The Role of Anti-Inflammatory Cytokines in Heart Failure

Abstract

Coronary occlusion promotes a state of ischaemia that results in myocardial infarction; it  is  a  major  cause  of  mortality  accounting  for  one  hospital  admission  every  three minutes. At the site of infarct, sterile inflammation is initiated due to pro-inflammatory secretions from cardiac and innate immune cells. The focus of this review is to explore the role of a newly discovered innate immune complex, the nod-like receptor family pyrin domain containing 3 inflammasome. This review discusses the potential of this immune  complex  in  decreasing  the  proportion  of  functional  myocardium  during ischaemia   and   ischaemia-reperfusion   injury.   Due   to   the   central   role   of   this inflammasome  in  promoting  cardiac  dysfunction  following  an  acute  myocardial infarction,  the  risk  of  port-infarction  heart  failure  increases.  With  an  intention  of highlighting the importance of improving current management of patients with acute myocardial  infarction,  this  review  addresses  novel  therapeutic  agents  that  have demonstrated  cardioprotective  outcomes  in  recent  studies.  This  follows  discussion concerning the therapeutic potential of these agents, intending to form the basis of heart failure therapy.