Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 1998;31:1070-1076

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Onwuanyi, A.
Right arrow Articles by Francis, C. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Onwuanyi, A.
Right arrow Articles by Francis, C. K.

(Hypertension. 1998;31:1070-1076.)
© 1998 American Heart Association, Inc.


Scientific Contributions

Hypertensive Vascular Disease as a Cause of Death in Blacks Versus Whites

Autopsy Findings in 587 Adults

Anekwe Onwuanyi; David Hodges; Amarnath Avancha; Linda Weiss; Daniel Rabinowitz; Steven Shea; ; Charles K. Francis

From the Division of Cardiology and Department of Medicine, Harlem Hospital Center (A.O., D.H., A.A., C.K.F.); the Divisions of Cardiology (D.H.) and General Medicine (L.W., S.S.), Department of Medicine, Columbia University College of Physicians and Surgeons; the Department of Statistics, Columbia University (D.R.); and the Division of Epidemiology, Columbia University School of Public Health (S.S.), New York, NY.

Correspondence to Dr Charles K. Francis, Department of Medicine, Room 14–401, Harlem Hospital Center, 506 Lenox Ave, New York, NY 10037.


*    Abstract
up arrowTop
*Abstract
down arrowIntroduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Abstract—Cardiovascular disease is the major cause of excess mortality among urban US blacks, but autopsy data comparing black-white differences in underlying pathological causes of cardiovascular death are lacking. We reviewed all 720 adult cases autopsied in 1991 in the New York City Medical Examiner's Office in which the coded cause of death was cardiovascular disease (International Classification of Diseases, 9th Revision, codes 391, 393 to 398, 401 to 404, 410, 411, 414 to 417, 420 to 438, and 440 to 444). After exclusion of 133 cases because race was missing or coded as other than black or white, gender was not coded, or there was an unusual circumstances of death or extreme obesity, 587 cases were available for analysis. There were 314 black and 273 white subjects. Black women were younger than white women at time of death (mean age, 54.7 versus 61.5 years; P<.001), whereas black and white men did not differ in mean age at death. Hypertensive vascular disease was the autopsy cause of death in 42% of blacks compared with 23% of whites (P<.001). Conversely, atherosclerotic heart disease was the autopsy cause of death in 64% of white subjects but only 38% of blacks. These patterns were consistent in both sexes and after adjustment for age. Hypertensive vascular disease was far more common than atherosclerotic heart disease as the cause of death at autopsy among blacks compared with whites in New York City, whereas atherosclerotic heart disease was more common in whites. These findings suggest that ineffective control of hypertension is a major factor contributing to excess cardiovascular mortality among urban blacks.


Key Words: atherosclerosis • autopsy • cardiovascular diseases • race


*    Introduction
up arrowTop
up arrowAbstract
*Introduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Cardiovascular disease remains the leading cause of death for both blacks and whites in the United States,1 but substantial differences in cardiovascular disease mortality rates between blacks and whites have been described.2 3 4 In particular, the interaction of poverty with race appears to play an important role in contributing to excess cardiovascular mortality among blacks living in impoverished urban areas, with the greatest increase in risk among younger age groups.5 6 7 Moreover, recent studies show adverse trends for cardiovascular disease mortality in African Americans compared with whites, with widening of the differential.2 8 Recent data also show a greatly increased risk of cardiovascular mortality among African Americans born in the United States compared with Caribbean-born blacks,9 and it has been suggested that these differences are mediated in part by acculturation and accompanying differences in health-related behaviors that influence cardiovascular risk.10 Several hypotheses have been put forward to explain differences between US-born blacks and whites, including different patterns of risk factors.11 12 In addition, it has been noted that blacks have lower rates than whites of utilization of high-technology cardiology services including coronary angiography, angioplasty, and revascularization,13 14 15 16 as well as other cardiovascular treatments.17 18 19 It has also been suggested that fatal cardiovascular disease in blacks involves less atherosclerosis of the epicardial coronary arteries than among whites.7

