With the increasing incidence of heart failure (HF) and the aging population, the incidence of atrial fibrillation (AF) is increasing. It was reported that angiotensin receptor blocker (ARB) decreases the incidence of AF in patients with hypertension. We investigate the role of angiotensin II in atrial remodeling in rats with HF induced by myocardial infarction (MI). Methods: 8 weeks old male SD rats were used. MI were induced by a ligation of left anterior descending artery. 2 days after MI, rats were given losartan (10mg/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 prevented fibrosis formation in losartan group. Duration of AF were increased in MI and decreased in losartan group. Atrial eNOS levels were decreased in MI and improved in losartan group. Conclusion: In rat myocardial infarction induced heart failure model, there were significant increase of atrial fibrosis and AF duration. Atrial tissue eNOS levels were decreased. But treatment with losartan prevents these changes. Atrial fibrosis and decrease eNOS levels lead to a substrate that can support prolonged AF under the appropriate conditions. Losartan, ARB, intervenes collagen fiber formation and prevent decrease of tissue eNOS levels may prevent subsequent AF induction