Optimizing outcomes in ST-segment elevation myocardial infarction.

During the past two decades, major advances in the treatment of acute ST-segment elevation myocardial infarction (STEMI), including coronary care units and thrombolysis, have lowered the mortality after hospital presentation to approximately 5%. However, in recent years, there has been little further improvement in survival (1). Neither newer fibrinolytic agents nor attempts to combine a reduced-dose fibrinolytic agent with a glycoprotein (GP) IIb/IIIa inhibitor, which increase 60to 90-min infarct-artery–related patency, have resulted in improved survival (2–4). Reasons for this apparent paradox may include poor myocardial perfusion through the microvasculature despite optimal epicardial coronary artery flow, continued myocardial cell death in ischemic border zones, or an inability to impact the high mortality associated with cardiogenic shock.