CLINICAL STUDIES
Racial differences in the significance of coronary calcium in asymptomatic black and white subjects with coronary risk factors
Terence M. Doherty, BAa,b,
Weiyi Tang, MDa,b and
Robert C. Detrano, MD, PhD, FACCa,b
a Division of Cardiology, Department of Medicine, Harbor-UCLA Medical Center, Torrance, California, USA
b Saint John’s Cardiovascular Research Center, Torrance, California, USA
Manuscript received July 14, 1998;
revised manuscript received March 25, 1999,
accepted May 10, 1999.
Reprint requests and correspondence: Robert C. Detrano, MD, PhD, FACC, Professor of Medicine, Division of Cardiology, Department of Medicine, Harbor-UCLA Medical Center and Saint John’s Cardiovascular Research Center, 1124 West Carson Street, Bldg. E5, Torrance, California 90502
detrano{at}harbor4.humc.edu
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Abstract
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OBJECTIVES
To compare the significance of a specific feature of coronary atherosclerosis—coronary calcium—in asymptomatic black and white subjects with coronary risk factors.
BACKGROUND
The natural history and clinical evolution of coronary atherosclerosis differs between blacks and whites. Differences in the underlying pathobiology of atherosclerosis may be one determinant of the ethnic variability in the clinical manifestation of coronary atherosclerosis.
METHODS
In 1,375 high-risk but asymptomatic subjects (93 blacks [6.8%] and 1,282 whites [93.2%]) with at least one risk factor but no prior evidence of coronary disease, we assessed coronary risk factors, calculated Framingham risk of a coronary event and evaluated coronary calcium with digital subtraction fluoroscopy. We then followed these subjects clinically for 70 ± 13 months, noting the occurrence of the following coronary events: death due to coronary heart disease (CHD); myocardial infarction (MI); angina pectoris; and performance of coronary bypass or angioplasty.
RESULTS
Risk factor profiles were similar in black and white subjects (6-year Framingham risk 15 ± 7% in blacks, 14 ± 8% in whites [NS]). Coronary calcium was present in 59.9% of white subjects but only 35.5% of black subjects (p = 0.0001). Nevertheless, after 70 months of follow-up, more blacks than whites (22 blacks [23.7%] vs. 190 whites [14.8%]; p = 0.04) suffered one of the following end points: CHD death, MI, angina or revascularization. The age, gender and coronary risk-adjusted odds ratio of black race for at least one event was 2.16 (95% CI 1.34 to 3.48).
CONCLUSIONS
Despite having a lowered prevalence of coronary calcium than high risk whites, high risk blacks suffer more CHD events. Coronary calcium therefore does not carry the same pathobiologic significance in blacks that it does in whites, consistent with the concept that there are specific racial differences in the natural history of CHD and its evolution into clinically manifest events.
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Abbreviations and Acronyms
| | CHD | = coronary heart disease | | CI | = confidence interval | | ECG | = electrocardiographic | | HDL | = high density lipoprotein | | LVH | = left ventricular hypertrophy | | MI | = myocardial infarction | | OR | = odds ratio |
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Blacks suffer an inordinately high degree of adverse cardiovascular events (1–3), posing an important but unsolved public health dilemma. While both underutilization (4) and diminished access to health care services (5) appear to significantly contribute, there are persistent suggestions that there may be ethnic differences in the pathobiology of atherosclerosis that may affect the clinical expression of the disease.
Ethnic differences in risk factors appear early in childhood (6,7) and may impact subsequent racial variation in clinical expression of the underlying substrate. For example, data from several sources indicate that smoking has a disproportionately lethal effect on blacks (8–10). The Atherosclerosis Research in Communities (ARIC) study (11) and other reports (12–14) have implicated socioeconomic status as a contributor to cardiovascular morbidity and mortality. However, data from the Meharry-Hopkins Study in black and white physicians, presumably of comparable socioeconomic status, indicate that systolic blood pressure has a higher adjusted odds ratio for coronary events in black physicians but serum cholesterol is more deleterious in white physicians (15). Recent 16 year follow-up data from the Coronary Artery Surgery Study (CASS) indicate that even after adjusting for all clinical and treatment variables, black race was a strong predictor of mortality in both the surgical and medical groups (8). Collectively, these data are consistent with the concept that there are ethnic differences in the pathobiology of atherosclerosis that affect its eventual clinical manifestations.
