Differences in Prevalence of and Risk Factors for Subclinical Vascular Disease Among Black and White Participants in the Cardiovascular Health Study

From the University of Pittsburgh, Pa (L.K.); the Cardiovascular Health Study Coordinating Center, Seattle, Wash (L. Fisher, R.M.); Johns Hopkins University, Baltimore, Md (L. Fried); the University of Vermont, Burlington (M.C.); Bowman Gray School of Medicine, Winston-Salem, NC (S.J.); and the National Heart, Lung, and Blood Institute, Bethesda, Md (T.M.).

Correspondence to Lewis H. Kuller, MD, DrPH, University of Pittsburgh, Department of Epidemiology, GSPH, 130 DeSoto St, Pittsburgh, PA 15261. E-mail kuller+{at}pitt.edu

	Abstract

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Abstract—A composite measure of subclinical vascular disease has been developed in the Cardiovascular Health Study (CHS). In previous reports, we measured the prevalence of subclinical disease among the original 5201 participants in the CHS, the relationship of risk factors to subclinical disease, and the association of subclinical disease to clinical coronary heart disease. In 1992 to 1993 (year 4 of the study), a larger cohort of 424 black women and 248 black men was added to the study. In this study, we have compared the prevalence of subclinical disease among blacks and whites in the CHS and the association with cardiovascular risk factors. The prevalence of subclinical disease for all participants (aged 65 years) was 41.3% for white women, 39.7% for black women, 41.9% for white men, and 43.7% for black men. The prevalence increased with age. The risk factor associations for subclinical disease were similar among blacks and whites. In multivariate analysis, age, systolic blood pressure, LDL cholesterol, smoking, and family history of myocardial infarction were independently associated with subclinical disease among both black and white women, while for white men, systolic blood pressure, use of antihypertensive medication, smoking, body mass index, and diastolic blood pressure (inverse) were related to subclinical disease. In black men, blood triglyceride level, use of antihypertensive medications, and family history of myocardial infarction (inverse) were associated with subclinical disease.

Key Words: cardiovascular disease • race • risk factors • subclinical disease

	Introduction

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An important issue in cardiovascular disease research is whether the relationship between risk factors and cardiovascular disease is similar among different races, sexes, and ethnic groups. Most epidemiological studies have focused primarily on white populations. We have previously reported the relationship between risk factors and subclinical disease among whites in the Cardiovascular Health Study (CHS)¹ and the association of subclinical disease among whites and risk of clinical disease over an approximate 2.4-year follow-up.² We have also documented the prevalence of individual components (ie, specific measurements) of subclinical disease and the relationship of these attributes to risk factors, among a smaller sample of blacks measured at baseline in the year from 1989 to 1990 of the CHS.³ The purpose of this study is to determine the risk factors for a composite measure of subclinical disease¹ among a larger sample of black and white participants in the CHS to determine whether there are any differences in key risk factors between blacks and whites.

There were 153 black women (5.2%) and 91 black men (4.1%) aged 65 years among the original 5201 CHS participants recruited in 1989 to 1990 (year 1 of the CHS). In 1992 to 1993 (year 4 of the study), a larger cohort, consisting of 424 black women and 248 black men, was added to the CHS. The recruitment methods, using the Medicare participant files as a sampling frame, were the same as those for the baseline population in 1989 to 1990.³ This study includes the total sample of blacks from both the baseline recruitment and the sample added with their baseline examination in year 4 of their examinations. The black participants are compared with the entire sample of white participants who had their baseline examination in 1989 to 1990.³

In the initial report of black/white comparisons in the CHS,³ black men and women had greater common carotid artery wall thickness than whites but lesser internal carotid artery wall thickness. Whites had a higher prevalence of carotid artery stenosis 50%. Blacks had a much higher prevalence of decreased ankle/brachial blood pressure 0.9 than whites, especially among black men, and greater echocardiographic and electrocardiographic evidence of increased left ventricular mass. Isolated ST-T segment abnormality and conduction defects on ECG were similar between blacks and whites. Atrial fibrillation prevalence was slightly higher in whites than blacks.³

