The main results of this study are as follows: (1) IMD1-53 treatment increased AERP, reduced atrial fibrillation inducibility, and shortened the atrial fibrillation duration in rats with MI; (2) IMD1-53 treatment reduced LAD and ameliorated cardiac function; (3) IMD1-53 treatment inhibited left-atrial fibrosis and collagen production; (4) IMD1-53 impacted TGF-β1/Smad3, and the TGF-β1/ALK5/Nox4 pathway inhibited atrial fibrosis. The gene discussed is SMAD3; the disease is myocardial infarction.