title: Statin treatment improves plasma lipid levels but not HDL subclass distribution in patients undergoing percutaneous coronary intervention.
abstract: Despite the established efficacy of statin therapy, the risk of cardiovascular events remains high in many patients. We examined high-density lipoprotein (HDL) subclass distribution profiles among statin-treated coronary heart disease (CHD) patients undergoing percutaneous coronary intervention (PCI). Plasma HDL subclasses were measured in 85 patients with established CHD and quantified by two-dimensional gel electrophoresis and immunoblotting. In CHD patients with statin treatment, the mean value of total cholesterol (TC) reached the desirable level and the triacylglycerol level (TAG) was borderline high. Moreover, low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), apolipoproteinA-I, and apolipoproteinB-100 levels in these patients resembled those in normolipidemic healthy subjects. The HDL subclass did not show a normal distribution and was characterized by the lower large-sized HDL(2b) contents and higher contents of small-sized preβ₁-HDL in CHD patients, compared to those in normolipidemic control subjects. Multiple stepwise regression analysis revealed that the severity of coronary stenosis, determined by the Gensini Score, was significantly and independently predicted by HDL(2b) and HDL(3b). Statin therapy was effective in modifying plasma lipids levels, but not adequate as a monotherapy to normalize the HDL subclass distribution phenotype of patients with CHD undergoing PCI. The HDL subclass distribution may aid in risk stratification, especially in patients with CHD and therapeutic LDL-C and HDL-C levels.
authors.affiliation: Laboratory of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu 610041, Sichuan, People's Republic of China.
authors.forename: Li
authors.initials: L
authors.lastname: Tian
authors.forename: Yucheng
authors.initials: Y
authors.lastname: Chen
authors.forename: Chuanwei
authors.initials: C
authors.lastname: Li
authors.forename: Zhi
authors.initials: Z
authors.lastname: Zeng
authors.forename: Yanhua
authors.initials: Y
authors.lastname: Xu
authors.forename: Shiyin
authors.initials: S
authors.lastname: Long
authors.forename: Mingde
authors.initials: M
authors.lastname: Fu
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D016632:Apolipoprotein A-I / Q000097:blood; D016022:Case-Control Studies; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003327:Coronary Disease / Q000097:blood* / Q000188:drug therapy* / Q000473:pathology / Q000601:surgery; D003331:Coronary Vessels / Q000473:pathology; D015180:Electrophoresis, Gel, Two-Dimensional; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008055:Lipids / Q000097:blood*; D008075:Lipoproteins, HDL / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D062645:Percutaneous Coronary Intervention
chemical_list: D016632:Apolipoprotein A-I; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL