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Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:2670-2676

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:2670.)
© 2000 American Heart Association, Inc.


Atherosclerosis and Lipoproteins

Distribution of ApoA-I–Containing HDL Subpopulations in Patients With Coronary Heart Disease

Bela F. Asztalos; Paul S. Roheim; Richard L. Milani; Michael Lefevre; Judith R. McNamara; Katalin V. Horvath; Ernst J. Schaefer

From the Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Center on Aging at Tufts University, and the Division of Endocrinology, Metabolism, Diabetes, and Molecular Medicine (B.F.A., J.R.M., K.V.H., E.J.S.), New England Medical Center, Boston, Mass; the Physiology Department (P.S.R.), Louisiana State University Medical Center, New Orleans; the Division of Cardiology (R.L.M.), Alton Ochsner Hospital, New Orleans, La; and Pennington Biomedical Research Center (M.L.), Baton Rouge, La.

Correspondence to Bela F. Asztalos, PhD, JM-USDA/HNRC at Tufts University, Lipid Metabolism Laboratory, 711 Washington St, Boston, MA 02111. E-mail belaasztalos{at}yahoo.com

Abstract—High density lipoproteins (HDLs) and their subspecies play a role in the development of coronary heart disease (CHD). HDL subpopulations were measured by 2-dimensional nondenaturing gel electrophoresis in 79 male control subjects and 76 male CHD patients to test the hypothesis that greater differences in apolipoprotein (apo)A-I–containing HDL subpopulations would exist between these 2 groups than for traditional lipid levels. In CHD subjects, HDL cholesterol (HDL-C) was lower (-14%, P<0.001), whereas total cholesterol and the low density lipoprotein cholesterol/HDL-C ratio were higher (9% [P<0.05] and 21% [P<0.01], respectively) compared with control levels. No significant differences were found for low density lipoprotein cholesterol, triglyceride, and apoA-I levels. In CHD subjects, there were significantly (P<0.001) lower concentrations of the large lipoprotein (Lp)A-I {alpha}1 (-35%), pre-{alpha}1 (-50%), pre-{alpha}2 (-33%), and pre-{alpha}3 (-31%) subpopulations, whereas the concentrations of the small LpA-I/A-II {alpha}3 particles were significantly (P<0.001) higher (20%). Because {alpha}1 was decreased more than HDL-C and plasma apoA-I concentrations in CHD subjects, the ratios of HDL-C to {alpha}1 and of apoA-I to {alpha}1 were significantly (P<0.001) higher by 36% and 57%, respectively, compared with control values. Subjects with low HDL-C levels (<=35 mg/dL) have different distributions of apoA-I–containing HDL subpopulations than do subjects with normal HDL-C levels (>35 mg/dL). Therefore, we stratified participants according to HDL-C concentrations into low and normal groups. The differences in lipid levels between controls and HDL-C–matched cases substantially decreased; however, the significant differences in HDL subspecies remained. Our research findings support the concept that compared with control subjects, CHD patients not only have HDL deficiency but also have a major rearrangement in the HDL subpopulations with significantly lower {alpha}1 and pre-{alpha}1–3 (LpA-I) and significantly higher {alpha}3 (LpA-I/A-II) particles.


Key Words: HDL subpopulations • coronary heart disease • lipids • lipoproteins • apolipoproteins




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