EFFECTS OF PRAVASTATIN ON PLASMA-LIPIDS, APOLIPOPROTEINS, LP(A), REMNANT-LIKE PARTICLE, CHOLESTERYL ESTER TRANSFER PROTEIN, AND LECITHIN - CHOLESTEROL ACYLTRANSFERASE - A 12-MONTH STUDY

Sixty-nine hypercholesterolemic patients at three hospitals received p ravastatin therapy (10-20 mg/day); 46 completed 12 months of therapy. Mean plasma total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) decreased by 16.5%, 14.8%, and 23.9% from 279, 149, and 200 mg/dl to 231, 127, and 151 mg/dl, respectively, by the 3rd month after initiation of therapy. In contrast, high-densi ty lipoprotein cholesterol (HDL-C) increased significantly by 14.6% fr om 46.6 to 53.4 mg/dl by the 3rd month. After the 3rd month, levels of all measures remained unchanged for the remaining 9 months of the stu dy. Lp(a) levels before and after 12 months of drug administration wer e not significantly different, nor were levels of apo A-II, apo C-III, and apo E. However, levels of apo B and apo C-II were reduced signifi cantly while the level of apo A-I was increased significantly. Before pravastatin administration, cholesteryl ester transfer protein (CETP) activity was significantly and inversely correlated with HDL-C and apo A-I (r=-0.60 and r=-0.55, respectively, P<0.01) while lecithin: chole sterol acyltransferase (LCAT) activity was significantly correlated wi th TC and apo B (r=-0.43, P<0.05 and r=-0.44, P<0.001, respectively). No significant changes in CETP activity or LCAT activity were observed during 12 months of drug administration. Remnant lipoproteins, design ated as remnant-like particles (RLPs), were isolated from fasting plas ma using immunoaffinity gel fixed with an anti-apo B-100 monoclonal an tibody and an anti-apo A-I monoclonal antibody. RLP-C was highly corre lated with TG, apo B, apo C-II, apo C-III, and apo E levels before the drug administration. Pravastatin administration for 12 months decreas ed both RLP-cholesterol and RLP-triglyceride significantly. We conclud e that pravastatin administration to hypercholesterolemic patients red uced not only LDL but also remnant lipoproteins while it did not affec t Lp(a) levels. In addition, although the pravastatin administration i ncreased HDL-C, it did not significantly change CETP or LCAT activity.