Acute myocardial infarction (AMI) often leads to myocardial ischemia reperfusion (MIRI), thereby causing myocardial remodeling. Percutaneous coronary intervention (PCI) is the primary treatment of AMI, but easily results in myocardial ischemia-reperfusion injury, leading to myocardial remodeling. It was showed that miR-24 plays a role in cardiac remodeling. However, miR-24 expression and effect in AMI after PCI treatment have not been fully elucidated. A total of 80 cases of AMI patients after PCI surgery were enrolled. Information about echocardiography ejection fraction (EF), left ventricular end systolic diameter (LVESD), left ventricular thickness, and left ventricular end diastolic diameter (LVEDD) were recorded. MiR-24 expression before and after PCI treatment was detected by real-time PCR and analyzed with cardiac function. Rat AMI model was established and transfected by miR-24 lentivirus. Cardiac function in rats was assessed by M-mode ultrasound. Type I collagen content was determined by ELISA. Bax and Bcl-2 protein expressions in rat myocardial cells were tested by Western blot. EF reduced, LVESD and LVEDD increased, left ventricular thickness decreased, and miR-24 downregulated significantly in AMI patients after PCI compared with the preoperative group (P < 0.05). MiR-24 was positively correlated with left ventricular thickness and EF, and negatively correlated with LVESD and LVEDD (P < 0.05). Overexpression of MiR-24 in AMI rats obviously improved heart function index, reduced type I collagen content, downregulated Bax level, and enhanced Bcl-2 expression compared with AMI group (P < 0.05). MiR-24 downregulated in AMI and increased after PCI treatment. MiR-24 overexpression improved cardiac function through reducing type I collagen, regulating apoptosis balance, and alleviating MIRI.