Intramyocardial AM administration in animals with acute myocardial infarction activated migration of macrophage, their infiltration of myocardial damage area, inflammatory response, and enhance matrix metalloproteinase-9 mRNA expression in the infarct area and peri-infarct zones, whereas disturbed fibrotic repair, then provoked acute cardiac rupture in acute myocardial infarction [23]. Here, MMP9 is linked to acute myocardial infarction.