Most of what is known about the effects of hypertension on mortality in blacks versus whites is based on information derived from epidemiological studies, clinical trials of drug treatment, or anecdotal clinical experience. Autopsy data offer an opportunity to compare the specific cardiovascular pathological findings that underlie the racial differences described in mortality statistics, but few autopsy studies addressing this issue have been published. The study by Strong et al20 focused on adolescents and young adults, while the study of Shirani et al21 included only subjects over the age of 80 years. The large studies reported by Roeske et al22 and Kitzman et al23 did not report the race of the subjects, whereas the study by Burke et al24 focused on plaque morphology in 113 men, all of whom had atherosclerotic coronary disease and died suddenly. The Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study, which included autopsy data for 1532 subjects aged 15 to 34 years who died of external causes, addressed risk factors for and the natural history of early atherosclerotic lesions.25 26 Thus, existing autopsy studies have not directly compared the underlying pathological causes of death in blacks and whites who died of cardiovascular disease. We reviewed the findings in all cases of cardiovascular death autopsied in the New York City Medical Examiner's Office in 1991. Because of the higher prevalence of hypertension among US-born blacks compared with whites,27 28 and the well-established effectiveness of hypertension treatment in both blacks and whites,29 we tested the hypothesis that hypertensive vascular disease contributes to cardiovascular mortality to a greater extent among blacks than whites.


*    Methods
up arrowTop
up arrowAbstract
up arrowIntroduction
*Methods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Data Source and Population
Data were derived from a consecutive series of autopsy records maintained in the New York City's Medical Examiner's Office. The autopsy series was drawn from the 72 421 deaths occurring within the city's geographic boundaries during 1991. Of these, 21 564 were reported to the Medical Examiner's Office, and autopsies were performed on 7162 of the decedents (9.8% of recorded deaths). All records in which the decedent was 20 years or older and in which the cause of death was coded as cardiovascular in origin (conditions corresponding to International Classification of Diseases, 9th Revision [ICD-9]30 codes: 391, 393 to 398, 401 to 404, 410, 411, 414 to 417, 420 to 438, and 440 to 444) were reviewed by two of us (A.O. and A.A.). There were 720 cases that met these criteria. Of these, 128 individuals were excluded from our sample because their race, as coded by the Medical Examiner's Office, was either missing, mixed, or other than black or white. Five other cases were excluded: 1 because gender was not indicated, 2 because of extreme obesity, and 2 because their deaths occurred under highly unusual circumstances (one during electric-shock therapy, the other from complications of childbirth), leaving a final analytic sample of 587. Individuals lacking data on heart weight (n=20), body weight (n=27), and clinical cause of death (n=144) were excluded from analyses that included those variables but were included in all other analyses.

Autopsy and Clinical Cause of Death: Definition of Terms
Autopsy cause of death was defined by the first cause of death listed by the medical examiner; this was identified as the principal cause of death. Only one autopsy cause of death was assigned per case. Autopsy causes of death were grouped by the investigators into atherosclerotic heart disease, hypertensive vascular disease, congestive heart failure, and "other cardiac causes," according to explicit criteria.

Atherosclerotic heart disease (ICD-9 codes 410 [acute myocardial infarction], 411 [other acute and subacute forms of ischemic heart disease], 414 [other forms of chronic ischemic heart disease], and 440 [atherosclerosis]) was considered the autopsy cause of death if the autopsy report described pathological evidence of either myocardial necrosis or significant epicardial coronary stenosis. Significant coronary stenosis was defined as >50% narrowing of the cross-sectional luminal diameter of the left main coronary artery or >75% narrowing of the cross-sectional luminal diameter of one or more of the major epicardial coronary arteries. The presence of recent myocardial infarction was noted if the autopsy record indicated acute infarction within 7 days.

Hypertensive vascular disease (ICD-9 codes 401 [essential hypertension], 402 [hypertensive heart disease], 403 [hypertensive renal disease], and 404 [hypertensive heart and renal disease]) was considered the autopsy cause of death if the autopsy report noted myocyte hypertrophy in the absence of other heart disease known to cause this lesion, including aortic valve stenosis or hypertrophic cardiomyopathy, systemic arteriolar changes consistent with hypertension, or microscopic evidence of glomerular or arteriolar damage in the kidneys in the absence of diabetes mellitus. Left ventricular hypertrophy was not formally assessed at autopsy. If atherosclerotic heart disease was present together with evidence of hypertensive vascular disease, the autopsy cause of death was considered to be hypertensive vascular disease if pathological evidence of myocardial necrosis or significant coronary artery stenosis was absent.

Congestive heart failure (ICD-9 codes 425 [cardiomyopathy] and 428 [heart failure]) was considered the autopsy cause of death if the left ventricle or all the heart chambers were dilated and/or if hepatic or pulmonary congestion was noted in the autopsy report.

