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Circulation. 2002;106:304-308
Published online before print June 24, 2002, doi: 10.1161/01.CIR.0000022664.21832.5D
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(Circulation. 2002;106:304.)
© 2002 American Heart Association, Inc.


Clinical Investigation and Reports

Heritability of Coronary Artery Calcium Quantity Measured by Electron Beam Computed Tomography in Asymptomatic Adults

Patricia A. Peyser, PhD; Lawrence F. Bielak, DDS, MPH; Julia S. Chu, BS; Stephen T. Turner, MD; Darrell L. Ellsworth, PhD; Eric Boerwinkle, PhD; Patrick F. Sheedy, II, MD

From the Department of Epidemiology, University of Michigan, Ann Arbor, Mich (P.A.P., L.F.B., J.S.C.); Division of Hypertension, Department of Internal Medicine (S.T.T.), and Department of Diagnostic Radiology (P.F.S.), Mayo Clinic and Foundation, Rochester, Minn; Gene and Drug Discovery Center, Windber Research Institute, Windber, Pa (D.L.E.); and Human Genetics Center and Institute of Molecular Medicine, University of Texas, Houston Health Science Center, Houston (E.B.).

Correspondence to Patricia A. Peyser, University of Michigan, Department of Epidemiology, 109 Observatory, Ann Arbor, MI 48109. E-mail ppeyser{at}umich.edu

Background Electron beam computed tomography is an accurate, noninvasive method to detect and quantify coronary artery calcification (CAC), a marker of subclinical and clinical coronary artery atherosclerosis. CAC quantity predicts future coronary artery disease end points in asymptomatic adults, but measured risk factors explain less than half the variability in CAC quantity. Although several candidate genes for CAC have been identified, the relative importance of genetic influences on CAC quantity has not been assessed in asymptomatic adults in a community.

Methods and Results We quantified the relative contributions of measured risk factors and genetic influences on CAC quantity measured by electron beam computed tomography in 698 asymptomatic white adults from 302 families. Before adjusting for any risk factors, 43.5% of the variation in CAC quantity was attributable to genetic factors (P=0.0007). Independent predictors of CAC quantity were identified with stepwise linear regression. After adjusting for these risk factors, including age, sex, fasting glucose level, systolic blood pressure, pack-years of smoking, and LDL cholesterol, 41.8% of the residual variation in CAC quantity was attributable to genetic factors (P=0.0003).

Conclusions These results demonstrate the importance of genetic factors in subclinical coronary atherosclerosis variation as measured by CAC quantity. The presence of genetic effects suggests that unknown genes that influence CAC quantity are yet to be identified.


Key Words: genetics • calcium • atherosclerosis • imaging • epidemiology




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