Apolipoprotein B but not LDL cholesterol is associated with coronary artery calcification in type 2 diabetic whites

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Abstract

OBJECTIVE - Evidence favors apolipoprotein B (apoB) over LDL cholesterol as a predictor of cardiovascular events, but data are lacking on coronary artery calcification (CAC), especially in type 2 diabetes, where LDL cholesterol may underestimate atherosclerotic burden. We investigated the hypothesis that apoB is a superior marker of CAC relative to LDL cholesterol. RESEARCH DESIGN AND METHODS - We performed cross-sectional analyses of white subjects in two community-based studies: the Penn Diabetes Heart Study (N = 611 type 2 diabetic subjects, 71.4% men) and the Study of Inherited Risk of Coronary Atherosclerosis (N = 803 nondiabetic subjects, 52.8% men) using multivariate analysis of apoB and LDL cholesterol stratified by diabetes status. RESULTS - In type 2 diabetes, apoB was associated with CAC after adjusting for age, sex, and medications [Tobit regression ratio of increased CAC for 1-SD increase in apoB; 1.36 (95% CI 1.06-1.75), P = 0.016] whereas LDL cholesterol was not [1.09 (0.85-1.41)]. In nondiabetic subjects, both were associated with CAC [apoB 1.65 (1.38-1.96), P < 0.001; LDL cholesterol 1.56 (1.30-1.86), P < 0.001]. In combined analysis of diabetic and nondiabetic subjects, apoB provided value in predicting CAC scores beyond LDL cholesterol, total cholesterol, the total cholesterol/HDL cholesterol and triglyceride/HDL cholesterol ratios, and marginally beyond non-HDL cholesterol. CONCLUSIONS - Plasma apoB, but not LDL cholesterol, levels were associated with CAC scores in type 2 diabetic whites. ApoB levels may be particularly useful in assessing atherosclerotic burden and cardiovascular risk in type 2 diabetes. © 2009 by the American Diabetes Association.

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Martin, S. S., Qasim, A. N., Mehta, N. N., Wolfe, M., Terembula, K., Schwartz, S., … Reilly, M. P. (2009). Apolipoprotein B but not LDL cholesterol is associated with coronary artery calcification in type 2 diabetic whites. Diabetes, 58(8), 1887–1892. https://doi.org/10.2337/db08-1794

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