title: Relationship between the cholesterol ester transfer protein TaqIB polymorphism and the lipid-lowering effect of atorvastatin in patients with coronary atherosclerotic heart disease.
abstract: This study aimed to investigate the relationship between the cholesterol ester transfer protein (CETP) gene TaqIB polymorphism and the lipid-lowering effect of atorvastatin in patients with coronary atherosclerotic heart disease. Two hundred eighty-eight patients were divided into a control group, an acute coronary syndrome (ACS) group, and a stable coronary heart disease (CHD) group. Blood biochemical indices were determined using the enzyme method, and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis was performed to study the TaqIB polymorphism of the CETP gene. The ACS and stable CHD groups were treated with atorvastatin, and blood lipid levels were reexamined after three months. Plasma levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and lipoprotein(a) were all significantly higher in the ACS and stable CHD groups compared to the control group (P < 0.05 or P < 0.01). After three months of treatment with atorvastatin, plasma levels of TC, LDL-C, triglycerides (TG) (only in patients with genotype B2B2), and lipoprotein(a) (only in patients with genotype B1B2) were all significantly decreased (P < 0.05 or P < 0.01). After treatment, the plasma level of TG was lower in patients with genotype B2B2 compared to patients with genotypes B1B1 or B1B2 (B1 carriers) (P < 0.01). Therefore, the CETP TaqIB polymorphism is associated with the lipid-lowering effect of atorvastatin in patients with CHD.
authors.affiliation: Department of Cardiology, Tongji Hospital, Tongji University, Shanghai, China jianlicncn@163.com.
authors.forename: J
authors.initials: J
authors.lastname: Li
authors.affiliation: Department of Cardiology, Tongji Hospital, Tongji University, Shanghai, China.
authors.forename: L
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Department of Cardiology, Tongji Hospital, Tongji University, Shanghai, China.
authors.forename: N Z
authors.initials: NZ
authors.lastname: Xie
authors.affiliation: Department of Cardiology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
authors.forename: B
authors.initials: B
authors.lastname: Deng
authors.affiliation: Department of Biochemistry, Medical School of Tongji University, Shanghai, China.
authors.forename: L X
authors.initials: LX
authors.lastname: Lv
authors.affiliation: Department of Biochemistry, Medical School of Tongji University, Shanghai, China.
authors.forename: L Q
authors.initials: LQ
authors.lastname: Zheng
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D000069059:Atorvastatin; D053480:Cholesterol Ester Transfer Proteins / Q000235:genetics*; D003324:Coronary Artery Disease / Q000097:blood / Q000188:drug therapy* / Q000235:genetics*; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D012150:Polymorphism, Restriction Fragment Length; D011758:Pyrroles / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D053480:Cholesterol Ester Transfer Proteins; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D011758:Pyrroles; D000069059:Atorvastatin