A composite subclinical cardiovascular disease measure was developed in the CHS based on the extent of intimal-medial thickness of the carotid artery 80th percentile and ankle/brachial blood pressure 0.9, major electrocardiographic abnormalities according to the Minnesota code, echocardiographic abnormalities of wall motion and ejection fraction, and positive response on the Rose questionnaire for either claudication or possible angina pectoris.¹ The prevalence of subclinical disease by this definition was very high at the baseline examination; 39.0% of all men and 35.9% of women age 65 years had evidence of subclinical but no evidence of clinical cardiovascular disease at baseline examinations in 1989 to 1990. The prevalence of subclinical cardiovascular disease increased with age in both men and women. Independent risk factors for subclinical disease included age, higher systolic blood pressure and LDL-C, lower HDL-C, higher fasting glucose, current smoking, and an elevated white blood cell count for women and age, systolic blood pressure, glucose, current smoking, and a history of high blood pressure in men, based on logistic regression analysis.¹ There were not enough black participants in the original baseline sample in 1989 to 1990 for a comparison of risk factors for this composite index of subclinical disease between blacks and whites.

In this study we have determined (1) the prevalence of clinical, subclinical, and no disease among men and women, both black and white, in the Cardiovascular Health Study and (2) the association for both blacks and whites between clinical, subclinical, and no disease and cardiovascular risk factors.

	Methods

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A description of the CHS has been previously published.^{4 5} The original cohort was recruited from four communities in the United States from a defined sample of Medicare beneficiaries aged 65 years. There were 5201 participants in the original sample, including 2955 women and 2246 men. Only 153 black women and 91 black men in the original sample were recruited in 1989 to 1990, the baseline year of the CHS.

In 1993 to 1994, year 4 of the study, a new cohort of 248 black men and 424 women was added to the study. The recruitment of the new black participants was similar to that for the original cohort of white and black participants. They were recruited from lists of Medicare beneficiaries in three of the four CHS communities: Pittsburgh, Pa, Winston-Salem, NC, and Sacramento, Calif. Eligible participants were ambulatory, expected to reside in the area for the next 3 years, able to give informed consent, and did not require a proxy response at baseline. Clinical cardiovascular disease at baseline was not an exclusion criterion.⁶

The baseline evaluation included a home interview and physical examination in the clinic. The components of these evaluations have been published.⁴ Prevalent cardiovascular disease was determined at baseline in year 1 for the original cohort and in year 4 for the new cohort, by self-report. Clinical cardiovascular disease was defined as a confirmed history of heart disease, including MI, angina pectoris, or use of nitroglycerine; congestive heart failure; coronary bypass surgery; atrial fibrillation, as detected by ECG (or use of a cardiac pacemaker); history of stroke, transient ischemic attack, or carotid artery surgery¹ ; or history of intermittent claudication or peripheral vascular surgery (Table 1).¹

Subclinical cardiovascular disease was defined as in the previous study^{1 2} and in the introduction to this study (ankle/arm index 0.9, internal carotid wall thickness >80th percentile, common carotid wall thickness >80th percentile, carotid stenosis >25%, major electrocardiographic abnormalities, Rose questionnaire claudication positive, or Rose questionnaire angina positive).

The echocardiogram was not done in year 4, ie, baseline for the new black cohort, but was done later, in year 6. Echocardiographic abnormalities as a measure of subclinical disease have therefore been excluded from this study for both blacks and whites. At the baseline evaluation there were only 45 women (4.2%) and 66 men (7.6%) that had either an abnormal ejection fraction or wall motion abnormalities on the echocardiogram that were considered a measure of subclinical disease, excluding participants with clinical disease.¹ In the original classification, only 11 participants with subclinical disease had wall motion or ejection fraction abnormalities as their only criterion for classification of subclinical disease.

The differences in the time of the baseline examination between the "new" black cohort recruited in 1992 to 1993 and the original predominantly white cohort recruited in 1989 to 1990 could present a potential bias if methods of data collection changed during the 3 years between examinations. To reduce this potential bias, the measurements of carotid duplex scanning at year 1 were reread, using the same readers who had read the year 4 carotid studies. The ECGs were read in the same laboratory using similar criteria. The ankle/brachial blood pressure was measured in the same way at years 1 and 4, and quality control methods were monitored in the study to assure consistency over time in laboratory methods. We compared the risk factor levels for blacks in the 1989 to 1990 with the 1992 to 1993 cohort. There were no consistent differences in the risk factors.

