This study conducted an exploratory investigation into the new mechanism of Wenxin Keli, it provided a detailed analysis of its regulation of the AMPK/SIRT1/PGC-1α pathway, promoting the flexible utilization of energy substrates in the myocardium and enhancing the oxidative capacity of mitochondria, thereby delaying the deterioration of cardiac function in heart failure after myocardial infarction and reducing the risk of concurrent ventricular arrhythmias. This evidence concerns the gene PPARGC1A and myocardial infarction.