title: Prolonged activation of fibrinolytic system induced by fibrin nonselective thrombolytic agent can contribute to preventing early reocclusion after coronary thrombolytic therapy.
abstract: The incidence of early reocclusion is reported to be higher in patients who receive fibrin-specific thrombolytic agents than nonspecific ones. The reason has yet to be clarified. In the present study, we focused on the difference in duration of fibrinolytic activity. The hemostatic parameters of 7 consecutive patients suffering from acute myocardial infarction treated with a fibrin-nonspecific thrombolytic agent (urokinase) were compared with 9 patients who received a fibrin-specific agent (tissue plasminogen activator, t-PA). The plasma concentrations of alpha 2-plasmin inhibitor (alpha 2-PI), plasmin alpha 2-PI complex (PLC), fibrin degradation products E fragment (FDP-E), and D-D dimer (D-dimer) were measured before, soon after, 1, 2, 3, 4, and 6 h and 2, 3, 4, and 7 days after thrombolytic therapy to estimate the hemostatic and fibrinolytic state. A significant decrease in alpha 2-PI (less than the lowest measurable level) with a simultaneous increase in FDP-E and D-dimer was induced soon after the administration of urokinase. FDP-E and D-dimer decreased, with a significant increase in alpha 2-PI, more than 6 h after thrombolytic therapy. In contrast, a less significant decrease in alpha 2-PI with a lesser amount and shorter duration of fibrinolysis were observed in patients who received t-PA. The amount of PIC soon after drug administration was not different between the two groups. Our data suggested that fibrinolytic activities induced by fibrin-nonspecific urokinase persisted longer than expected by its plasma half-life.The fibrinolytic activities might be terminated by the production of alpha 2-PI.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Cardiopulmonary Division, Keio University, 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: Handa
authors.forename: E
authors.initials: E
authors.lastname: Takahashi
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; D005337:Fibrin / Q000378:metabolism*; D005342:Fibrinolysis / Q000187:drug effects* / Q000502:physiology; D006487:Hemostasis / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy*; D011994:Recombinant Proteins / Q000008:administration & dosage; D012008:Recurrence; D015912:Thrombolytic Therapy; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*; D014568:Urokinase-Type Plasminogen Activator / Q000008:administration & dosage; D000979:alpha-2-Antiplasmin / Q000378:metabolism
chemical_list: D011994:Recombinant Proteins; D000979:alpha-2-Antiplasmin; D005337:Fibrin; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator