The morbidity and mortality rates of coronary heart disease (CHD) are high worldwide. The primary pathological changes in CHD involve stenosis and ischemia caused by coronary atherosclerosis (AS). Extensive research on the pathogenesis of AS has revealed chronic immunoinflammatory processes and cell proliferation in all layers of coronary vessels, including endothelial cells (ECs), vascular smooth muscle cells, and macrophages. m6 A methylation is a common posttranscriptional modification of RNA that is coordinated by a variety of regulators (writers, readers, erasers) to maintain the functional stability of modified mRNAs and ncRNAs. In recent years, there has been increasing focus on the involvement of m6 A methylation in the incidence and progression of CHD, which starts with atherosclerotic plaque formation, leads to myocardial ischemia, and ultimately results in the occurrence of myocardial infarction (MI). m6 A regulators modulate relevant signaling pathways to participate in the inflammatory response, programmed death of cardiomyocytes, and fibrosis. Therefore, diagnostic models based on m6 A profiling are helpful for the early detection of CHD, and m6 A methylation shows promise as a sensitive target for new drugs to treat CHD in the future.