The category "other cardiac causes" included ICD-9 codes 391 and 393 to 398 (acute and chronic rheumatic heart disease), 415 to 417 (acute and chronic pulmonary heart disease), 420 (pericarditis), 421 (endocarditis), 422 (myocarditis), 423 (other pericardial diseases), 424 (other endocardial diseases), 426 (conduction disorders), 427 (cardiac dysrhythmias), 429 (ill-defined heart disease), and 430 to 438 (cerebrovascular disease).

Clinical cause of death was determined by the investigators after evaluating all available clinical and necropsy data, including heart weight and descriptions of the events immediately preceding the death. Myocardial infarction was considered the clinical cause of death based on pathological evidence for recent myocardial necrosis and clinical evidence of recent myocardial infarction. All 57 subjects who at autopsy had evidence of recent myocardial infarction were classified in terms of clinical cause of death as dying of myocardial infarction. One additional subject had clinical evidence supporting recent myocardial infarction and was classified in this category of clinical cause of death.

Sudden cardiac death was specified as the clinical cause of death if an unforeseen death occurred within 1 hour of onset of symptoms. Sudden cardiac death was a clinical cause of death but not an autopsy cause of death, and some subjects whose autopsy cause of death was atherosclerotic heart disease, hypertensive vascular disease, congestive heart failure, or other cardiac cause were classified as sudden cardiac death in terms of clinical cause of death.

The criteria for congestive heart failure and "other cardiac causes" were the same as for autopsy cause of death, as described above. A single clinical cause of death could not be asssigned for 144 of the decedents (63 blacks and 81 whites). In such cases, clinical cause of death was listed as "undetermined." The assigned categories for all cases were reviewed by A.A. and A.O.

Statistical Methods
Descriptive statistics were developed to characterize the sample by race, age, gender, mean heart weight, and autopsy and clinical causes of death and to examine autopsy and clinical causes of death according to race and gender. Logistic regression was used to calculate age-adjusted odds ratios for the most frequent causes of death in blacks versus whites. Differences in heart weights according to race, gender, and cause of death were compared using Student's t tests. Differences in heart weight were also examined using multiple linear regression analysis in which age, gender, body weight, and race were entered simultaneously within each stratum of autopsy or clinical cause of death. Two-tailed values of P>.05 were considered nonsignificant.


*    Results
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
*Results
down arrowDiscussion
down arrowReferences
 
The ages of the 587 study subjects at time of death ranged from 22 to 95 years. Black men did not differ from white men in mean age at time of death (51.7 versus 51.2 years; P=NS) (FigureDown, A), but black women were significantly younger at time of death (mean age 54.7 versus 61.5 years; P<.001) (FigureDown, B). There were 417 men and 170 women in this autopsy series, but the proportions of males and females did not differ significantly by race (69% males among blacks versus 72% among whites) (Table 1Down).



View larger version (45K):
[in this window]
[in a new window]
 
Figure 1. Age distributions of male (A) and female (B) study subjects by race.


View this table:
[in this window]
[in a new window]
 
Table 1. Characteristics of Sample Population

Atherosclerotic heart disease and hypertensive vascular disease were the predominant autopsy causes of death among both blacks and whites (Table 1Up). However, hypertensive vascular disease was approximately twice as frequent among blacks compared with whites (42% versus 23%; P<.001) as the autopsy cause of death. In contrast, atherosclerotic heart disease was more frequent among whites compared with blacks (64% versus 38%).

Analysis of the clinical causes of death showed that sudden cardiac death was responsible for 274 of the 587 (47%) total deaths, accounting for 156 of 314 (50%) of the deaths among blacks and 118 of 273 (43%) deaths among whites (Table 1Up). Blood toxicology findings were available for 485 (86%) of the subjects. Toxicology results were positive for cocaine in 14 of the 267 (5.2%) blacks and 1 of 218 (0.5%) whites in whom these data were available and for opiates in 12 (4.5%) blacks and 8 (3.7%) whites.

The predominance of hypertensive vascular disease as the autopsy cause of death among blacks compared with whites was present among both men and women (Table 2Down). Hypertensive vascular disease was the pathological cause of death among 41% of black males compared with 24% of white males (P<.001) and 44% of black females compared with 19% of white females (P<.001). Atherosclerotic heart disease was the pathological cause of death among 64% of white males compared with 39% of black males and 64% of white females compared with 36% of black females.


