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Serial Changes in Coagulant Activities After Thrombolytic Therapy for Acute Myocardial Infarction

Cardiopulmonary Division, Keio University School of Medicine

Yohko Kawai

Department of Laboratory Medicine, Keio University School of Medicine

Sumihisa Abe

Cardiopulmonary Division, Keio University School of Medicine

Eiichi Takahashi

Cardiopulmonary Division, Keio University School of Medicine

Shunnosuke Handa

Cardiopulmonary Division, Keio University School of Medicine

Satoshi Ogawa

Cardiopulmonary Division, Keio University School of Medicine

Kiyoaki Watanabe

Department of Laboratory Medicine, Keio University School of Medicine

Shingo Hori

Department of Emergency Medicine, Keio University School of Medicine, Tokyo, Japan

Yasuo Ikeda

Division of Hematology, Department of Medicine, Keio University School of Medicine

Early reocclusion and bleeding complications are still unresolved problems in throm bolytic therapy for acute myocardial infarction (AMI). In the present study, 16 patients treated with either fibrin-specific tissue-type plasminogen activator (t-PA) or nonspecific urokinase (UK) were studied to determine the effects of thrombolytic therapy on serial hemostatic states. Hemostatic states of each patient were estimated by measuring various plasma markers at one- to two-hour intervals during the first six hours of therapy, daily during the next three days, and subsequently on day 7.

Two markers of plasma thrombin generation, thrombin antithrombin III complex (TAT) and prothrombin fragment 1+2 (F 1+2), showed an activated coagulant state imme diately after thrombolytic therapy The amount of thrombin generation indicated by these markers showed significant positive correlation with direct markers of fibrinolysis such as fibrin degradation products (FDP), while it did not show any correlation with the markers for plasmin generation. The potential for coagulation as indicated by prothrombin time (%) decreased with thrombolysis using fibrin nonselective agents, owing perhaps to destruction of coagulant factors by free plasmin. (continued on next page)

Fibrinolytic activity induced by thrombolytic therapy for AMI caused transient activa tion of the coagulant system, which could contribute to early reocclusion. Fibrin nonse lective agents decreased the potential for coagulation by destroying clotting factor through the generation of free plasmin. These data provide theoretical support for simultaneous administration of anticoagulant therapy with fibrin-specific thrombolytic agents.

Angiology, Vol. 45, No. 4, 273-281 (1994)
DOI: 10.1177/000331979404500403


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