SOLUBLE THROMBOMODULIN ANTIGEN IN PLASMA IS INCREASED IN PATIENTS WITH ACUTE MYOCARDIAL-INFARCTION TREATED WITH THROMBOLYTIC THERAPY

Thrombomodulin (TM) is an integral endothelial cell membrane protein t hat functions as a cofactor for thrombin mediated activation of protei n C. The anticoagulant functions of the protein C system are important in contributing to a hemostatic balance and prevention of thromboembo lic disease. It has been suggested that impaired TM cofactor function could also constitute a prothrombotic abnormality leading to thromboem bolic diseases. TM exists not only on the surface of endothelial cells but also as soluble fragment(s) circulating in plasma. The concept of a thrombotic occlusion as the critical event in acute myocardial infa rction (AMI) forms the rationale for thrombolytic therapy. After succe ssful reperfusion, patients remain at substantial risk for recurrent i nfarctions due to rethrombosis. The balance between procoagulant and a nticoagulant mechanisms in the postthrombolytic phase have not been st udied in detail. We have studied whether the plasma levels of soluble TM are influenced by thrombolytic therapy with streptokinase in patien ts suffering from AMI. Soluble TM concentrations increased significant ly by 24 to 48h after thrombolytic treatment, simultaneously with an i ncrease in C-reactive protein (CRP, a marker of the inflammatory compo nent of the cell damage) and in thio-barbituric acid reactive substanc es (TEARS, an indirect marker of lipid peroxidation).