There were 244 blacks in the original cohort (91 men and 153 women) and 672 in the new cohort (248 men and 424 women) in year 4. The mean values of risk factors in the original black cohort and the new black cohort were, respectively, age 72.6 and 73.1 years, diastolic blood pressure 75 and 75 mm HG (NS), systolic blood pressure 141 and 142 mm Hg (NS), BMI 28 and 29 kg/(m)² (NS), cholesterol 207 and 210 mg/dL (NS), and fasting glucose 120 and 119 mg/dL (NS). A history of current cigarette smoking and alcohol use was also similar between the original and new cohorts. A history of MI was reported by 19% of the original and 15% of the new cohort (NS), stroke 7.4% and 9.8%, diabetes 22% and 21% (NS), and history of hypertension 63% and 68% (NS). The only significant difference between the two cohorts was use of antihypertensive therapy, at 55% in the original and 63% in the new cohort, which could be a time-dependent change in the community. If the prevalence of antihypertensive drug use had been 63% at both time periods, the number of blacks on drug therapy would have been 578 rather than 559 of 971 participants (Table 2).

Statistical Methods
All analyses excluded those individuals not classified as either white or black. Potential categorical risk factors for subclinical disease that were examined included history of hypertension, history of diabetes, familial history of MI in a first-degree relative aged <65 years, current smoking, use of antihypertensive medications, and use of lipid-lowering medications. Continuous risk factors considered included age, systolic blood pressure, diastolic blood pressure, BMI, WHR, total cholesterol, LDL-C, HDL-C, triglycerides, fasting glucose, serum insulin, and white blood cell count.

All risk factors of interest were compared across races stratified by sex and disease status (where disease status is either clinical, subclinical, or no disease). For the categorical risk factors, age-adjusted percentages were calculated by using a logistic regression model with the risk factor as the dependent variable and age as the explanatory variable. A separate model was fit for each disease/sex/race combination, and these models were then used to predict the proportion of participants with the risk factor of interest within each stratum, adjusted for age. The age-adjusted significance levels were based on an age-adjusted logistic regression model for the risk factor of interest. For continuous risk factors, age-adjusted means were calculated for each disease/sex/race stratum. These means were recalculated, excluding those participants using antihypertensive medication. The significance levels were based on an analysis of variance model for the risk factor of interest, adjusted for age.

Logistic regression was used to model the risk of subclinical disease, excluding those individuals with clinical disease. The analysis was stratified by sex and race. Within each sex/race stratum, variables were entered into the model using a forward stepwise selection procedure beginning with all of the risk factors listed above. For comparison between races, an expanded model was fit using a common set of explanatory variables across races within a sex (the union of the variables selected in the forward stepwise procedures).

Logistic regression was used to obtain a model for each outcome, with age as the explanatory variable. A separate model was fit for each disease/sex/race combination, and this model was used to predict the percentages (evaluated at the mean age for the white population in the original cohort). The significance levels are based on the Wald statistic in a logistic regression. For any effect, the probability value is adjusted for age, as well as any other effects of the same or lower order. For example, the two-way interactions are adjusted for age, all main effects, and all other two-way interactions. Note that different models were used to arrive at the predicted values versus the probability values.

All statistical analyses were performed using the Statistical Package for the Social Sciences (SPSS for Windows), release 6.1. (Probability values are shown in the tables).

	Results

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There were 2791 white women (48%) and 2136 white men (36%) in the analysis.¹ There were 577 black women (10%) and 339 black men (6%). The black women included 192 aged 65 through 69, 180 aged 70 through 74, 123 aged 75 through 79, 57 aged 80 through 84, and 25 aged >80 years. The black men included 117 aged 65 through 69, 121 aged 70 through 74, 56 aged 75 through 79, 29 aged 80 through 84, and 16 aged 80 years.

Prevalence of Subclinical and Clinical Disease
The prevalence of clinical cardiovascular disease was 26.2% among white women, 35.4% among black women, 37.2% among white men, and 37.3% among black men (Tables 1 and 3). There was a higher prevalence of stroke, MI, angina pectoris, and congestive heart failure in black women than in white women (Table 1). There was a higher prevalence of stroke and a lower prevalence of bypass surgery and/or angioplasty in black men than in white men. It is important to note that any participant could have more than one clinical disease or procedure (Table 1).

