number of Mexican American females and males had hypertension (1.5 and 1.4 million; 2.3% and 2.2%, respectively). The number of Mexican American adults as a percentage of the total hypertension burden was 33.8% lower than what would be predicted by the percentage of Mexican American adults in the general US population (6.8% total; 3.4% males; 3.4% females).
Other adult subpopulations were analyzed, including persons identified as non-Mexican American Hispanic or Latino, American Indian or Alaskan Native, or Asian Pacific Islander. More than 5 million other adults had hypertension (8.1%; Table 3, Figure 3). Slightly more other females than other males had hypertension (2.8 and 2.4 million; 4.2% and 3.8%, respectively). The number of other adults as a percentage of the US hypertension burden was 11.0% lower than what would be predicted by the percentage of other adults in the general US population, because of differences in the male group (9.1% total; 4.9% males; and 4.2% females).
Age-adjusted hypertension prevalence rates for 1999 to 2000 for non-Hispanic black men were 36.9% higher than non-Hispanic white men, 30.7% higher than Hispanic American men, and 41.5% higher than other men (P
0.01; Table 2, Figure 4). Rates for non-Hispanic black females were 48.5% higher than non-Hispanic white females, 41.1% higher than Hispanic American females, and 27% higher than other women (P<0.01). Mexican American adults had hypertension rates that were similar to non-Hispanic white adults. Profiles for other adults were closest to those for Mexican Americans. Similar patterns were also evident for 1988 to 1994, except that other adults had the lowest hypertension prevalence rates.
|
| Discussion |
|---|
|
|
|---|
More than 65 million US adults had hypertension in 1999 to 2000. This number is significantly higher than the
50 million estimated for the 1988 to 1994 period.3 The total US hypertension burden and prevalence rate estimated in this study are
9% and 11% higher compared with a recent NHANES-based report.6 This difference is a very important one given the anticipated impact on total length and quality of life, health and other resource use, and overall societal costs directly and indirectly attributable to the additional adults with hypertension, hypertensive complications, and other comorbid conditions typically associated with hypertension.5 If the burden-based strategic cost estimate was
$110 billion for US residents with hypertension alone or with hypertensive complications and comorbidities, a 10% underestimation of the total hypertension burden could result in a strategic underallocation of
$11 billion in necessary resources. The significant differences between these studies are associated with application of group-specific methodology to estimate the total burden of hypertension for the overall population as well as for specific subpopulations, a total prevalence rate that is based on broader population data, use of population data matched for the same analysis time period, and inclusion of adults who were told on at least 2 occasions that they had high BP. The latter inclusion matches methodology used in the original NHANES III analysis.3 The higher estimated hypertension values for 1999 to 2000 compared with 1988 to 1994 reflect an increase in the actual proportion and number of obese and older persons in the US population.
The increase in US hypertension burden could reflect an increase in the rate of new-onset high BP in adults that is not sufficiently counterbalanced by important successes in hypertension-related primary prevention efforts.1,15,16 The higher 1999 to 2000 hypertension burden may also reflect an increased number of persons with hypertension who live longer as a result of healthier lifestyles and/or better BP control rates associated with hypertension-related public health effectiveness and medical care quality improvement. This phenomenon could be referred to as a higher control/higher survival/higher burden effect or a "higher control-survival-burden paradox."
The larger total hypertension burden is of particular concern in the context of the epidemic of overweight and obesity affecting the US.17,18 The prevalence of obesity has increased over the same time period of this study. Obesity is one of the major risk factors for hypertension. A weight loss of
10 kg is associated with
5 to 10 mm Hg reduction in systolic BP.1 The upward trend in hypertension burden is of added concern in the context of low national rates of self-reported moderate or vigorous physical activity at recommended frequencies among US adults during leisure time (
33%), even though physical activity is known to prevent hypertension and improve BP control.7,8,19
The majority of US adults with hypertension were non-Hispanic white persons. This racialethnic subpopulation comprised
69% of the total number of US adults with hypertension. This finding is consistent with their representation in the overall population.
Women are disproportionately impacted by hypertension. More women than men had hypertension. Postmenopausal status and differences in sex-specific life expectancy may contribute to this phenomenon.1
Non-Hispanic black adults continue to be disproportionately impacted by hypertension. An over-representation of hypertension was not observed in other subpopulations. The lower hypertension prevalence rate for the Mexican American population was associated with a younger overall age for this group.
Aging adults are also disproportionately impacted by hypertension. Approximately 81% of all US adults with hypertension were at least 45 years of age, even though this group comprised only 46% of the US population. The size of this group is expected to continue to increase, making age-dependency of hypertension prevalence even more important. Hypertension-focused primary prevention interventions are likely to be most beneficial when applied to individuals before 45 years of age. This fact does not diminish the secondary benefits of healthy lifestyles on BP control rates, pointing to usefulness of healthy behaviors across the lifespan. Population-wide approaches such as incremental reduction in sodium content of processed foods, combined with strategies to mitigate a counterbalancing increase in sodium added to foods by individual consumers, may positively impact primary prevention of hypertension and BP control rates over a wide range of age.2026
Qualifications and Limitations
Crude hypertension rates were estimated using a nonpregnant and noninstitutionalized US civilian sample population. These rates could be even higher if specific institutionalized populations were included in the survey sample. This assumption seems reasonable because a greater proportion of persons living in nursing homes and many chronic disease hospitals are older and more likely have hypertension. The underestimation bias for crude rates is substantially counterbalanced by the use of US Census Bureau population data that includes institutionalized and pregnant resident civilians to estimate the US hypertension burden.
