title: Serial changes in coagulant activities after thrombolytic therapy for acute myocardial infarction.
abstract: Early reocclusion and bleeding complications are still unresolved problems in thrombolytic 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 immediately 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. Fibrinolytic activity induced by thrombolytic therapy for AMI caused transient activation of the coagulant system, which could contribute to early reocclusion. Fibrin nonselective 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.
authors.affiliation: Cardiopulmonary Division, Keio University School of Medicine, Tokyo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Goto
authors.forename: Y
authors.initials: Y
authors.lastname: Kawai
authors.forename: S
authors.initials: S
authors.lastname: Abe
authors.forename: E
authors.initials: E
authors.lastname: Takahashi
authors.forename: S
authors.initials: S
authors.lastname: Handa
authors.forename: S
authors.initials: S
authors.lastname: Ogawa
authors.forename: K
authors.initials: K
authors.lastname: Watanabe
authors.forename: S
authors.initials: S
authors.lastname: Hori
authors.forename: Y
authors.initials: Y
authors.lastname: Ikeda
mesh_terms: D000368:Aged; D000933:Antifibrinolytic Agents / Q000378:metabolism; D000990:Antithrombin III / Q000187:drug effects / Q000378:metabolism; D001777:Blood Coagulation / Q000187:drug effects*; D005340:Fibrinogen / Q000187:drug effects / Q000378:metabolism; D005341:Fibrinolysin / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy*; D010447:Peptide Hydrolases / Q000187:drug effects / Q000378:metabolism; D011517:Prothrombin Time; D015912:Thrombolytic Therapy; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*; D014568:Urokinase-Type Plasminogen Activator / Q000627:therapeutic use*; D000979:alpha-2-Antiplasmin
chemical_list: D000933:Antifibrinolytic Agents; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C037742:plasmin-plasmin inhibitor complex; D000990:Antithrombin III; D005340:Fibrinogen; D010447:Peptide Hydrolases; D010959:Tissue Plasminogen Activator; D005341:Fibrinolysin; D014568:Urokinase-Type Plasminogen Activator