Effect of Complementary Intracoronary Streptokinase Administration Immediately After Primary Percutaneous Coronary Intervention on Microvascular Perfusion and Late Term Infarct Size in Patients With Acute Myocardial Infarction

Mechanical reperfusion for acute myocardial infarction (AMI) targets optimal revascularization of the epicardial artery but also aims at improved myocardial salvage. The goal of reperfusion therapies has shifted to include reperfusion downstream at the level of capillary bed, and it might be more appropriate that the hypothesis now be termed "the time dependent open artery and open microvascular hypothesis." Failure to achieve myocardial reperfusion despite the presence of a patent coronary artery has been termed the "no-reflow" phenomenon and attributed to microvascular dysfunction. It has become apparent that clinical outcomes are not only associated with patency of the epicardial artery, but also with patency of the microcirculation. Persistent impairment of microcirculation is associated with poor clinical outcome. Complete reperfusion in AMI settings necessitates reopening of the all consecutive vascular compartments all the way through the coronary circulation. But, embolization following percutaneous coronary intervention (PCI) and in situ microthrombi generation at the microvascular level makes this goal difficult to achieve. For this reason, mechanical intervention to the epicardial coronary artery with or without using distal protection wouldn't be enough to achieve ideal reperfusion at the ultimate (microvascular) level. At this point, it has become more evident that we need to develop more competent and feasible reperfusion strategies which can help us to achieve reperfusion as complete as possible at all levels.