Several lines of indirect evidence support the inclusion of adults determined to be hypertensive by medical history alone in NHANES III and in this study. Use of single or multiple lifestyle modifications by hypertensive adults lowers BP, and thus could increase the likelihood of a normal point BP measurement.1,8,2629 Hypertensive adults who successfully lower dietary sodium and urinary sodium excretion are more likely to maintain a lower BP after withdrawal of antihypertensive medication.7 Withdrawal of antihypertensive therapy in hypertensive adults can be followed by 1 to 4 years of normal BP, and lifestyle modifications, including weight control, enhance the odds of being able to defer reinstitution of antihypertensive medication.30
Perspectives
The hypertension burden increased since 1988 to 1994. Although most of the burden comprised non-Hispanic white adults, hypertension continues to disproportionately impact several other subpopulations. The fact that hypertension continues to be a major attributable cause of stroke, coronary heart disease, heart failure, atrial fibrillation, and end-stage renal disease predicts an added future negative impact of the growing hypertension burden.31 These findings underscore the importance of effective health policy, medical care, and public health actions that improve hypertension prevention and control.
| Acknowledgments |
|---|
Received April 14, 2004; first decision April 28, 2004; accepted May 18, 2004.
| References |
|---|
|
|
|---|
This article has been cited by other articles:
![]() |
R. D. Smith and P. J. Levy Review: New techniques for assessment of vascular function Therapeutic Advances in Cardiovascular Disease, October 1, 2008; 2(5): 373 - 385. [Abstract] [PDF] |
||||
![]() |
Y. Papanikolaou and V. L. Fulgoni III Bean Consumption Is Associated with Greater Nutrient Intake, Reduced Systolic Blood Pressure, Lower Body Weight, and a Smaller Waist Circumference in Adults: Results from the National Health and Nutrition Examination Survey 1999-2002 J. Am. Coll. Nutr., October 1, 2008; 27(5): 569 - 576. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Hwang, R. A. Kloner, M. T. Kleinman, and B. Z. Simkhovich Direct and Acute Cardiotoxic Effects of Ultrafine Air Pollutants in Spontaneously Hypertensive Rats and Wistar--Kyoto Rats Journal of Cardiovascular Pharmacology and Therapeutics, September 1, 2008; 13(3): 189 - 198. [Abstract] [PDF] |
||||
![]() |
V. F. Panoulas, G. S. Metsios, A. V. Pace, H. John, G. J. Treharne, M. J. Banks, and G. D. Kitas Hypertension in rheumatoid arthritis Rheumatology, September 1, 2008; 47(9): 1286 - 1298. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. Wang, X. Liao, K. Fukuda, S. Knappe, F. Wu, D. L. Dries, J. Qin, and Q. Wu Corin Variant Associated With Hypertension and Cardiac Hypertrophy Exhibits Impaired Zymogen Activation and Natriuretic Peptide Processing Activity Circ. Res., August 29, 2008; 103(5): 502 - 508. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. M. Egan, S. D. Nesbitt, and S. Julius Review: Prehypertension: should we be treating with pharmacologic therapy? Therapeutic Advances in Cardiovascular Disease, August 1, 2008; 2(4): 305 - 314. [Abstract] [PDF] |
||||
![]() |
P. P. Shi, X. R. Cao, E. M. Sweezer, T. S. Kinney, N. R. Williams, R. F. Husted, R. Nair, R. M. Weiss, R. A. Williamson, C. D. Sigmund, et al. Salt-sensitive hypertension and cardiac hypertrophy in mice deficient in the ubiquitin ligase Nedd4-2 Am J Physiol Renal Physiol, August 1, 2008; 295(2): F462 - F470. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. A. Pearce, M. M. Love, B. J. Shelton, N. E. Schoenberg, M. A. Williamson, M. A. Barron, and J. M. Houlihan Cardiovascular Risk Education and Social Support (CaRESS): Report of a Randomized Controlled Trial from the Kentucky Ambulatory Network (KAN) J Am Board Fam Med, July 1, 2008; 21(4): 269 - 281. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. J. Viera, L. W. Cohen, C. M. Mitchell, and P. D. Sloane High Blood Pressure Knowledge Among Primary Care Patients with Known Hypertension: A North Carolina Family Medicine Research Network (NC-FM-RN) Study J Am Board Fam Med, July 1, 2008; 21(4): 300 - 308. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. F. Pereira and M. J. Franz Prevention and Treatment of Cardiovascular Disease in People With Diabetes Through Lifestyle Modification: Current Evidence-Based Recommendations Diabetes Spectr, July 1, 2008; 21(3): 189 - 193. