Objective To study the protective effect of fluvastatin on cardiac remodeling and cardiac function, and to investigate its effect on Von Willebrand factor (VWF). Methods The rat model of cardiac heart failure (CHF) was in-duced by isoproterenol injection (170 mg/kg) via subcutaneous. Eighteen model rats were randomly divided into fluvastatin (20 mg ·kg-1·d-1) group, placebo group and control group. Rats were treated with normal saline in placebo group and control group. After 6-week treatment, the structure and function of hearts were measured by echocardiography in three groups. The ventricular weight index, the serum levels of VWF and B-type natriuretic peptide (BNP) were measured by ELISA assay. The levels of VWF mRNA in cardiac muscle were measured by RT-PCR. Results Compared with control group, the val-ues of left ventricular end-diastolic diameter (LVEDD) and left ventricular end systolic diameter (LVESD) were significantly increased in placebo group and fluvastatin group, while values of left ventricular ejection fraction (LVEF) and left ventricular ejection fraction shortening (LVFS) were significantly decreased (P＜0.05). The values of left ventricular wet weight/body weight (LVRW) and right ventricular wet weight/body weight (RVRW) were increased in placebo group and fluvastatin group. The expression of VWF mRNA in cardiac tissues was enhanced significantly (P＜0.01). Compared with placebo group, the values of LVEDD, LVRW and RVRW were significantly decreased in fluvastatin group. The expression of VWF mRNA in cardiac tissues was significantly decreased (P＜0.01), and the values of LVEF and LVFS were significant increased in fluvas-tatin group (P＜0.05). The level of VWF was positively corrected with BNP(r=0.996). Conclusion Fluvastatin could im-prove the cardiac function and cardiac remodeling, which may be by reducing the level of VWF and improving endothelial function.