ABSTRACT
Introduction In the mid-1970s, Davies et al 1 demonstrated that the mechanism of acute myocardial infarction (AMI) in most cases results from rupture of an atherosclerotic plaque leading to thrombosis and occlusion of the coronary artery. The recognition that the prompt restoration of flow salvages myocardium, reduces infarct size, and prolongs life has been the driving force behind a large number of clinical trials assessing reperfusion therapy for AMI. The goal of reperfusion therapy in ST-elevation myocardial infarction (STEMI) is to achieve early, full, and sustained coronary blood flow in the culprit vessel. Both primary percutaneous coronary intervention (PPCI) and fibrinolytic therapy fulfill some but not all of these goals.