The pathobiologic substrates underlying these ethnic differences are unknown, but recent studies suggest the distinct possibility that coronary calcium—a specific and widely prevalent feature of coronary plaque—does not carry the same significance in blacks that it does in whites. For example, black subjects have a lower incidence of coronary calcification compared to whites, despite having a similar risk factor profile (16,17) and thus a roughly comparable risk of coronary heart disease (CHD) events. Furthermore, even after adjusting for the effects of all known determinants of coronary calcium (age, gender, and 1 ,25(OH)2D3 [16,18]) as well as all other coronary risk factors, high risk asymptomatic blacks still have less coronary calcium than high risk asymptomatic whites (16). Based on available data on the prognostic significance of coronary calcium (19–24), this lesser amount of calcium in blacks should predict fewer subsequent events.
On the contrary, we report that although blacks have a lower prevalence of coronary calcium than whites, they nevertheless suffer greater numbers of coronary events, even after adjusting for the effects of risk factors. Therefore, coronary calcium is of different pathobiologic significance in black subjects with coronary risk factors compared to white subjects with similar risk factors.
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Methods
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Subjects.
All subjects gave written informed consent to voluntarily participate in this investigation and no subject was required to pay for testing. The study received approval from the Human Subjects Committee at our institution. Subjects were excluded if they had history or electrocardiographic evidence of a prior myocardial infarction (MI) or if they answered affirmatively to the first and two other questions from the following angina questionnaire: a) Do you suffer from chest discomfort? b) Does it last less than 15 minutes? c) Does the pain come on when you exert yourself? d) Is the pain relieved by rest or nitroglycerin? This definition of angina is similar to that used by Diamond and Forrester (25) and that used by the Framingham investigators (26).
A total of 1,461 subjects satisfied these enrollment criteria. Eighty six subjects from ethnic groups other than black or white (82 Asian Americans, 4 Native Americans) were excluded from analysis in this report. The remaining 1,375 subjects were either black (n = 93; 6.8%) or white (n = 1,282; 93.2%), were asymptomatic at the time of coronary calcium assessment, underwent risk factor evaluation at the time of coronary calcium screening, and were followed prospectively thereafter by the South Bay Heart Watch Clinic to determine coronary events. Details of recruitment, selection and risk factor evaluation methodology have been previously published (23,24,27).
Our cohort was, by design, high-risk but asymptomatic, with no clinical or electrocardiographic (ECG) evidence of CHD, but all had >8% risk of a coronary heart disease event within six years, based on risk factor analysis and calculations utilizing the Framingham risk algorithm (26,28). All 1,375 subjects underwent evaluation of coronary calcium using digital subtraction fluoroscopy (23,24,27,29) and were evaluated annually thereafter.
Risk factor analysis.
The following risk factors were assessed for each subject at the time of digital fluoroscopic coronary calcium assessment: age, gender, total serum cholesterol, high-density lipoprotein (HDL) cholesterol, systolic blood pressure, body mass index, history of hypertension, history of diabetes mellitus, history of smoking, family history of coronary heart disease, and left ventricular hypertrophy (LVH) by ECG (Romhilt-Estes LVH score) (Table 1). We also obtained information on current medication usage (Table 2). Details of risk factor assessment methodology are reported elsewhere (23,24,27).
Ethnicity.
Ethnicity was determined by a clinical research nurse who questioned subjects regarding their ethnic ancestry and classified each subject as African American, Asian American, white, or Native American. Of the 1,461 subjects enrolled, there were a total of 1,282 whites (87.7%), 93 blacks (6.4%), 82 Asian Americans (5.6%) and 4 Native Americans (0.3%). The proportion of minority subjects enrolled was roughly comparable to the ethnic compositions of the communities from which these subjects originated (17).
Digital subtraction fluoroscopy.
We performed digital fluoroscopy in all subjects in the 60° left anterior oblique projection utilizing a Philips digital cinefluoroscopic x-ray imaging system. Further details of the image acquisition protocol have been reported elsewhere (17,23,24,27). Although there are no published head-to-head comparisons of digital fluoroscopy with the newer radiographic technology, electron beam computed tomography, we expect that the former technology will be somewhat less sensitive than the latter. All fluoroscopic images were assessed for the presence or absence of calcium in the distribution of each of the coronary arteries by two observers (RCD and WT), both blinded to risk factor information as well as to the other observer’s interpretation. Interobserver differences in interpretation occurred in 7.7% of cases and were resolved by the two observers after review and consensus decision (30).
