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* Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Center on Aging at Tufts University and Division of Endocrinology, Metabolism, Diabetes, and Molecular Medicine, New England Medical Center, Boston, MA
Physiology Department, Louisiana State University Medical Center, New Orleans, LA
Cardiology Division, Newton-Wellesley Hospital, Newton, MA
1 To whom correspondence should be addressed. e-mail: basztalos{at}hnrc.tufts.edu
We investigated the effects of atorvastatin on the lipid and the apoA-I-containing HDL subpopulation profiles in 86 patients with established coronary heart disease (CHD). The entire drug treatment period lasted 12 weeks (4-week periods of 20 then 40, then 80 mg/day). Each dose of atorvastatin treatment resulted in significant reductions in plasma total-C, LDL-C, and triglyceride (TG), and non-significant increases in HDL-C levels compared with placebo treatment. ApoA-I levels did not change significantly during any of the treatment periods. Despite the modest increase of HDL-C (6%, 7%, 5%) and no change in apoA-I levels, the distribution of the apoA-I-containing HDL subpopulations changed significantly during each treatment period. There were significant increases in the concentrations of the large LpA-I 
-1 (24%, 39%, 26%) and pre-1 (51%, 61%, 63%) subpopulations at the expense of the small lipoprotein LpA-I:A-II -3 subpopulations which decreased on all doses, and the decreases were significant on the 40 and 80 mg/day doses (6%, 5%).
Atorvastatin influences the lipid-related risk for CHD in two ways: first, it significantly decreases LDL-C and TG levels while increasing HDL-C, and second, it significantly shifts the HDL subpopulation profile of CHD patients toward that observed in subjects without CHD.
Abbreviations: apo, apolipoprotein; CHD, coronary heart disease; TG, triglyceride
Supplementary key words CHD • lipids • lipoproteins • apolipoproteins • statin
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