ABSTRACT
Two considerations have had a tremendous impact on the modern management of STsegment elevation acute myocardial infarction (STEMI). First, occlusive thrombosis superimposed on a ruptured plaque in an epicardial coronary artery was firmly established as the usual proximate cause of STEMI [1]. Coronary artery occlusion sets off a wave front of myocardial necrosis, spreading from endocardium to epicardium, with an inverse relation between the time to perfusion and the ultimate size and extent of transmurality of the infarct [2]. Transmural myocardial infarction, as opposed to subendocardial myocardial infarction, is characterized pathologically by necrosis involving not only the inner half but also significant amounts of the outer half of the ventricular wall, and electrocardiographically by the ST-segment elevation/Q-wave pattern. Secondly, restoration of coronary artery patency was found to correlate with survival. Recanalization can be achieved by pharmacologic dissolution of the coronary clot (fibrinolysis). Current fibrinolytic therapy consists of intravenous bolus administration of a plasminogen activator that dissolves the fibrin matrix of a thrombus. Alternatively, mechanical interventions within the occluded coronary artery may restore patency. Although the link between patency and survival is intuitively appealing and was firmly supported by laboratory animal experiments, only in the early 1990s did the Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries (GUSTO) I study convincingly establish the ‘‘open-artery hypothesis’’ (Fig. 1).
GUSTO-I AND THE OPEN ARTERY