View this table:
[in this window]
[in a new window]
 
Table 2. Autopsy and Clinical Causes of Death for Men (n=417) and Women (n=170)

The age-adjusted odds ratio (OR) for hypertensive vascular disease as the autopsy cause of death for blacks versus whites was 2.2 (P<.001) among men and 3.1 (P=.01) among women (Table 3Down). Blacks were correspondingly less likely than whites to have atherosclerotic heart disease as the autopsy cause of death (age-adjusted OR, 0.4 for men, P<.001; age-adjusted OR, 0.4 for women, P<.01). The age-adjusted ORs comparing clinical causes of death for blacks versus whites indicated that recent myocardial infarction was less frequent among blacks versus whites for both men (age-adjusted OR, 0.5; P<.05) and women (age-adjusted OR, 0.2; P<.05).


View this table:
[in this window]
[in a new window]
 
Table 3. Age-Adjusted Odds Ratios1 and 95% Confidence Intervals for Black vs White Autopsy and Clinical Causes of Death

Mean heart weight was significantly greater in bivariate analyses among black women compared with white women (460 versus 384 g; P<.001) (Table 4Down) but not among black men compared with white men. Mean heart weight was greater among both blacks (536 versus 416 g; P<.001) and whites (487 versus 432 g; P<.01) whose autopsy cause of death was hypertension compared with those with atherosclerotic heart disease. Comparison of black versus white mean heart weight stratified by autopsy cause of death showed no significant differences except among subjects with hypertensive vascular disease as the autopsy cause of death, where blacks had higher mean heart weight than whites (536 versus 487 g, P<.05), strongly suggesting that the overall increased mean heart weight among blacks was explained by the greater prevalence and severity of hypertension. Comparison of black versus white mean heart weight stratified by clinical cause of death (lower panel of Table 4Down) showed no significant differences between blacks and whites. Multiple linear regression analyses of mean heart weight in relation to age, gender, body weight, and race were conducted within each stratum of autopsy and clinical cause of death. In these analyses, mean heart weight was associated with race (P=.046) among subjects with hypertensive vascular disease as the autopsy cause of death, but not in any of the other strata, consistent with the bivariate findings.


View this table:
[in this window]
[in a new window]
 
Table 4. Autopsy Heart Weights in Grams

Among the 274 subjects who died of sudden cardiac death, 234 had either atherosclerotic heart disease or hypertensive vascular disease as the underlying autopsy cause of death (Table 5Down), whereas the remainder had congestive heart failure or other cardiac causes as the autopsy cause of death. In this subgroup of 234 subjects, among blacks atherosclerotic heart disease was the autopsy cause of death in 42% versus hypertensive vascular disease in 58%, whereas among whites these proportions were 68% and 32% (P<.001). This pattern was present among both men and women (Table 5Down).


View this table:
[in this window]
[in a new window]
 
Table 5. Autopsy Causes of Death in Blacks vs Whites Among 234 Subjects Who Died of Sudden Cardiac Death


*    Discussion
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
The main finding of this study is that hypertensive vascular disease was substantially more common than atherosclerotic heart disease as the underlying cause of death among black adults dying of cardiovascular disease and coming to autopsy in the New York City Medical Examiner's Office in 1991. Among comparable white adults, this pattern was reversed, and atherosclerotic heart disease was considerably more frequent than hypertensive vascular disease as the underlying cause of cardiovascular death. These race-specific patterns were consistent in both men and women and persisted after adjustment for age. Mean heart weight, reflecting left ventricular hypertrophy, was increased in both blacks and whites dying of hypertensive vascular disease, compared with other cardiovascular causes, but was not associated with race after the underlying cause of death and other covariates were taken into account.

In considering whether the findings in this autopsy series can shed light on the differential cardiovascular disease mortality rates in blacks versus whites, a key issue is the basis for selection of deaths for autopsy by the medical examiner. Because selection was largely based on the circumstances of death, our case series should not be viewed as a representative sample, and the actual rates of specific cardiovascular causes of death observed for blacks and whites should not be applied directly to these populations as a whole. The finding that there were large differences by race within this autopsy series in the relative rates of hypertensive vascular disease and atherosclerotic heart disease does suggest that this pattern may be present in the population as a whole. While it is possible that factors leading to selection for autopsy differed systematically between blacks and whites, this seems unlikely because the Medical Examiner's Office was not aware of the race of the decedent at the time it decided whether to take a case. Selection biases are therefore unlikely to account for the large differences between blacks and whites in the underlying pathology responsible for the cardiovascular deaths in this series. Our series included all adult autopsied cardiovascular deaths in New York City in 1991, excluding only those whose autopsy reports did not record their race, whose race was recorded as neither black nor white, who were morbidly obese, or who died under highly unusual circumstances.