The prevalence of subclinical disease at baseline among all CHS participants (Table 3) was similar in black and white men and women. The prevalence was higher in men than women. Blacks had significantly lower ankle/brachial blood pressure, greater common carotid artery wall thickness 80th percentile, and higher prevalence of major electrocardiographic abnormalities, while whites had a much higher prevalence of carotid artery stenosis (Table 4). The prevalence of subclinical and clinical disease increased with age in all four race/sex groups (Figs 1 and 2).

View larger version (62K): [in this window] [in a new window]   Figure 1. Top, Distribution of prevalent disease by age in white females; bottom, distribution of prevalent disease by age in black females. Solid portion of bars represents clinical disease; dark shaded portion, subclinical disease; and light shaded portion, no disease.

View larger version (63K): [in this window] [in a new window]   Figure 2. Top, Distribution of prevalent disease by age in white males; bottom, distribution of prevalent disease by age in black males. Solid portion of bars represents clinical disease; dark shaded portion, subclinical disease; and light shaded portion, no disease.

Risk Factors and Subclinical and Clinical Disease, Discrete Variables
The distribution of discrete and continuous risk factors in Tables 5 and 6 are shown by clinical, subclinical, and no-disease categories and by comparison by sex and race and possible interaction terms.

The distribution of categorical diseases, diabetes, and hypertension was as expected. The prevalence was highest in participants with clinical disease, next highest with subclinical disease, and lowest for those with no disease for all four race and sex groups. The prevalence of hypertension was higher in blacks than whites. Even in older individuals (except for black men), a history of MI in a first-degree relative <65 years of age was more prevalent in those with clinical disease (and next for subclinical disease) than in those with neither subclinical nor clinical disease.

The use of antihypertensive medications was lowest in participants with no disease and highest in those with clinical disease. The use of antihypertensive medication was higher among blacks than whites, especially for black women. The use of lipid-lowering drugs was much less than of antihypertensive drug therapy (Table 5) and was higher for clinical disease and subclinical disease than for those with no disease.

A history of current cigarette smoking provided a somewhat different pattern, in that the highest prevalence was found among individuals with subclinical disease and next for clinical disease, with the lowest prevalence in those with no disease. The percent of current smoking was higher among blacks with subclinical disease and was about twice as high as for the no-disease group among blacks.

Continuous Variables
The association of continuous risk factors (Table 6) with clinical disease was also similar among the four race and sex groups and was also consistent with risk factors for clinical disease among younger individuals. The levels of systolic blood pressure, LDL-C, triglycerides, fasting glucose, and insulin were higher for individuals with either subclinical or clinical disease than for those with no disease. There was a weak, but overall significant, association of BMI and WHR with subclinical and clinical disease compared with no disease. White men and black women with subclinical and clinical disease had higher BMIs than those with no subclinical disease. Similarly, for WHR, the differences among the three categories were relatively small.

HDL-C levels were, as expected, higher in women than in men and higher in blacks than in whites, lowest for individuals with clinical disease, and higher for individuals with no disease. Black women with no subclinical or clinical disease had HDL-C levels that were 19 mg/dL higher than levels in white men with clinical disease.

The diastolic blood pressure varied little among the three disease categories. In general, the levels were highest for participants with no subclinical or clinical disease and lower for those with clinical disease.

The white blood cell count, which may be a measure of inflammation related to atherosclerosis, was highest for individuals with clinical disease and lowest for those with neither subclinical nor clinical disease for all four race and sex groups. White blood cell counts were higher in whites than in blacks, consistent with previous studies.⁷

The high prevalence of antihypertensive drug use in this study and the possible effects of antihypertensive drugs such as diuretics and beta-blockers on other risk factors, especially blood pressure, lipids, and glucose, could effect the associations noted in Tables 5 and 6. The entire analysis of risk factors and disease was repeated, excluding those who were on antihypertensive therapy. The risk factor analysis for the relationships of subclinical, clinical, and no subclinical or clinical disease was similar to that for the entire sample, which included the participants on antihypertensive therapy.

