Endothelial lipase genetic polymorphisms and the lipid-lowering response in patients with coronary artery disease on rosuvastatin.
BACKGROUND
Endothelial lipase (EL) plays an important role in the regulation of lipid metabolism by reducing the high density lipoprotein cholesterol (HDL-C) levels and inducing the macrophages to take up native low density lipoprotein cholesterol (LDL-C). Our purpose was to investigate the impact of EL genetic polymorphisms on the lipid-lowering effects of rosuvastatin in Chinese coronary artery disease (CAD) patients.


METHODS
One hundred twenty-one unrelated CAD patients, who underwent the treatment with rosuvastatin (10mg/day) for four to eight weeks, were enrolled in this study. Before and after treatment, serum lipids levels were measured. Genotypes of EL 2037T/C and 2237 G/A polymorphisms were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method.


RESULTS
Patients with EL 2037C allele (CC + CT) had significantly lower LDL-C levels than those with TT genotype (CC + CT: 2.60 ± 0.74 mmol/l; TT: 2.90 ± 0.87 mmol/l; P = 0.047), before rosuvastatin treatment. No significant differences between baseline lipid levels and the EL 2237G/A genotypes were observed. After treatment with rosuvastatin, total cholesterol (TC), high triglyceride (TG) and LDL-C levels decreased from baseline, on average, by 23.09 % (4.59 ± 0.96 mmol/l to 3.47 ± 0.83 mmol/l), 6.36 % (2.01 ± 1.18 mmol/l to 1.68 ± 1.16 mmol/l), 32.48 % (2.77 ± 0.83 mmol/l to 1.79 ± 0.62 mmol/l), respectively (all P < 0.05) in all patients. While changes in HDL-C levels did not reach statistical significance. No significant effects of EL 2037T/C or 2237G/A polymorphism were observed on lipid-lowering effects of rosuvastatin.


CONCLUSIONS
EL 2037T/C and 2237 G/A polymorphisms might not affect the lipid-owing effects of rosuvastatin in Chinese CAD patients.
Department of Cardiology, Wujin Hospital Affiliated to Jiangsu University, Changzhou, Jiangsu Province, China. cgj982@126.com.
Gaojun
G
Cai
Department of Pathology and Molecular Medicine, McMaster University, Ontario, Canada.
Bifeng
B
Zhang
Department of Cardiology, Wujin Hospital Affiliated to Jiangsu University, Changzhou, Jiangsu Province, China.
Ganwei
G
Shi
Department of Cardiology, Wujin Hospital Affiliated to Jiangsu University, Changzhou, Jiangsu Province, China.
Weijin
W
Weng
Department of Cardiology, Wujin Hospital Affiliated to Jiangsu University, Changzhou, Jiangsu Province, China.
Liping
L
Yang
Department of Cardiology, Wujin Hospital Affiliated to Jiangsu University, Changzhou, Jiangsu Province, China.
Sheliang
S
Xue
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D044466:Asian People; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood / Q000188:drug therapy* / Q000235:genetics* / Q000473:pathology; D005260:Female; D005838:Genotype; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage; D008049:Lipase / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D000068718:Rosuvastatin Calcium / Q000008:administration & dosage*; D014280:Triglycerides / Q000097:blood
D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D014280:Triglycerides; D000068718:Rosuvastatin Calcium; C410382:LIPG protein, human; D008049:Lipase
Coronary artery disease; Endothelial lipase; Rosuvastatin; Single nucleotide polymorphism