The left ventricle constitutes the main component of the mean heart weight, particularly in the hypertrophied heart.31 The propensity of the left ventricle to hypertrophy is strongly related to blood pressure level.32 33 The relationship of left ventricular hypertrophy to race and skin color is controversial. Some studies have shown no relationship after taking account of severity and duration of hypertension,34 35 whereas others have found such relationships.36 37 Left ventricular hypertrophy defined electrocardiographically33 and echocardiographically38 was shown in the Framingham Heart Study to be strongly associated with incident cardiovascular events after adjustment for other cardiovascular risk factors, including blood pressure.33 The relationship in our study between mean heart weight and autopsy-based classification of underlying cause of death, with higher mean heart weight among those with hypertensive vascular disease, supports the validity of this classification.

Sudden death was the clinical cause of death in 274 of the 587 (47%) of the total deaths in our study. This high frequency of sudden death was not explained by acute cocaine or opiate use, since blood toxicology was positive in only a small proportion of subjects. It was also not explained by acute myocardial infarction or past myocardial infarction, since pathological evidence of recent infarction was present in only 57 subjects and past myocardial infarction in 46 additional subjects. Left ventricular hypertrophy has been found to predispose to ventricular arrhythmias39 40 and sudden death,41 and it is likely that hypertensive heart disease and left ventricular hypertrophy contributed to the high frequency of sudden death, especially among blacks, in whom hypertensive vascular disease was more common than atherosclerotic heart disease. The high proportion of deaths that met clinical criteria for sudden death may also in part reflect autopsy selection factors, since the Medical Examiner's Office autopsies cases in which death is unexpected or unexplained.

National data show that the incidence of sudden death is greater among blacks compared with whites or Hispanics.42 We found that in whites who died of suddent death, atherosclerotic coronary disease, presumably leading to acute or chronic myocardial ischemia, was the predominant autopsy finding. In contrast, among blacks who died of sudden death, hypertensive vascular disease was more common at autopsy than atherosclerotic heart disease.

Autopsy data from the Medical Examiner's Office have several limitations. Documentation may be imprecise once it has been ascertained that death was due to natural causes, so that attention to subtle distinctions among etiologic causes may have varied from case to case. The fact that several persons performed the autopsies may also have contributed to variability in accuracy. The rigorous autopsy techniques followed by hospital or research pathologists may not have been uniformly or generally followed in all cases in this series. This variability or imprecision in classification of specific cardiovascular cause of death, however, is unlikely to have been systematically different in blacks compared with whites. Thus, possible misclassification of specific cause of death due to inaccuracy would not explain the observed differences between blacks and whites in our study, and, indeed, would lead to an underestimation of the odds ratios. Another limitation is that clinical information on many of the cases was sparse and probably unreliable. It is for this reason that we based our analysis almost entirely on autopsy findings, the main exception being the suddenness of death, a variable that involves a minimum of subjectivity. Several studies have reported that heart weight adjusted for body mass index is superior to heart weight alone as an index of hypertensive left ventricular hypertrophy.43 44 We were unable to calculate body mass index for our subjects because of lack of height data, but we were able to adjust heart weight for body weight, as well as for other covariates in our analysis.

Hypertension causes or contributes to mortality through damage of organs other than the heart, in particular via its pathogenic role in stroke.3 Our study focused on cardiac causes of death based on the ICD-9 codes for the first cause of death assigned by the Medical Examiner's Office. We therefore excluded subarachnoid hemorrhage and other hypertension-related strokes.

National data2 4 7 8 45 show that the greatest excess cardiovascular disease mortality risk among blacks is in younger age groups, and particularly among blacks in their 40s and 50s. While this excess risk is present among both men and women, it is greater among black women, compared with white women, than among black men, compared with white men. National data for 1991, the year in which the subjects in our study died, show these same patterns, with the greatest excesses in large core metropolitan areas compared with large fringe metropolitan, medium/small metropolitan, urban nonmetropolitan, or rural areas.45 These data are based on ICD-9 diagnoses derived from death certificates, rather than autopsy findings, and do not permit direct comparison of hypertensive vascular disease with atherosclerotic heart disease as specific, autopsy-validated causes of cardiovascular death. Consistent with these national data, the black subjects in our study were younger at time of death than whites, and this age difference was present among women but not men.

