Department of Cardiology, Xiangya Hospital, Central South University, Changsha 41008, China

Objective To determine the effect of different doses of atorvastatin and withdrawal of atorvastatin on vascular endothelial function and inflammation factors in the patients with hypercholesterolemia and obesity and to explore the possible mechanism. MethodsFiftyfive patients with hypercholesterolemia and obesity and 58 healthy controls were recruited to observe brachial artery endothelialdependent vasodilation, serum concentration of NO, soluble Eselectin (SE), and high sensitive Creactive protein(hsCRP). The 55 patients were randomly, doubleblindly divided into 2 groups：Group A (n=27), received atorvastatin 10 mg per day, and Group B (n=28), received atorvatatin 10 mg per day for 8 weeks at the base of diet control. Endothelial dependent flowmediated vasodilation (FMD), NO, SE, hsCRP，and blood lipid were evaluated before the treatment, after 8 weeks of atorvastatin treatment, and 1 week of therapy termination.ResultsAtorvastatin treatment for 8 weeks reduced total cholesterol (TC), low density lipoprotein cholesterol (LDLC), SE, and hsCRP, and improved NO and FMD obviously in patients (P<0.01). Comparing with the Group A, the abovementioned changes in the Group B were more profound. Withdrawal of atorvastatin for a week, TC and LDLC levels were significantly increased compared with those after 8 weeks treatment (P<0.05), but still lower than those before treatment (P<0.05 or P<0.01) in the two groups. The levels of NO and FMD decreased whereas the SE and hsCRP levels were elevated than those after 8 weeks treatment (P<0.01), and there was no obvious changes compared with those before the treatment (P>0.05). ConclusionAtorvastatin 20 mg per day reduces TC, LDLC, protects endothelial function, and inhibits inflammation to a greater extent than 10 mg per day. Sudden withdrawal of atorvastatin therapy, the beneficial effects on endothelial function and inflammation inhibition were attenuated. Effects of therapy termination on vascular endothelial function and inflammation factors are independent of cheolesterol adjustment.