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The thrombolytic regimen with half dose r-PA and abciximab had a benefical influence on platelet activation and induced a more marked decrease of platelet-monocyte, and in part, platelet-granulocyte aggregates compared with the r-PA regimen. This could contribute to a probably lesser monocyte activation state with favourable effects on monocyte-endothelial adhesion and a consecutively possible influence of myocardial damage, a reduction of the additionally acute local inflammatory processes and a reduction of adherence of platelet-granulocyte aggregates to subendothelium.

Background-Thrombolytic therapy in patients with acute myocardial infarction (AMI) is hampered by procoagulant effects. In vitro studies have indicated that plasmin stimulation activates the kallikrein-contact-phase system, resulting in thrombin activation. This prospective comparative study was designed to examine the procoagulant effects of streptokinase or alteplase in AMI. Methods and Results-Sixty-one patients with AMI received 1.5 million U of streptokinase or front-loaded alteplase (up to 100 mg) and systemic heparin. Twenty-four patients with AMI and no thrombolytic therapy and 30 control subjects were examined for comparison. Molecular markers of thrombin, plasmin activation, and coagulation activities were determined before therapy and serially for up to 10 days. Streptokinase and alteplase increase TAT to 50Ϯ17 and 51Ϯ18 g/L at 3 hours and to 50Ϯ17 and 33Ϯ14 g/L at 6 hours, respectively (PϽ0.01). Kallikrein activity is elevated (PϽ0.01) to 76Ϯ5 and 71Ϯ7 U/L at 3 hours and 64Ϯ6 and 47Ϯ5 U/L by streptokinase and alteplase, respectively, at 6 hours. Reductions in fibrinogen and increases in D-dimers and plasmin-antiplasmin complexes are more marked (PϽ0.05 and 0.01) after streptokinase versus alteplase. Correlations were found among TAT, kallikrein activity, and plasmin activation (PϽ0.01). Conclusions-The data indicate a more marked procoagulant action of the streptokinase regimen compared with front-loaded alteplase, thus supporting the hypothesis of a plasmin-mediated kallikrein activation with consecutive procoagulant action in vivo.