Follow-up.
Subjects were assessed annually after enrollment, risk factor assessment and coronary calcium fluoroscopy, and then followed for 70 ± 13 months (successful follow-up was obtained in over 98% of subjects). The mean follow-up duration was 72 ± 13 months and 70 ± 13 months for blacks and whites, respectively (p = NS).
There were a total of six follow-up evaluations during the 70 ± 13 month follow-up period. Of the 93 black subjects in the cohort, 91 (97.8%) returned to the South Bay Heart Watch Clinic for at least one visit. Of the 1,282 white subjects, 1,248 (97.3%) returned to our clinic for at least one visit. The first two annual follow-up evaluations occurred principally in the South Bay Heart Watch Clinic, and the remaining four evaluations were largely by telephone.
At each follow-up visit evaluation, we assessed CHD status using review of medical records and transcriptions of conversations with families for infarctions, revascularizations and CHD deaths and the responses to the same angina questionnaire administered as on the initial visit (23,24,27). Three cardiologists met quarterly to decide by majority rule on all cases for which at least one member had diagnosed an MI (using criteria specified below, and previously reported [23,24,27]). Subjects unable or unwilling to return to the clinic were contacted by telephone by a research nurse and were either visited in their home by staff personnel or were mailed a questionnaire to obtain information on angina and hospital admissions.
Medical records were obtained for all but two hospital admissions (one black and one white subject). For subjects who died outside of a hospital, we obtained transcriptions of conversations with next of kin regarding circumstances and symptoms preceding death. Coronary heart disease end points were: 1) angina pectoris; 2) acute MI; 3) myocardial revascularization; and 4) CHD death. Evaluation of medical records to determine CHD end points was performed by a committee of three board-certified cardiologists without knowledge of coronary calcium results, ethnic origin or risk factor data. Evaluations by committee members were performed separately, and the entire committee would then meet periodically to decide by majority rule only those cases where there was not unanimous agreement among committee members whether or not an event had occurred. At follow-up, angina pectoris was defined as present by a score of 4 on the angina questionnaire that had been administered at screening. Thus, an increase in angina score from baseline of at least two was required in order to achieve this endpoint.
Coronary heart disease death was determined by the committee without knowledge of coronary calcium, ethnicity or other data by review of medical records (23,24,27). The committee also attributed each death either to CHD or non-CHD causes.
Statistical analysis.
Two-tailed Fisher’s exact test was used to evaluate ethnic differences in coronary calcification and CHD events. Either two-tailed Fisher’s exact test or Student’s t test was performed to compare differences in risk factors between ethnic groups. These tests were utilized to provide the most conservative method possible to test our hypotheses. Logistic regression was performed to evaluate the influence of risk factors and ethnicity on the occurrence of CHD events. Kaplan-Meier curves were compared using the Wilcoxon test. An alpha value <0.05 was considered significant.
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Results
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Risk factors.
Coronary heart disease risk factor data comparing black and white subjects are depicted in Table 1. Black subjects had a significantly higher systolic blood pressure (p = 0.002) and body mass index (p = 0.02), a higher incidence of diabetes mellitus (p = 0.01) and more frequent history of hypertension (p = 0.03) compared to white subjects. However, white subjects were significantly older (p = 0.0001) and had a greater incidence of positive family history of CHD compared to black subjects (p = 0.01). There were no significant ethnic differences in gender, total cholesterol, HDL cholesterol, history of smoking, current smoking status, LVH by ECG, or calculated Framingham risk of a coronary event in six years (Table 1). There were also no significant ethnic differences in medication usage (Table 2), although there were trends towards more use of both beta blockers and other antihypertensive agents in black subjects (p = 0.06 for both comparisons).
Coronary calcium prevalence.
The prevalence of any coronary calcium was 58.2% (n = 801) in the entire cohort. The prevalence of coronary calcium in black subjects was 35.5% (n = 33) and in white subjects was 59.9% (n = 768); this difference was highly significant (p < 0.0001).