The contribution of hypertension to the pathological processes observed in this series of autopsies goes beyond those subjects whose autopsy findings documented hypertensive vascular disease as the underlying cause of death, since hypertension is also a major contributing cause to atherosclerotic heart disease and congestive heart failure.32 These three causes of cardiovascular death accounted for more than 80% of all the cardiovascular deaths in this autopsy series, with other cardiac causes explaining only 16% of the total. Despite the demonstrated effectiveness of antihypertensive medications in lowering blood pressure and preventing the complications of hypertension,29 national surveillance data continue to show substantial gaps in detection, awareness, treatment, and control.46 Rates of hypertension control are lower among minority and socially disadvantaged groups.47 48 Studies of patients with hypertensive emergencies49 and severe uncontrolled hypertension50 found that almost all of these hypertensive persons had been previously treated. Lack of access to primary care50 and financial barriers51 are key problems for uninsured or underinsured groups and groups with large out-of-pocket costs for medications, although other studies have found low rates of hypertension control even in fully insured healthcare workers.52 The findings in this large autopsy series underscore the importance of hypertension in the excess cardiovascular mortality experienced by blacks in the United States.


*    Acknowledgments
 
We wish to acknowledge the help and cooperation of the Medical Examiner's Office of the New York City Department of Health.

Received November 25, 1997; first decision November 25, 1997; accepted December 5, 1997.


*    References
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
up arrowDiscussion
*References
 

