Are Native Anticoagulant Mechanisms

T he evolving concept that coronary artery patency after myocardial infarction is associated with improved shortand long-term survival1'2 and left ventricular function34 has intensified efforts to open thrombosed vessels. The importance of maintaining vessel patency has also become clear. Ohman et a15 found that patients with documented reocclusion had more complicated hospital courses, higher in-hospital mortality rates, and worse infarct zone function. Efforts to maintain patency have been hampered by a significant rate of reocclusion, approximately 12-18% after successful thrombolytic therapy for acute myocardial infarction.6,7 Because this rethrombosis occurs in the setting of a systemic fibrinolytic state, therapeutic efforts have been directed toward inhibition of platelet activation and aggregation. This has focused attention on anticoagulant mechanisms native to the vessel itself.