Statin has pleiotropic effects. Statin can prevents cardiomyocyte hypertrophy and has antioxidant effects. Recently there are several reports about relation of atrial fibrillation (AF) with oxidative stress and inflammatory process. Patients with elevated CRP level were related with increased incidence of AF. Recent research showed prednisone prevented atrial tachycardia related atrial remodeling. We investigate role of eNOS and fibrosis in AF prevention by simvastatin in rat heart failure model induced by myocardial infarction (MI). Methods: 8 week old male SD rats were used. MI was induced by a ligation of left anterior descending artery. 2 days after MI, rats were given simvastatin (2 mg/kg/day) for 10 weeks. Sham operated rats were served as controls. 10 weeks after MI, echocardiography were done and AF induction studies were done under open chest state. Bipolar lead was hocked in right atrial appendage then AF was induced by atrial burst pacing. Masson trichorome staining for fibrosis analysis and eNOS western blotting study were done. Results: Ejection fraction were decreased in MI. Fibrosis analysis showed increased left atrial fibrosis in MI and prevention of fibrosis formation in simvastatin group. Duration of AF were increased in MI and decreased in simvastatin group, Atrial eNOS levels were decreased in MI and improved in simvastatin group. Conclusion: Simvastatin suppress HF induced AF promotion. Simvastatin suppressed fibrosis formation and AF promotion by prevention of eNOS down-regulation in rat left atrial tissue. To my knowledge, it is first report about statin induced promotion of eNOS can suppress left atrial remodeling in HF tissue