The next assessment was limited to participants with either subclinical or no subclinical and clinical disease, using bivariate analyses similar to those in Tables 5 and 6. For white women, significant differences were found for all of the risk factors listed in Table 6 except BMI; for black women, systolic blood pressure, WHR, LDL-C, and HDL-C; for white men, age, systolic blood pressure, BMI, WHR, HDL-C, triglycerides, and fasting glucose; and for black men, age only (data not shown); P<.05 between subclinical and no subclinical disease. For categorical variables similar to Table 5, current cigarette smoking was significantly greater among those with subclinical disease for all four race and sex groups. A history of diabetes was more frequent among subclinical disease for all groups except black men, and hypertension history more frequent for all groups except black women. Family history of coronary heart disease was more frequent for white women with subclinical disease than for those with no subclinical disease (not shown).

Regression Analysis
The results of forward stepwise logistic regression analysis of the risk factors for the composite index of subclinical disease, excluding those individuals with clinical disease, are shown by race and sex in Table 7.

Current smoking and indicators of elevated blood pressure (either measured systolic blood pressure or history of hypertension) were significantly related to subclinical disease in all four race and sex groups in multivariate models (Table 7). LDL-C and fasting blood glucose (in whites) were significant independent predictors of subclinical disease in women, but not in men. White blood cell count and family history of MI were significant independent predictors of subclinical disease in white women. BMI was significantly different between subclinical and no subclinical disease for white men only in both univariate and multivariate models (Table 7). Although WHR was a significant independent predictor in bivariate analyses, the addition of blood pressure measures, LDL-C, and BMI to the multivariate model reduced WHR as a significant variable for white women, black women, and white men, respectively.

	Discussion

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There were three key observations based on the results in this study: (1) The prevalence of either subclinical or clinical disease was very high, (2) risk factors for subclinical and clinical disease were similar for blacks and whites, and (3) most risk factors for subclinical and clinical disease among older individuals were similar to those for clinical disease among younger individuals.

The prevalence of either clinical or subclinical vascular disease was very high in older men and women, both black and white. Only 25% of black women and 19% of black men had neither subclinical nor clinical cardiovascular disease at age 65 years, compared with 32% of white women and 21% of white men. Black women had significantly higher prevalence of clinical disease than white women. The prevalence of subclinical disease increased with age in all four race/sex groups. The distribution of the attributes of subclinical disease is different for blacks and whites. Blacks had a greater prevalence of common carotid artery wall thickness 80th percentile. White men had a significantly higher prevalence of internal carotid artery wall thickness 80th percentile than black men. Whites had a much greater prevalence of carotid artery stenosis >25% (Table 4). Similar observations have been reported previously by the CHS³ and the Atherosclerosis Risk in Communities study.⁸

The absence of good genetic markers, ie, host susceptibility, detailed lifetime measures of risk factors, and other unmeasured risk factors, limits our interpretation of any differences in prevalence of components of subclinical disease (ie, ankle/brachial blood pressure, common and intimal carotid artery wall thickness) between blacks and whites.

Second, the risk factors for prevalent subclinical vascular disease and clinical disease among blacks were similar to those for whites. The interaction term of disease, sex, and race was significant only for systolic blood pressure. There was also a significant disease/race interaction for LDL-C levels, showing a stronger association for blacks, especially black women.

The lack of an association of history of hypertension with subclinical disease among black women in multivariate analysis is likely due to the very high prevalence of hypertension, ie, 62% of those without subclinical disease versus 66% with subclinical disease among black women. As noted in Table 5, the prevalence of hypertension was about 11/2 to 2 times as high for black as for white women with no clinical or subclinical disease. As the prevalence of any of these risk factors (eg, hypertension) begins to approach 100% among participants without subclinical or clinical disease, the likelihood of finding any significant associations across prevalent disease categories becomes much smaller. For example, if all black women were hypertensive, there clearly could be no way of identifying any association of the risk factor (ie, hypertension) and prevalent subclinical or clinical versus no disease in this study. The prevalence of a history of diabetes was higher in blacks than whites and in women than men for all prevalent subclinical or clinical cardiovascular disease categories (see Table 5), consistent with the literature. The odds ratios for HDL-C, white blood cell count, and family history of MI were similar for black and white women.

