Primary Coronary Intervention for Acute Myocardial Infarction

DESPITE DRAMATIC IMPROVEments in the treatment of acute ST-segment elevation myocardia l infarct ion (STEMI) during the past decade, approximately 1 in 10 patients still die of this disease. Three critical factors in the immediate management of patients with STEMI result in reduced mortality: prompt diagnosis, immediate treatment with aspirin, and rapid reestablishment of blood flow in the infarctrelated artery. The latter aim may be achieved either pharmacologically, with administration of thrombolytic therapy, or mechanically, with percutaneous coronary intervention (PCI). Primary PCI refers to the strategy of emergent angiography followed by mechanical recanalization of the occluded artery with a balloon catheter, without prior administration of thrombolytic therapy. In its early years, the data regarding primary PCI were limited to observational studies from specialized centers. With the publication of randomized controlled trials (RCTs)comparingPCIwith thrombolytic therapy, however, primary PCI has become accepted as part of the standard armamentarium in the treatment of STEMI. The most recent RCTs on this topic have begun to examine the role of primary PCI in specific subsets of patients with STEMI and the role of adjunctive therapies in patients undergoing primary PCI. Pathophysiology of STEMI ST-segment elevation myocardial infarction is the clinical correlate of fullthickness ischemia and infarction of myocardium and is the result of sudden thrombotic occlusion of its blood supply. The transition from a diseased but patent coronary artery to one that is occluded by thrombus begins with either rupture or erosion of a coronary atherosclerotic plaque. The cellular and molecular events within the plaque that lead to its disruption remain incompletely understood but are clearly unrelated to the severity of the preexisting luminal stenosis. In fact, the majority of STEMI evolve from mild to moderate stenoses. Plaque disruption results in exudation of its lipid-rich core into the lumen and adherence of platelets to the arterial subendothelium. The platelets become activated and develop high affinity for fibrinogen, causing their crosslinking and degranulation. Simultaneously, the release of tissue factor from the lipid-rich core results in activation of the coagulation cascade and generation of thrombin. The result is a luminal thrombus consisting of aggregated platelets, cross-linked fibrin strands, and entrapped red blood cells (FIGURE 1). The enlarging thrombus can interrupt blood flow and lead to an imbalance between oxygen supply and demand that, if severe and persistent, causes transmural infarction of the myocardium.