Objectives To investigate the cardioprotection and its mechanism of the different doses of simvastatin on cardiomyocyte apoptosis induced by myocardium of rabbits with congestive heart failure.

Methods Sixty male wistar rabbitts were randomly divided into five groups: normal control group (n = 12), high dose group (n = 12, HF + S, received simvastatin 3mg · kg -1·d -1 by gastric irrigation diet for 12 weeks), middle dose group (n = 12, HF + S, received simvastatin 1.5mg · kg -1·d -1 by gastric irrigation diet for 12 weeks),little dose group (n = 12, HF + S, received simvastatin 0.3mg · kg -1·d -1 by gastric irrigation diet for 12 weeks)and heart failure group (n = 12), Left ventricular remodelling and function were evaluated by echocardiography and hemodynamic measurements 10 weeks after operation, The apoptotic eardiomyoeytes of myocardial tissue were tested by TUNEL,sFas were measured with ELISA.

Results Left ventricular ejection fraction (LVEF)and Left ventricular end-systolic diameter (LVESD)improved significantly (P < 0.05) in the MD-SIM Compared with those LD-SIM, HD-SIM and CHF, HE shows that there are severe fibrosis and inflammatory cell infiltration in CHF;however there were less ibrosis and inflammatory cell infiltration in the MD-SIM Compared with those LD-SIM and HD-SIM, Compared with normal control group the numbers of apoptotic cardiomyocytes as well as the expression of sFas in myocardial tissue were significantly increased in HF group (P < 0.01 or 0.05), LD-SIM and MD-SIM and HD-SIM have the expression of sFas and numbers of apoptotic cardiomyocytes,but only the MD-SIM in myocardia1 tissue were remarkably reduced in simvastatin groups.

Conclusions Apoptosis is associated with the development of HF,sFas which may play a role in acceleration of apoptosis, The simvastatin can inhibit the myocardocyet apoptosis, 1.5mg · kg -1·d -1 of simvastatin is the best option.