The absence of significance for some of the variables in multiple logistic analysis for blacks compared with whites, in spite of similar point estimates, is due to much smaller sample sizes among blacks, especially black men. The significant variables in logistic regression are not necessarily the primary causal variables but provide a summary statistic of many interrelated variables in the causal pathway of atherosclerosis and clinical disease.

Third, the risk factor associations for older individuals for subclinical disease, especially systolic blood pressure, cigarette smoking, and measures of lipoproteins, were similar to risk factors for clinical cardiovascular disease among younger individuals.⁹ Diastolic blood pressure was lower for older individuals with clinical and subclinical disease.

The absence of a strong association of LDL-C and subclinical or clinical cardiovascular disease among older men^{10 11 12} could be related to selective survival to older ages (eg, men with higher LDL-C cholesterol levels have already died from cardiovascular disease), possible decrease in LDL-C with increasing age,¹³ and the possibility of greater misclassification of subclinical and no subclinical disease for older men compared with women because the overall prevalence of atherosclerosis is higher in older men than women. The lower prevalence of current cigarette smoking among participants with clinical disease (Table 5) may be due to (1) changes in cigarette smoking after the onset of clinical disease, (2) a higher mortality following the development of clinical disease among cigarette smokers than non–cigarette smokers, and (3) higher mortality among smokers with subclinical disease.

BMI was not significantly associated with subclinical compared with no disease for black men and both black and white women, even before the inclusion of other cardiovascular risk factors in the multivariate analysis. The absence of an association of BMI with subclinical vascular disease among women was not primarily due to the confounding of the BMI with the other cardiovascular risk factors. Weight gain and obesity may be more important risk factors for cardiovascular disease among premenopausal and younger perimenopausal and postmenopausal women than among older women.^{14 15 16 17}

BMI or waist measurements may be an inadequate measure of body fatness among older individuals.^{18 19} There is an increase in body fat percentage and a decrease in muscle and bone with increasing age, especially for women.^{20 21} The development of osteoporosis of the spine results in a decrease in the size of vertebral bodies and in compression fractures, with a concomitant loss of height, thereby modifying the estimated BMI (weight/[height]² ).

Individual composites of subclinical disease are probably measures of systemic atherosclerotic disease. There are high correlations among the specific components, ie, ankle/brachial blood pressure and carotid artery wall thickness or stenosis, and each component has previously been shown to be a predictor of risk of clinical disease.^{22 23 24 25}

There is not a perfect correlation of specific measures of atherosclerosis or subclinical disease at different anatomical sites. The measurement of subclinical disease at more than one anatomical site may provide a better distinction of subclinical from no subclinical disease than would measures limited to one anatomical site (ie, carotid or ankle/brachial blood pressure). It is important to recognize, however, that even this combination of measures of subclinical disease does not fully discriminate individuals with no disease from those with measures of subclinical atherosclerosis. There are errors associated with all of these measures. We did not have an independent noninvasive measure of the amount and characteristics of atherosclerosis in the coronary arteries.

We did not include echocardiographic measurements in this analysis. There is, however, a strong correlation in the CHS between electrocardiographic criteria for increased left ventricular mass and echocardiographic measurements.²⁶ Both measures (ie, electrocardiographic and echocardiographic left ventricular mass) were related to similar risk factors, including prevalent clinical coronary artery disease, blood pressure levels, and obesity at baseline. Both electrocardiographic measures of ischemia and left ventricular hypertrophy and echocardiographic measures of left ventricular hypertrophy have been related to carotid artery disease.²⁷ Left ventricular hypertrophy, based on both echocardiographic and electrocardiographic^{28 29 30 31} criteria, is much more prevalent in blacks than whites.

