To examine the procoagulant effects of thrombolytic agent on h emostasis and study the role of hemostatic markers as predictors of clinical outcomes. Methods. In the present study, eighteen patients with acute m...To examine the procoagulant effects of thrombolytic agent on h emostasis and study the role of hemostatic markers as predictors of clinical outcomes. Methods. In the present study, eighteen patients with acute myocardial in farction(AMI) received 1.5 or 2.0 million U nonspecific urokinase(UK), or 70～80 mg fibrin specific recombinant tissue plasminogen activator(rt PA)and did not use heparin until 8 hours after intravenous injection of the above agents. Eig ht patients with AMI and without thrombolytic therapy were enrolled as controls. Coagulant and thrombolytic activity markers included thrombin antithrombin Ⅲ complex (TAT), D dimer, fibrinogen (Fg), FMPV/Amax. All markers were determined before,immediately,1,2,4 and 8 hours after the administration of thrombolytic a gents respectively. Results. Molecular marker of thrombin generation——TAT showed an activated coa gulant state immediately after thrombolytic therapy. Level of TAT showed no sign ificant changes between every two observed phases in controls. However, level of TAT increased significantly from 4.95±1.75μg/L ( 4.63±1.37μg/L) to 14.71±3 .31μg/L ( 14.25±2.53μg/L) before and immediately after administration of thro mbolytic agents UK(or rt PA). There was significant difference between level of serum TAT of patients with and without thrombolytic therapy (P< 0.05). Patients achieving clinical reperfusion had lower TAT level than those failing in thromb olytic therapy, and higher FMPV/Amax level than controls. D dimer, a surrogate of thrombolytic activity increased markedly and Fg significantly declined afte r thrombolytic therapy(P< 0.05).Conclusions. Thrombin generation occurred in plasma in response to excess fibri nolysis induced by thrombolytic therapy. Both urokinase and rt PA had procoagul ant action. This transient activation of the coagulant system might contribute t o early reocclusion. These data provided the theoretical support for simultaneou s administration of anticoagulant therapy with thrombolytic agents. These result s also suggested that TAT might be useful in predicting clinical outcomes of p atients treated with thrombolytic therapy for AMI.展开更多
文摘To examine the procoagulant effects of thrombolytic agent on h emostasis and study the role of hemostatic markers as predictors of clinical outcomes. Methods. In the present study, eighteen patients with acute myocardial in farction(AMI) received 1.5 or 2.0 million U nonspecific urokinase(UK), or 70～80 mg fibrin specific recombinant tissue plasminogen activator(rt PA)and did not use heparin until 8 hours after intravenous injection of the above agents. Eig ht patients with AMI and without thrombolytic therapy were enrolled as controls. Coagulant and thrombolytic activity markers included thrombin antithrombin Ⅲ complex (TAT), D dimer, fibrinogen (Fg), FMPV/Amax. All markers were determined before,immediately,1,2,4 and 8 hours after the administration of thrombolytic a gents respectively. Results. Molecular marker of thrombin generation——TAT showed an activated coa gulant state immediately after thrombolytic therapy. Level of TAT showed no sign ificant changes between every two observed phases in controls. However, level of TAT increased significantly from 4.95±1.75μg/L ( 4.63±1.37μg/L) to 14.71±3 .31μg/L ( 14.25±2.53μg/L) before and immediately after administration of thro mbolytic agents UK(or rt PA). There was significant difference between level of serum TAT of patients with and without thrombolytic therapy (P< 0.05). Patients achieving clinical reperfusion had lower TAT level than those failing in thromb olytic therapy, and higher FMPV/Amax level than controls. D dimer, a surrogate of thrombolytic activity increased markedly and Fg significantly declined afte r thrombolytic therapy(P< 0.05).Conclusions. Thrombin generation occurred in plasma in response to excess fibri nolysis induced by thrombolytic therapy. Both urokinase and rt PA had procoagul ant action. This transient activation of the coagulant system might contribute t o early reocclusion. These data provided the theoretical support for simultaneou s administration of anticoagulant therapy with thrombolytic agents. These result s also suggested that TAT might be useful in predicting clinical outcomes of p atients treated with thrombolytic therapy for AMI.