Distribution of coronary calcium.
Of the entire cohort, a total of 409 subjects (29.7%) had calcium in one coronary artery, 239 subjects (17.4%) had calcium in two coronary arteries and 153 subjects (11.1%) had calcium in all three coronary arteries.
Racial differences in the topographic distributions of coronary calcium are summarized in Table 3. Of the black cohort, 20 subjects (21.5%) had calcium in one coronary artery, 8 subjects (8.6%) had calcium in two coronary arteries and 5 (5.4%) had calcium in all three coronary arteries. Of the white cohort, 389 (30.3%) had calcium in the distribution of only one coronary vessel, 231 subjects (18.0%) had calcium in two coronary arteries, while 148 (11.5%) had calcium in all three coronary vessels.
Determinants of coronary calcium.
Multivariate logistic regression analysis demonstrated black race to be a significant, independent and inverse predictor of the presence of coronary calcium (odds ratio [OR] 0.47; 95% confidence interval [CI], 0.29, 0.75). Age, male gender, smoking status, family history, diabetes mellitus, LVH, and serum total cholesterol were significant independent predictors of the presence of coronary calcium by digital fluoroscopy. These results are summarized in Table 4, along with the corresponding ORs and 95% CIs.
Coronary heart disease events.
Despite having a lower prevalence of coronary calcium, more black subjects than white subjects suffered a CHD endpoint during the 70 month follow-up period. This difference was highly significant (p = 0.001), and is depicted in Figure 1, which shows event-free survival for blacks and whites as a function of time.
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Figure 1 Kaplan-Meier event-free survival curves in black and white subjects during the 70 month follow-up period. Black subjects were significantly more likely than white subjects to suffer a coronary event (p = 0.001; Wilcoxon test).
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Table 5 shows ethnic differences in the occurrence of end points during the follow-up period. The occurrence of any end point (CHD death, nonfatal MI, new onset angina, or performance of a revascularization procedure) was more frequent in black subjects than in white subjects (22 blacks [23.7%]; 190 whites [14.8%]; p = 0.04). Blacks were also significantly more likely to suffer either CHD death, MI or new onset angina compared to white subjects (20 blacks [21.5%]; 162 whites [12.6%]; p = 0.03).
There were a total of 126 deaths in the entire cohort (11 [11.8%] blacks and 115 [9.0%] whites; p = 0.35). The majority (85 [67.5%]) of deaths were not attributed to CHD by the Adjudication Committee. In all instances where the Adjudication Committee decided a death was due to CHD, the decision was based upon the occurrence of either a sudden unexpected death or an MI death. There were no autopsy-determined CHD deaths.
There were more MIs (either fatal or nonfatal) in black subjects compared to white subjects (9 blacks [9.7%]; 62 whites [4.8%]; p = 0.05). Black subjects were also more likely to suffer new onset angina (14 blacks [15.1%]; 97 whites [7.6%]; p = 0.02). There was also a trend towards more hard events (CHD death or MI) in black subjects compared to whites, but the difference did not reach statistical significance (11 blacks [11.8%]; 86 whites [6.7%]; p = 0.09). The performance of revascularization procedures (percutaneous coronary angioplasty or coronary bypass) did not differ between the races (4 blacks [4.3%]; 76 whites [5.9%]; p = 0.65). There was also no significant ethnic difference in the occurrence of CHD deaths during the follow-up period (4 blacks [4.3%]; 37 whites [2.9%]; p = 0.35).
Table 6 shows the relationship between calcification and end points (CHD death, MI, angina, or revascularization) in blacks and whites. Multivariate logistic regression analysis using the occurrence of any of these end points as the dependent variable revealed that black race was a significant and independent predictor of the occurrence of a CHD end point (OR 2.16; 95% CI 1.34, 3.48) (Table 7). Additional significant and independent predictors of a CHD event included the presence of LVH by ECG (OR 2.18; 95% CI 1.35, 3.52), a history of diabetes mellitus (OR 1.21; 95% CI 1.02, 1.43;), the number of calcified coronary vessels (OR 1.16; 95% CI 1.01, 1.33;), a history of hypertension (OR 1.34; 95% CI 1.02, 1.76) and total serum cholesterol (OR 1.03; 95% CI 1.00, 1.06). High-density lipoprotein cholesterol was a significant inverse predictor of a coronary endpoint (OR 0.84; 95% CI 0.75, 0.93). Age, history of smoking, gender and family history of CHD were not significant independent predictors of a CHD event.
