Inflammasome Activation in Reperfusion Injury

W ith 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 area 2 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.