Abstract: AIM: To investigate the effects of simvastatin on membrane sodium ion channel current (INa) in left ventricular myocytes from rabbits suffering from acute myocardial infarction (AMI) in order to explore the cellular (ionic) basis of statin treatment for antiarrhythmia. METHODS: Rabbits were infarcted by ligation of the left anterior descending coronary artery after the administration of oral simvastatin 5 mg/(kg·d) (statin group) or placebo (AMI group) for 3 days. After 24 h, single ventricular myocytes were isolated enzymatically from the epicardial zone of the infarcted region. Whole cell patch clamp technique was used to record INa. RESULTS: No significant difference in serum cholesterol concentration was observed among the three groups. Peak INa current density (at 30 mV) in CON, AMI group and statin group was, respectively, (42.78±5.48)(n=16), (23.26±5.18)(n=12), and (39.23±5.45) pA/pF (n=13) (AMI group vs. CON and statin group, P<0.01). CONCLUSION: Our findings indicate that AMI induces significant reduction in Ina, and INa downregulation may underlie the altered electrical activity of the surviving ventricular myocytes. Pretreatment with simvastatin can attenuate this change without lowering serum cholesterol level, suggesting that simvastatin may reverse this electrical remodeling, which may be part of the ionic mechanism in statin treatment for antiarrhythmia.