The complement system, discovered over one hundred years ago, is a major component of innate mechanisms of immune responses. A group of approximately 40 proteins that comprise the complement system, participates in the defense of the host against various agents, e.g. microorganisms, through facilitation of phagocytosis and enhancement of ongoing inflammatory reaction. There are three complement activation pathways: conventional, alternative and lectin pathway. Activation of the complement system results in formation of membrane attacking complex (MAC) and death of the lytic target cell. Complement activation and MAC formation are regulated by specific cellular and serum proteins. It is constitutively active and potentially could damage the body own cells. Cells of ischemic myocardium become foreign cells for the immune system for antigenic reasons. This results in activation of the complement system and formation and deposition of MAC that damages myocardial cells. By binding their surface, it exacerbates myocardial injury caused by infarction. The aim of this paper is to elaborate on the role of complements and their inhibitors in etiology of myocardial infarction basing on literature data concerning this condition.