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Table 7 Independent Predictors of Any Coronary Event by Multivariate Logistic Regression, Along With Odds Ratios and 95% Confidence Intervals
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Discussion
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Coronary calcium indicates concomitant atherosclerotic disease (31), and prospective studies have demonstrated that subjects with coronary calcium have a higher risk of subsequent coronary events compared to similar subjects without coronary calcium (19–24). However, we report here that in a cohort of asymptomatic subjects with coronary risk factors, coronary calcium detected with digital fluoroscopy was less prevalent in blacks than in whites, yet more blacks than whites suffered coronary events during a 70 month follow-up period. These results indicate that there are differences in a measurable pathobiologic characteristic of coronary lesions—calcific deposits—detected in vivo, in two ethnic groups destined to suffer similar numbers of adverse outcomes.
Potential explanations for ethnic differences.
1. Differences in prevalence of atherosclerosis
It is possible that our black subjects had a lesser prevalence of coronary calcium because they had less coronary atherosclerosis than our white subjects. There are conflicting data on the prevalence and severity of coronary atherosclerosis in blacks and whites. Autopsy studies prior to the 1980s (32,33) have shown that blacks have less severe coronary atherosclerosis than whites, but more recent post-mortem data indicate that these differences are not significant (34). However, pathologic studies also have shown that blacks have less atherosclerotic calcium than whites (35,36). For example, Strong and McGill have reported that aortic lesions in whites were calcified 1.6 times more frequently than similar lesions in blacks (36). Consistent with these findings, our data also suggest that blacks have a lower frequency and severity of coronary calcium, despite similar or even greater risk of CHD events.
The National Institutes of Health has planned a large, multiethnic investigation to determine the interaction of coronary calcification and ethnicity in the prediction of CHD events (37). This study should more fully define the relationship of calcium quantity to CHD events in several ethnic groups.
2. Differences in calcium metabolism
Ethnic differences in bone metabolism have been previously reported; for example, despite a lower calcium intake (38), blacks have greater bone mass (39) and a lower incidence of osteoporosis and hip fractures (40) compared to whites. Severalstudies (41–43) have demonstrated racial differences in endocrine factors that affect bone metabolism and that, given the similarities between atherosclerotic calcification and osteogenesis (44,45), could affect mineralization at lesion sites. We have recently shown that serum levels of 1,25(OH)2D3 are inversely related to calcium mass (16,18), that blacks have higher levels of 1,25(OH)2D3, but these differences are not sufficient to fully account for the observed racial differences in coronary calcium (16). It is therefore conceivable that ethnic differences in endocrine mechanisms in addition to vitamin D metabolism may be contributing factors. However, these possibilities, while perhaps explaining racial differences in the amount of coronary calcium, do not explain why blacks have more events than whites.
3. Myocardial mass
Recent studies suggest that myocardial mass may be a more important factor leading to sudden cardiac death in blacks than in whites (15,46). This relationship might be pertinent to our findings. Although both a history of hypertension and LVH by ECG were significant independent predictors of events in the entire cohort, we did not find a more significant independent association between LVH (by ECG) and coronary events in blacks, perhaps due to inadequate power in our study.
4. Differing importance of risk factors
Population-based epidemiologic studies indicate that predictors of CHD mortality were similar in blacks and whites except that cigarette smoking carried a greater risk for blacks, while serum cholesterol carried a greater risk in whites (1,9). Data from the Meharry-Hopkins Study which prospectively evaluated risk factors in black and white physicians suggest that systolic blood pressure is a relatively more important predictor of CHD events in black compared to white physicians, but serum cholesterol is more important in white physicians (15). Although Framingham risk in our black and white cohorts was identical, risk factor differences (Table 1 and Results) could have accounted for some of the observed differences in CHD events.
Blacks with symptomatic CHD have a poorer prognosis compared to whites (3,47,48), which at least in part appears to be due to limited access of blacks to care (49) and decreased utilization of revascularization procedures by blacks (4,6,50,51). Since our subjects were asymptomatic and had no evidence of coronary disease at enrollment and since rates of revascularization were similar, any effects of ethnic differences in access to care on our results would probably have been minimal, but cannot be excluded.
