Abstract：Acute myocardial infarction (AMI) induced cardiomyocyte death causes a series of pathophysiological responses of the heart. The process involves proinflammatory reaction and extracellular matrix degradation, and antiinflammatory reaction and new scars formation. However, the redundancy of inflammatory reaction caused by tissue injury would lead to excessive cardiac fibrosis and antagonistic cardiac remodeling, eventually developing into adverse cardiovascular events such as heart failure. It is helpful to prevent and treat the adverse prognosis after AMI as far as understanding the inflammatory regulation mechanism. This review introduces the key inflammatory factors involved in cardiac repair after AMI, especially interleukin, matrix metalloproteinase and reactive oxygen species, influence the infarct area and left ventricular function after AMI through pro and antiinflammatory effects of themselves. These factors regulate cardiac repair after AMI, and provide references and strategies for clinically improving the prognosis of patients with AMI.
