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Serum Adiponectin and Coronary Heart Disease Risk in Older Black and White Americans

University of California (A.M.K., C.W.F., E.V.), San Francisco, San Francisco, California 94115; Department of Nutrition (P.J.H.), University of California, Davis, Davis, California 95616; Department of Aging and Geriatric Research (M.C.), University of Florida, Gainesville, Florida 32611; Wake Forest University Medical Center (B.N.), Winston-Salem, North Carolina 27157; Laboratory of Epidemiology (T.H.), Demography and Biometry, Intramural Research Program, National Institutes of Health, Bethesda, Maryland 20892; University of Pittsburgh (A.B.N.), Pittsburgh, Pennsylvania 15260; University of Tennessee (S.S.), Knoxville, Tennessee 37996; and California Pacific Medical Center (S.R.C.), San Francisco, California 94118

Address all correspondence and requests for reprints to: Alka M. Kanaya, M.D., 1635 Divisadero Street, Suite 600, San Francisco, California 94115. E-mail: Alka.Kanaya{at}ucsf.edu.

Context: Adiponectin may influence the risk of coronary heart disease (CHD) independently of traditional cardiovascular risk factors.

Objective: Because body composition and adiponectin levels vary by race, we examined the relationship of adiponectin with prevalent and incident CHD in a cohort of older Black and White adults.

Design and Setting: We conducted a cross-sectional and prospective cohort study at two U.S. clinical centers.

Participants: Participants included 3075 well-functioning adults between ages 70 and 79 yr enrolled in the Health, Aging, and Body Composition study.

Main Outcome Measures: Prevalent CHD was defined as history of myocardial infarction, coronary artery bypass graft, percutaneous coronary transluminal angioplasty, angina, or major electrocardiogram abnormalities. After excluding those with prevalent CHD, incident CHD was defined as hospitalized myocardial infarction or CHD death.

Results: At baseline, 602 participants (19.6%) had CHD. During 6 yr of follow-up, 262 (10.6%) incident CHD events occurred. Whites had higher median adiponectin than Blacks (12 vs. 8 µg/ml, P < 0.001). Race modified the effect of adiponectin (P for interaction was 0.002 for prevalent CHD, and P = 0.02 for incident CHD). Among Whites, an inverse association of adiponectin with CHD was explained by high-density lipoprotein and glucose. Among Blacks, a doubling of adiponectin was associated with a 40% higher risk of both prevalent CHD (odds ratio, 1.41; 95% confidence interval, 1.11–1.78) and incident CHD (hazards ratio, 1.37; 95% confidence interval, 1.01–1.87) after adjusting for explanatory variables.

Conclusion: High circulating concentrations of adiponectin were associated with higher risk of CHD in older Blacks, even accounting for traditional CHD risk factors.

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