  1. Trends in ischemic heart disease deaths: United States, 1990–1994. MMWR Morb Mortal Wkly Rep. 1997;46:146–150.[Medline] [Order article via Infotrieve]
  2. Sempos C, Cooper R, Kovar MG, McMillen M. Divergence of the recent trends in coronary mortality for the four major race-sex groups in the United States. Am J Public Health. 1988;78:1422–1427.[Abstract/Free Full Text]
  3. Gillum RF. Cardiovascular disease in the United States: an epidemiologic overview. In: Saunders E, ed. Cardiovascular Diseases in Blacks. Philadelphia, Pa: FA Davis; 1991:3–16.
  4. Pappas G, Queen S, Hadden W, Fisher G. The increasing disparity in mortality between socioeconomic groups in the United States, 1960 and 1986. N Engl J Med. 1993;329:103–108.[Abstract/Free Full Text]
  5. McCord C, Freeman HB. Excess mortality in Harlem. N Engl J Med. 1990;322:173–177.[Abstract]
  6. Geronimus AT, Bound J, Waidmann TA, Hillemeier MM, Burns PB. Excess mortality among blacks and whites in the United States. N Engl J Med. 1996;335:1552–1558.[Abstract/Free Full Text]
  7. US Department of Health and Human Services. Report of the Working Group on Research in Coronary Heart Disease in Blacks. US Public Health Service, National Institutes of Health; March 1994.
  8. Liao Y, Cooper R. Continued adverse trends in coronary heart disease mortality among blacks, 1980–91. Public Health Rep. 1995;110:572–579.[Medline] [Order article via Infotrieve]
  9. Fang J, Madhavan S, Alderman MH. The association between birthplace and mortality from cardiovascular causes among black and white residents of New York City. N Engl J Med. 1996;335:1545–1551.[Abstract/Free Full Text]
  10. Gillum RF. The epidemiology of cardiovascular disease in black Americans. N Engl J Med. 1996;335:1597–1599.[Free Full Text]
  11. Keil JE, Sutherland SE, Knapp RG, Lackland DT, Gazes PC, Tyroler HA. Mortality rates and risk factors for coronary disease in black as compared with white men and women. N Engl J Med. 1993;329:73–78.[Abstract/Free Full Text]
  12. Lewis C, Raczynski JM, Oberman A, Cutter GR. Risk factors and the natural history of coronary heart disease in blacks. Cardiovasc Clin. 1991;21:29–45.[Medline] [Order article via Infotrieve]
  13. Goldberg KC, Hartz AJ, Jacobsen SJ, Krakauer H, Rimm AA. Racial and community factors influencing coronary artery bypass graft surgery rates for all 1986 Medicare patients. JAMA. 1992;267:1473–1477.[Abstract]
  14. Mirvis DM, Burns R, Gaschen L, Cloar FT, Graney M. Variation in utilization of cardiac procedures in the Department of Veteran Affairs health care system: effect of race. J Am Coll Cardiol. 1994;24:1297–1304.[Abstract]
  15. Wenneker MB, Epstein AM. Racial inequalities in the use of procedures for patients with ischemic heart disease in Massachusets. JAMA. 1989;261:253–257.[Abstract]
  16. Carlisle DM, Leake BD, Shapiro MF. Racial and ethnic disparities in the use of cardiovascular procedures: associations with type of health insurance. Am J Public Health. 1997;1987:263–267.
  17. Yedidia MJ. The impact of social factors on the content of care: treatment of ischemic heart disease at a public and a voluntary hospital. Arch Intern Med. 1992;152:595–600.[Abstract]
  18. Escarce JJ, Epstein KR, Colby DC, Schwartz JS. Racial differences in the elderly's use of medical procedures and diagnostic tests. Am J Public Health. 1993;83:948–954.[Abstract/Free Full Text]
  19. Yedidia MJ. Differences in treatment of ischemic heart disease at public and a voluntary hospital: sources and consequences. Milbank Q. 1994;72:299–325.[Medline] [Order article via Infotrieve]
  20. Strong JP, Oalmann MC, Newman WP III, Tracy RE, Malcom GT, Johnson WD, McMahan LH, Rock WA Jr, Guzman MA. Coronary heart disease in young black and white males in New Orleans: community pathology study. Am Heart J. 1984;108:747–759.[Medline] [Order article via Infotrieve]
  21. Shirani J, Yousefi J, Roberts WC. Major cardiac findings at necropsy in 366 American octogenarians. Am J Cardiol. 1995;75:151–156.[Medline] [Order article via Infotrieve]
  22. Roeske WR, Savage RM, O'Rourke R, Bloor CM. Myocardial infarction: how representative are autopsied subjects with this clinical entity? Arch Pathol Lab Med. 1981;105:642–646.[Medline] [Order article via Infotrieve]
  23. Kitzman DW, Scholz DG, Hagen PT, Ilstrup DM, Edwards WD. Age-related changes in normal human hearts during the first 10 decades of life, II (maturity): a quantitative anatomic study of 765 specimens from subjects 20 to 99 years old. Mayo Clin Proc. 1988;63:137–146.[Medline] [Order article via Infotrieve]
  24. Burke AP, Farb A, Malcom GT, Liang Y-H, Smialek J, Virmani R. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. N Engl J Med. 1997;336:1276–1282.[Abstract/Free Full Text]
  25. Pathobiological Determinants of Atherosclerosis inYouth (PDAY) Research Group. Relationships of atherosclerosis in young men to serum lipoprotein cholesterol concentrations and smoking: a preliminary report from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group. JAMA. 1990;264:3018–3024.[Abstract]
  26. Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group. Natural history of aortic and coronary atherosclerotic lesions in youth: findings from the PDAY Study. Arterioscler Thromb. 1993;13:1291–1298.[Abstract/Free Full Text]
