Antithrombin Therapy for Acute ST-Segment Elevation Myocardial Infarction

Thrombus formation at the site of plaque rupture has long been recognized as the inciting event in the pathophysiology of ST-segment elevation myocardial infarction (STEMI). Fibrinolysis remains the most common mode of revascularization worldwide and has the recognized limitation of creating large amounts of activated thrombin as a byproduct of its mechanism of action. Several antithrombin agents have been developed as adjuncts to either pharmacologic or mechanical revascularization strategies for this patient population. Unfractionated heparin remains a very important agent although low-molecular weight heparins and direct thrombin inhibitors have been developed and studied in these patients. How each class of antithrombin therapies will be optimally utilized for patients with STEMI remains to be defined. At the core of any antithrombin therapy rests the goals of minimizing ischemic complications while simultaneously avoiding any bleeding complications.