Inflammasome activation in reperfusion injury: friendly fire on myocardial infarction?

With the advances in percutaneous coronary intervention technology and accompanying medical therapy, the prognosis of patients with acute coronary syndromes has greatly improved over the last decades. Still, approximately 6% of admitted patients do not survive to hospital discharge,1 and despite the implementation of rapid interventional protocols, loss of cardiac tissue, and a consecutive decrease in cardiac function is the frequent consequence of acute myocardial infarction. In addition, increasing experimental and clinical evidence demonstrates that revascularization itself triggers a harmful inflammatory response, termed ischemiareperfusion (I/R) injury, that might contribute up to 50% of the ultimate infarction area2 and that can exert deleterious effects even beyond the initially affected perfusion territory. Since the first description of I/R injury by Jennings et al in the 1960s,3,4 a large number of studies have aimed to unravel the basic mechanisms of this complex pathophysiological process. It became evident that I/R injury is an inflammatorydriven mechanism, in part depending on the infiltration of bone marrow-derived cells and the activation of classic inflammatory pathways.5 However, none of the experimental strategies has evolved into a clinically applicable adjuvant therapy for the treatment of acute coronary syndromepatients, demonstrating the complexity of I/R injury.