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Tanaka, Y. Ishikawa, M. Yokoyama, H. Origasa, M. Matsuzaki, Y. Saito, Y. Matsuzawa, J. Sasaki, S. Oikawa, H. Hishida, et al. Reduction in the Recurrence of Stroke by Eicosapentaenoic Acid for Hypercholesterolemic Patients: Subanalysis of the JELIS Trial Stroke, July 1, 2008; 39(7): 2052 - 2058. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. G. Pickering, N. H. Miller, G. Ogedegbe, L. R. Krakoff, N. T. Artinian, and D. Goff Call to Action on Use and Reimbursement for Home Blood Pressure Monitoring: A Joint Scientific Statement From the American Heart Association, American Society of Hypertension, and Preventive Cardiovascular Nurses Association Hypertension, July 1, 2008; 52(1): 10 - 29. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. B. Green, A. J. Cook, J. D. Ralston, P. A. Fishman, S. L. Catz, J. Carlson, D. Carrell, L. Tyll, E. B. Larson, and R. S. Thompson Effectiveness of Home Blood Pressure Monitoring, Web Communication, and Pharmacist Care on Hypertension Control: A Randomized Controlled Trial JAMA, June 25, 2008; 299(24): 2857 - 2867. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. S. Gidding Measuring Children's Blood Pressure Matters Circulation, June 24, 2008; 117(25): 3163 - 3164. [Full Text] [PDF] |
||||
![]() |
S. B. Wyatt, E. L. Akylbekova, M. R. Wofford, S. A. Coady, E. R. Walker, M. E. Andrew, W. J. Keahey, H. A. Taylor, and D. W. Jones Prevalence, Awareness, Treatment, and Control of Hypertension in the Jackson Heart Study Hypertension, March 1, 2008; 51(3): 650 - 656. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. A. Mensah Public Health and the Control of High Blood Pressure at the State Level: Asleep at the Switch or Running Low on Fuel? Circulation, February 19, 2008; 117(7): 860 - 862. [Full Text] [PDF] |
||||
![]() |
W. Rosamond, K. Flegal, K. Furie, A. Go, K. Greenlund, N. Haase, S. M. Hailpern, M. Ho, V. Howard, B. Kissela, et al. Heart Disease and Stroke Statistics--2008 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee Circulation, January 29, 2008; 117(4): e25 - e146. [Full Text] [PDF] |
||||
![]() |
S. E Judd, M. S Nanes, T. R Ziegler, P. W. Wilson, and V. Tangpricha Optimal vitamin D status attenuates the age-associated increase in systolic blood pressure in white Americans: results from the third National Health and Nutrition Examination Survey Am. J. Clinical Nutrition, January 1, 2008; 87(1): 136 - 141. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Oyama, P. Gona, C. J. Salton, M. L. Chuang, R. R. Jhaveri, S. J. Blease, A. R. Manning, M. Lahiri, R. M. Botnar, D. Levy, et al. Differential Impact of Age, Sex, and Hypertension on Aortic Atherosclerosis: The Framingham Heart Study Arterioscler. Thromb. Vasc. Biol., January 1, 2008; 28(1): 155 - 159. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. M. Ferrario, J. Basile, W. Bestermann, E. Frohlich, M. Houston, D. T. Lackland, R. D. Smith, and D. L. Wise Review: The role of noninvasive hemodynamic monitoring in the evaluation and treatment of hypertension Therapeutic Advances in Cardiovascular Disease, December 1, 2007; 1(2): 113 - 118. [Abstract] [PDF] |
||||
![]() |
Y. Chen-Izu, L. Chen, T. Banyasz, S. L. McCulle, B. Norton, S. M. Scharf, A. Agarwal, A. Patwardhan, L. T. Izu, and C. W. Balke Hypertension-induced remodeling of cardiac excitation-contraction coupling in ventricular myocytes occurs prior to hypertrophy development Am J Physiol Heart Circ Physiol, December 1, 2007; 293(6): H3301 - H3310. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. S. Bowman, J. M. Gaziano, J. E. Buring, and H. D. Sesso A Prospective Study of Cigarette Smoking and Risk of Incident Hypertension in Women J. Am. Coll. Cardiol., November 20, 2007; 50(21): 2085 - 2092. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Coresh, E. Selvin, L. A. Stevens, J. Manzi, J. W. Kusek, P. Eggers, F. Van Lente, and A. S. Levey Prevalence of Chronic Kidney Disease in the United States JAMA, November 7, 2007; 298(17): 2038 - 2047. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. M. MacDonnell, H. Kubo, D. M. Harris, X. Chen, R. Berretta, M. F. Barbe, S. Kolwicz, P. O. Reger, A. Eckhart, B. F. Renna, et al. Calcineurin inhibition normalizes beta-adrenergic responsiveness in the spontaneously hypertensive rat Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H3122 - H3129. [Abstract] [Full Text] [PDF] |
||||