Optimal therapy for ST-segment elevation myocardial infarction: the role of residual thrombus.

Strategies that enhance functional reperfusion and translate into better clinical outcomes for ST-segment elevation myocardial infarction (STEMI) remain the holy grail of reperfusion therapy. In the absence of complete understanding of the vascular and cellular processes that are initiated with plaque rupture and thrombotic coronary artery occlusion, we have had to rely on therapies that shorten the duration of occlusion as well as result in effective thrombolysis. Because the initial events of a myocardial infarction appear to be mediated by acute thrombosis, it would seem logical that effective therapy would focus on pharmacologic strategies that would directly result in clot lysis, and/or enhance intrinsic fibrinolysis. Thrombolytic agents administered soon after the onset of an acute myocardial infarction achieve reperfusion in a majority of patients and save lives. Moreover, fibrin-specific thrombolytic agents achieve higher rates of vessel patency and are associated with lower mortality rates than non–fibrin-specific agents such as streptokinase. Finally, the ease of administration and life-saving characteristics of thrombolytics thrust this therapy into position as first-line treatment for an acute myocardial infarction in the 1980s and 1990s, and as a Class I, Level of Evidence: A, recommendation for STEMI (1).