  27. Hypertension Detection and Follow-up Program Cooperative Group. Race, education and prevalence of hypertension. Am J Epidemiol. 1977;106:351–361.[Abstract/Free Full Text]
  28. Hildreth C, Saunders E. Hypertension in blacks: clinical overview. In: Saunders E, ed. Cardiovascular Disease in Blacks. Philadelphia, Pa: FA Davis Co; 1991:85–96.
  29. Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. The Fifth Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC-V). Arch Intern Med. 1993;153:154–183.[Medline] [Order article via Infotrieve]
  30. International Classification of Diseases, 9th Revision, Clinical Modification. 4th ed. Los Angeles, Calif: Practice Management Information Corp; 1993.
  31. Reiner L, Mazzoleni A, Rodriguez FI, Freudenthal RR. The weight of the human heart, II: hypertensive cases. Arch Pathol. 1961;71:180–201.[Medline] [Order article via Infotrieve]
  32. Dawber TR. The Framingham Heart Study. Cambridge, Mass: Harvard University Press; 1980:205–210.
  33. Kannel WB. Blood pressure as a cardiovascular risk factor: prevention and treatment. JAMA. 1996;275:1571–1576.[Abstract]
  34. Hammond IW, Alderman MH, Devereux RB, Lutas EM, Laragh JH. Contrast in cardiac anatomy and function between black and white patients with hypertension. J Natl Med Assoc. 1984;76:247–255.[Medline] [Order article via Infotrieve]
  35. Coresh J, Klag MJ, Whelton PK, Kuller L. Left ventricular hypertrophy and skin color among American blacks. Am J Epidemiol. 1991;134:129–136.[Abstract/Free Full Text]
  36. Gottdiener JS, Reda DJ, Materson BJ, Massie BM, Notargiacomo A, Hamburger RJ, Williams DW, Henderson WG. Importance of obesity, race and age to cardiac structural and functional aspects of hypertension. J Am Coll Cardiol. 1994;15:1492–1498.
  37. Chaturvedi N, Athanassopoulos G, McKeigue PM, Marmot MG, Nihoyannopoulos P. Echocardiographic measures of left ventricular structure and their relation with rest and ambulatory blood pressure in blacks and whites in the United Kingdom. J Am Coll Cardiol. 1994;15:1499–1505.
  38. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med. 1990;322:1561–1566.[Abstract]
  39. Messerli FH, Ventura HO, Elizardi DJ, Dunn FG, Frohlich ED. Hypertension and sudden death: increased ventricular ectopy in left ventricular hypertrophy. Am J Med. 1984;77:19–22.[Medline] [Order article via Infotrieve]
  40. McLenachan JM, Henderson E, Morris KI, Dargie HJ. Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy. N Engl J Med. 1987;317:787–792.[Abstract]
  41. Kannel WB, Gordon T, Offutt D. Left ventricular hypertrophy by electrocardiogram: prevalence, incidence, and mortality in the Framingham study. Ann Intern Med. 1969;71:254–258.
  42. Gillum RF. Sudden cardiac death in Hispanic Americans and African Americans. Am J Public Health. 1997;87:1461–1466.[Abstract/Free Full Text]
  43. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man: anatomic validation of the method. Circulation. 1977;55:613–618.[Abstract/Free Full Text]
  44. Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular mass and geometry to morbidity and mortality in men and women with uncomplicated essential hypertension. Ann Intern Med. 1991;114:345–352.
  45. National Center for Health Statistics. Health, United States, 1993. Hyattsville, Md: US Public Health Service; 1994.
  46. Whelton PK, Brancati FL. Hypertension management in populations. Clin Exp Hypertens. 1993;15:1147–1156.
  47. Moorman PG, Hames CG, Tyroler HA. Socioeconomic status and morbidity and mortality in hypertensive blacks. In: Saunders E, ed. Cardiovascular Disease in Blacks. Philadelphia, Pa: FA Davis Co; 1991:179–194.
  48. Kaplan NM. Ethnic aspects of hypertension. Lancet. 1994;344:450–451.[Medline] [Order article via Infotrieve]
  49. Bennett NM, Shea S. Hypertensive emergency: case criteria, sociodemographic profile, and previous care of 100 cases. Am J Public Health. 1988;78:636–640.[Abstract/Free Full Text]
  50. Shea S, Misra D, Ehrlich MH, Field L, Francis CK. Predisposing factors for severe, uncontrolled hypertension in an inner-city minority population. N Engl J Med. 1992;327:776–781.[Abstract]
  51. Shulman NB, Martinez B, Brogan E, Carr AA, Miles CG. Financial costs as an obstacle to hypertension threapy. Am J Public Health. 1986;76:1105–1108.[Abstract/Free Full Text]
  52. Stockwell DH, Madhaven S, Cohen H, Gibson G, Alderman MH. The determinants of hypertension awareness, treatment, and control in an insured population. Am J Public Health. 1994;84:1768–1774.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
J Am Coll CardiolHome page
T. C. Lee, P. G. O'Malley, I. Feuerstein, and A. J. Taylor
The prevalence and severity of coronaryartery calcification on coronary arterycomputed tomography in black and white subjects
J. Am. Coll. Cardiol., January 1, 2003; 41(1): 39 - 44.
[Abstract] [Full Text] [PDF]


Home page
Arch Intern MedHome page
F. G. McMahon, K. Fujioka, B. N. Singh, C. M. Mendel, E. Rowe, K. Rolston, F. Johnson, and A. D. Mooradian
Efficacy and Safety of Sibutramine in Obese White and African American Patients With Hypertension: A 1-Year, Double-blind, Placebo-Controlled, Multicenter Trial
Arch Intern Med, July 24, 2000; 160(14): 2185 - 2191.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Onwuanyi, A.
Right arrow Articles by Francis, C. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Onwuanyi, A.
Right arrow Articles by Francis, C. K.