ABSTRACT
INTRODUCTION Despite the success of catheter-based reperfusion for acute myocardial infarction (MI), many patients have poor recovery of ventricular function in the infarct zone, due to prolonged ischemic injury, as well as suboptimal restoration of flow at a tissue level. Mechanisms contributing to this “myocardial no-reflow” phenomenon are not well understood but are thought to include ischemia-induced microvascular damage, distal embolization, and reperfusion injury. Because infarct size is still the most important determinant of survival, these observations have prompted the search for new adjunctive therapies to enhance tissue level perfusion, augment myocardial salvage, and improve clinical outcome.