The relevance of this composite measure of subclinical disease for blacks compared with whites will ultimately depend on the ability of the index to predict clinical cardiovascular disease among blacks, as it has for whites.² It is possible that the composite measure of subclinical disease will not have a similar relationship to either relative or attributable risk of cardiovascular disease for blacks compared with whites, because of differences in the components of subclinical disease, in which case, the individual measures of some clinical disease (ie, carotid artery disease, carotid stenosis, increased wall thickness in the common carotid artery, decreased ankle/brachial blood pressure) may be better measures for blacks than whites. Whether the composite index is a better predictor of clinical disease in terms of both relative and attributable risks compared with any of the specific components of subclinical disease (ie, carotid artery wall thickness, ankle/brachial blood pressure) or to traditional risk factors such as cholesterol and blood pressure levels³² will be determined.³³

	Selected Abbreviations and Acronyms

 

BMI = body mass index HDL-C = HDL cholesterol LDL-C = LDL cholesterol MI = myocardial infarction WHR = waist-hip ratio

	Appendix 1

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Participating Institutions and Principal Staff
Forsyth County, NC; Bowman Gray School of Medicine of Wake Forest University: Gregory L. Burke, Sharon Jackson, Alan Elster, Walter H. Ettinger, Curt D. Furberg, Gerardo Heiss, Dalane Kitzman, Margie Lamb, David S. Lefkowitz, Mary F. Lyles, Cathy Nunn, Ward Riley, John Chen, and Beverly Tucker.

Forsyth County, NC; Bowman Gray School of Medicine, ECG Reading Center: Farida Rautaharju and Pentti Rautaharju.

Sacramento County, Calif; University of California, Davis: William Bommer, Charles Bernick, Andrew Duxbury, Mary Haan, Calvin Hirsch, Lawrence Laslett, Marshall Lee, John Robbins, and Richard White.

Washington County, Md; The Johns Hopkins University: M. Jan Busby-Whitehead, Joyce Chabot, George W. Comstock, Adrian Dobs, Linda P. Fried, Joel G. Hill, Steven J. Kittner, Shiriki Kumanyika, David Levine, Joao A. Lima, Neil R Powe, Thomas R Price, Jeff Williamson, Moyses Szklo, and Melvyn Tockman.

Washington County, Md; The Johns Hopkins University, MRI Reading Center: R Nick Bryan, Norman Beauchamp, Carolyn C. Meltzer, Naiyer Iman, Douglas Fellows, Melanie Hawkins, Patrice Holtz, Michael Kraut, Grace Lee, Larry Schertz, Cynthia Quinn, Earl P. Steinberg, Scott Wells, Linda Wilkins, and Nancy C. Yue.

Allegheny County, Pa; University of Pittsburgh: Diane G. Ives, Charles A. Jungreis, Laurie Knepper, Lewis H. Kuller, Elaine Meilahn, Peg Meyer, Roberta Moyer, Anne Newman, Richard Schulz, Vivienne E. Smith, and Sidney K Wolfson.

University of California, Irvine; Echocardiography Reading Center (baseline): Hoda Anton-Culver, Julius M. Gardin, Margaret Knoll, Tom Kurosaki, and Nathan Wong.

Georgetown Medical Center; Echocardiography Reading Center (follow-up): John Gottdiener, Eva Hausner, Stephen Kraus, Judy Gay, Sue Livengood, Mary Ann Yohe, and Retha Webb.

Geisinger Medical Center; Ultrasound Reading Center: Daniel H. O'Leary, Joseph F. Polak, and Laurie Funk.

University of Vermont; Central Blood Analysis Laboratory: Edwin Bovill, Elaine Cornell, Mary Cushman, and Russell P. Tracy.

University of Arizona, Tucson; Respiratory Sciences: Paul Enright.

University of Washington, Seattle; Coordinating Center: Alice Arnold, Annette L. Fitzpatrick, Bonnie K Lind, Richard A. Kronmal, Bruce M. Psaty, David S. Siscovick, Lynn Shemanski, Will Longstreth, Patricia W. Wahl, David Yanez, Paula Diehr, Maryann McBurnie, Chuck Spieker, Scott Emerson, Cathy Tangen, and Priscilla Velentgas.

NHLBI Project Office: Diane E. Bild, Robin Boineau, Teri A. Manolio, Peter J. Savage, and Patricia Smith.

	Acknowledgments

 
This study was supported by contracts NO1-HC-85079, NO1-HC-85080, NO1-HC-85081, NO1-HC-85082, NO1-HC-85083, NO1-HC-85084, NO1-HC-85085, NO1-HC-85086, and NO1 to 9 from the National Heart, Lung, and Blood Institute.

Received July 8, 1997; accepted October 25, 1997.

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