Study limitations
Though ours was a population based study of the South Bay suburbs of Los Angeles, there is the possibility that differing referral patterns between whites and blacks might have influenced the results. Education and socioeconomic status have been shown to have an effect on CHD outcomes. These were not controlled for in our study. Our study has limited power for determining the predictive accuracy of coronary calcium in blacks. There were few black women in our sample and for this and other reasons, our results may not be applicable to other populations. Therefore, despite the fact that this was not significant in our cohort (Table 6), larger multi-ethnic sample sizes may clarify these issues (37).
Conclusion
Our results demonstrate that black subjects with coronary risk factors have a lower prevalence of coronary calcium than similar white subjects, but have at least as many CHD events on follow-up. Our black sample was too small to determine if coronary calcium is predictive of outcomes in blacks. Further investigations into ethnic differences in the mechanistic determinants of coronary heart disease events are needed and are underway. It is hoped that such data may result in improved treatment to minimize the morbidity and mortality of CHD, particularly in blacks.
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Acknowledgments
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This work was supported by grants from the National Heart, Lung and Blood Institute, the Saint John’s Cardiovascular Research Center and the Kenneth T. and Eileen L. Norris Foundation.
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Footnotes
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Supported by grants from: The National Heart, Lung, and Blood Institute (7RO1-HL-43277-02), National Institutes of Health, Bethesda, MD; Saint John’s Cardiovascular Research Institute, Santa Monica, CA; and the Kenneth T. and Eileen L. Norris Foundation.
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References
|
|---|
1. Keil JE, Sutherland SE, Knapp RG, et al. 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]
2. Gillum RF. Cardiovascular disease in the United States: an epidemiologic overview. Saunders E. Cardiovascular disease in blacks. Cardiovascular Clinics. Philadelphia: F. A. Davis Company; 1991. p. 3–16
3. Gillum RF. Coronary heart disease in black populations. I. Mortality and morbidity. Am Heart J. 1982;104:839–851[CrossRef][Medline]
4. Peterson ED, Shaw LK, DeLong ER, et al. Racial variation in the use of coronary revascularization procedures. Are the differences real? Do they matter? N Engl J Med. 1997;336:480–486[Abstract/Free Full Text]
5. Gillum RF, Gillum BS, Francis CK. Coronary revascularization and cardiac catheterization in the United States: trends in racial differences. J Am Coll Cardiol. 1997;29:1557–1562[Abstract]
6. Webber LS, Harsha DW, Phillips GT, et al. Cardiovascular risk factors in hispanic, white, and black children: the Brooks County and Bogalusa Heart Studies. Am J Epidemiol. 1991;133:704–714[Abstract/Free Full Text]
7. Belcher JD, Ellison RC, Shepard WE, et al. Lipid and lipoprotein distributions in children by ethnic group, gender, and geographic location S preliminary findings of the Child and Adolescent Trial for Cardiovascular Health (CATCH). Prev Med. 1993;22:143–153[CrossRef][Medline]
8. Taylor HA Jr, Mickel MC, Chaitman BR, et al. Long-term survival of African Americans in the Coronary Artery Surgery Study (CASS). J Am Coll Cardiol. 1997;29:358–364[Abstract]
9. Keil JE, Sutherland SE, Hames CG, et al. Coronary disease mortality and risk factors in black and white men. Arch Intern Med. 1995;155:1521–1527[Abstract/Free Full Text]
10. Wagenknecht LE, Cutter GR, Haley NJ, et al. Racial differences in serum cotinine levels among smokers in the coronary artery risk development in (young) adults study. Am J Public Health. 1990;80:1053–1056[Abstract/Free Full Text]
11. Diez-Roux AV, Nieto FJ, Tyroler HA, et al. Social inequalities and atherosclerosis. The Atherosclerosis Risk in Communities Study. Am J Epidemiol. 1995;141:960–972[Abstract/Free Full Text]
12. 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;329:103–109[Abstract/Free Full Text]
13. Buring JE, Evans DA, Fiore M, et al. Occupation and risk of death from coronary heart disease. JAMA. 1987;258:791–792[Abstract/Free Full Text]
14. Pocock SJ, Shaper AG, Cook DG, et al. Social class differences in ischaemic heart disease in British men. Lancet. 1987;2:197–201[Medline]
