Background: Atrial fibrillation (AF) is the most common arrhythmia. Recent evidence shows that increased atrial oxidative stress might play an important role in AF. The Rho GTPase Rac1 regulates NADPH oxidase activity and is critical for generating oxidative stress. Here, we investigated AF developing effects of Rac1 in HF rats.. We also studied anti-AF effects of simvastatin by its Rac 1 suppression mechanism. Methods: A rat myocardial infarction (MI) model was used. Two days after induction of MI, rats were randomized into 3 groups: the sham group, the MI group, and the MI+Simva (simvastatin 2 mg/kg/day for 10 weeks) group. Echocardiography, AF induction, and atrial fibrous tissue content analysis were done. Western blotting of active form of Rac1, and sarcoplasmic reticulum Ca²⁺ ATPase2a (SERCA2a), and sodium calcium exchanger (NCX) were. Results: Ejection fractions were significantly decreased in MI group. Fibrosis quantification showed significantly increased left atrial fibrosis in MI and significantly attenuated in MI+Simva group. Duration of AF were increased in MI group and significantly decreased in MI+Simva group. The expression of atrial SERCA2a was significantly decreased in the MI group and significantly improved in the simvastatin group. The expression of atrial NCX and active form Rac1 were significantly increased in the MI group and those were significantly decreased in the simvastatin group. Conclusion: Simvastatin suppressed the HF induced AF promotion and it might be related with suppressing active form rac1. Simvastatin could be another drug for the prevention of AF in HF.