Myocardial infarction (MI) is the one of the most severe manifestations of coronary artery disease which may lead to severe complications as heart failure. MI is also still an important cause of death in both developed and western countries. One of the most crucial mechanisms causing MI induced complications is inflammasome activation and subsequent release of inflammatory cytokines. A significant rise in cardiac enzymes troponin I and creatine kinase-MB (CK-MB) was observed, also significant rise in inflammatory markers interleukin 1β (IL-1β) serum levels, toll like receptor 4 (TLR4) and NF-κB were observed in MI. Moreover, increase in the expression of all inflammasome components as NLRP3 and caspase-1 was detected along with histopathological and electrocardiographic abnormalities as changes in ST segment elevation and QT interval prolongation. The current study shows that targeting the inflammatory cascade through inhibiting one of its important activators the inflammasome may be a novel strategy for management of MI and preventing its complications.