15. Thomas J, Thomas DJ, Pearson T, et al. Cardiovascular disease in African American and white physicians: The Meharry cohort and Meharry-Hopkins cohort studies. J Health Care for the Poor and Underserved. 1997;8:270–284[Medline]
16. Doherty TM, Tang W, Descalos S, et al. Ethnic origin and serum levels of 1,25-dihydroxyvitamin D3 are independent predictors of coronary calcium mass quantitated by electron beam computed tomography. Circulation. 1997;96:1477–1481[Abstract/Free Full Text]
17. Tang W, Detrano RC, Brezden OS, et al. Racial differences in coronary calcium prevalence among high risk adults. Am J Cardiol. 1995;75:1088–1091[CrossRef][Medline]
18. Watson KE, Abrolat ML, Malone LL, et al. Active serum vitamin D levels are inversely correlated with coronary calcification. Circulation. 1997;96:1755–1760[Abstract/Free Full Text]
19. Doherty TM, Wong ND, Shavelle RM, et al. Coronary heart disease deaths and infarctions in people with little or no coronary calcium. Lancet. 1999;353:41–42[CrossRef][Medline]
20. Detrano RC, Wong ND, Doherty TM, et al. Coronary calcium does not accurately predict near-term coronary events in high risk adults. Circulation. 1999;99:2633–2638[Abstract/Free Full Text]
21. Secci A, Wong N, Tang W, et al. Electron beam computed tomographic (EBCT) coronary calcium as a predictor of coronary endpoints. Comparison of two protocols. Circulation. 1997;96:1123–1129
22. Detrano R, Hsiai T, Wang S, et al. Prognostic value of coronary calcification and angiographic stenoses in patients undergoing coronary angiography. J Am Coll Cardiol. 1996;27:285–290[Abstract]
23. Detrano RC, Wong ND, Doherty TM, Shavelle R. Prognostic significance of coronary calcific deposits in asymptomatic high-risk subjects. Am J Med. 1997;102:344–349[CrossRef][Medline]
24. Detrano RC, Wong ND, Tang W, et al. Prognostic significance of cardiac cinefluoroscopy for coronary calcific deposits in asymptomatic high risk subjects. J Am Coll Cardiol. 1994;24:354–358[Abstract]
25. Diamond GA, Forrester JS. Analysis of probability as an aid in the clinical diagnosis of coronary artery disease. N Engl J Med. 1979;300:1350–1358[Abstract]
26. Abbott RD, McGee D. The probability of developing certain cardiovascular diseases in eight years at specified values of some characteristics. In: Kannel WB, Wolf PA, Garrison RJ (eds), The Framingham Study. An Epidemiological Investigation of Cardiovascular Disease. National Heart, Lung, and Blood Institute. U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health; NIH Publication No. 87-2284. August, 1987.
27. Detrano RC, Wong ND, French WJ, et al. Prevalence of fluoroscopic coronary calcific deposits in high-risk asymptomatic persons. Am Heart J. 1994;127:1526–1532[CrossRef][Medline]
28. Anderson KM, Wilson PWF, Odell PM, Kannel WB. An updated coronary risk profile. A statement for health professionals. Circulation. 1991;83:356–362[Free Full Text]
29. Detrano R, Markovic D, Simpfendorfer C, Salcedo E. Digital subtraction fluoroscopy: a new method of detecting coronary calcification with improved sensitivity for the prediction of coronary disease. Circulation. 1985;71:725–732[Abstract/Free Full Text]
30. Tang W, Young E, Detrano R, et al. Reproducibility of digital subtraction fluoroscopic readings for coronary artery calcification. Invest Radiol. 1994;29:147–149[CrossRef][Medline]
31. Wexler L, Brundage B, Crouse J, et al. Coronary artery calcification: Pathophysiology, epidemiology, imaging methods and clinical implications. A statement for health professionals from the American Heart Association. Circulation. 1996;94:1175–1192[Free Full Text]
32. Strong JP, McGill HC Jr. The natural history of coronary atherosclerosis. Am J Pathol. 1962;40:37–49[Medline]
33. Tejeda C, Strong JP, Montenegro MR, et al. Distribution of coronary and aortic atherosclerosis by geographic location, race, and sex. Lab Invest. 1968;18:509–526[Medline]
34. Strong JP, Oalmann MC, Newman WP III, et al. Coronary heart disease in young black and white males in New Orleans: community pathology study. Am Heart J. 1984;108:747–759[CrossRef][Medline]
35. Eggen DA, Strong JP, McGill HC Jr. Coronary calcification. relationship to clinically significant coronary lesions and race, sex, and topographic distribution. Circulation. 1965;32:948–955[Abstract/Free Full Text]
36. Strong JP, McGill HC. The natural history of aortic atherosclerosis: relationship to race, sex and coronary lesions in New Orleans. Exp Mol Pathol. 1963;(Suppl I):15–27
37. National Heart, Lung, and Blood Institute, National Institutes of Health. NHLBI-HC-98-XX. Subclinical Cardiovascular Disease Study. Request for Proposals. 1998.
