The role of coronary thrombosis in the pathogenesis of acute myocardial infarction (AMI) is well established, and has led to great efforts at early recanalization of the infarct-related vessel. However, in up to 20"/" of the patients after initially successful thrombolysis, reocclusion by a new thrombus occurs (1). It has not yet been proven in clinical studies that the frequency of reocclusion can be influenced by anticoagulation (2).Therefore it appears to be an important question, whether and at what time during thrombolysis an activation of coagulation is demonstrable.
Recently an enzyme immuno assay of thrombin-antithrombinlll complex (TAT) plasma levels was developed by PELZER et al. (Thromb. Haemost. 54:24,1985). This test appears to be useful in the detection of intravasal thrombin generation, since all of 17 patients (pts.) with pulmonary embolism and 15 of 16 pts. with deep vein thrombosis (DVT) showed elevated values above 3 ng/ml.In 9 pts. with acute myocardial infarction (AMI) the TAT levels increased significantly (p 0.001) 3 to 6 hours after thrombolytic therapy with 1.5 million units streptokinase (SK) over 30 minutes. A concomitant increase of fibrinopeptide A (FPA) levels (p=0.048) was observed. In contrast, 8 AMI pts. treated with heparin showed an insignificant increase of TAT and FPA. In 7 DVT pts. the TAT levels rose significantly (p 0.001) within 6 hours after start of urokinase (UK) infusion, while the FPA levels were enhanced prior to treatment and showed no further increase.In order to assess the in vitro effects of SK and UK on TAT levels, clots obtained by recalcification of citrated plasma were incubated in heparin (2 units/ml) plasma. An increase of TAT occurred after addition of SK or UK, which was less pronounced when the clots were rinsed extensivly or squeezed before incubation. When SK or UK were added to plasma in the absence of a clot, still a small increase of TAT occurred which was absent in saline controls.The data suggest that SK and UK action is associated with the generation of TAT complexes. In vivo, thrombin or thromboplastic material might be released by enhanced "wash out" from the recanalized coronary artery or from the reperfused in-farcted myocardium. Thrombin might also be released from binding sites on fibrin clots or fibrinogen. It is conceivable that these findings contribute to the understanding of reocclusion of infarct vessels after thrombolytic therapy. This points to the importance of careful anticoagulation in patients receiving thrombolytic therapy.
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