38. Eck L, Hackett-Renner C. Calcium intake in youth: sex, age and racial differences in NHANES II. Prev Med. 1992;21:473–482[CrossRef][Medline]
39. Heaney RP. Bone mass, the mechanostat, and ethnic differences. J Clin Endocrinol Metab. 1995;80:2289–2290[CrossRef][Medline]
40. Farmer ME, White LR, Brody JA, Bailey KR. Race and sex differences in hip fracture incidence. Am J Public Health. 1984;74:1374–1380[Abstract/Free Full Text]
41. Bell NH, Greene A, Epstein S, et al. Evidence for alteration of the vitamin D-endocrine system in blacks. J Clin Invest. 1985;76:470–473[Medline]
42. Wright NM, Renault J, Willi S, et al. Greater secretion of growth hormone in black than in white men: Possible factor in greater bone mineral density. J Clin Endocrinol Metab. 1995;80:2291–2297[Abstract]
43. Richards RJ, Svec F, Bai W, et al. Steroid hormones during puberty: racial (black-white) differences in androstenedione and estradiol. The Bogalusa Heart Study. J Clin Endocrinol Metab. 1992;75:624–631[Abstract]
44. Doherty TM, Detrano RC, Mautner SL, et al. Coronary calcium: The good, the bad, and the uncertain. Am Heart J. 1999;137:806–814[CrossRef][Medline]
45. Doherty TM, Detrano RC. Coronary arterial calcification as an active process: A new perspective on an old idea. Calcif Tissue Int. 1994;54:224–230[CrossRef][Medline]
46. Liao Y, Cooper RS, McGee DL, et al. The relative effects of left ventricular hypertrophy, coronary artery disease, and ventricular dysfunction on survival among black adults. JAMA. 1995;273:1592–1597[Abstract/Free Full Text]
47. Cooper RS, Ghali JK. Coronary heart disease: black-white differences. Cardiovasc Clin. 1991;21:205–225[Medline]
48. Castaner A, Simmons BE, Mar M, Cooper R. Myocardial infarction among black patients: poor prognosis after hospital discharge. Ann Intern Med. 1988;109:33–35[CrossRef][Medline]
49. Ford E, Cooper R, Castaner A, et al. Coronary arteriography and coronary bypass surgery among whites and blacks relative to hospital-based incidence rates for coronary artery disease: findings from the National Hospital Discharge Survey. Am J Public Health. 1989;79:437–440[Abstract/Free Full Text]
50. Whittle J, Conigliaro J, Good CB, Lofgren RP. Racial differences in the use of invasive cardiovascular procedures in the Department of Veterans Affairs medical system. N Engl J Med. 1993;329:621–627[Abstract/Free Full Text]
51. Ayanian JZ, Udvarhelyi S, Gatsonis CA, et al. Racial differences in the use of revascularization procedures after coronary angiography. JAMA. 1993;269:2642–2646[Abstract/Free Full Text]
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|
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6(2):
147 - 153.
[Abstract]
[PDF]
|
|
|
|
|
|
|
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308 - 309.
[Full Text]
[PDF]
|
|
|
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|
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T. M. Doherty and R. C. Detrano
Reply
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July 1, 2000;
36(1):
309 - 309.
[Full Text]
[PDF]
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