title: Rate of fibrinogen breakdown related to coronary patency and bleeding complications in patients with thrombolysis in acute myocardial infarction--results from the PRIMI trial.
abstract: Four hundred and one patients with acute myocardial infarction of less than 4 h duration were randomized to receive intravenous thrombolytic treatment with either 80 mg of full length unglycosylated single-chain-urokinase plasminogen activator (INN saruplase) or 1.5 million IU of streptokinase delivered over a 60 min period. Angiographic patency rates were higher at 60 min in saruplase treated patients (71.8% vs 48%; P less than 0.001), but did not differ significantly at 90 min (71.2% vs 63.9%; P = 0.15). Fibrinogen levels dropped markedly in both groups, the decrease being delayed and less pronounced with saruplase. Total fibrin and fibrinogen degradation products and D-dimer values rose earlier and to higher peak values in streptokinase treated patients. In both groups marked plasminogen and alpha 2-antiplasmin consumption was observed. Lower fibrinogen levels, and in particular the faster rate of fibrinogen breakdown, were associated with higher patency rates at 90 min (P less than 0.05). Patients with bleeding complications had lower 'lowest points' and a more rapid decrease in fibrinogen (P less than 0.05). These findings were not related to the drug used. Increased heparin levels at 6 to 12 h were correlated to bleeding complications in streptokinase treated patients. It is concluded that the rate of fibrinogen breakdown during and following thrombolytic treatment for acute myocardial infarction is related to early vessel patency and bleeding complications.
authors.affiliation: Department of Internal Medicine, University of Münster, Germany.
authors.forename: H
authors.initials: H
authors.lastname: Ostermann
authors.forename: U
authors.initials: U
authors.lastname: Schmitz-Huebner
authors.forename: J
authors.initials: J
authors.lastname: Windeler
authors.forename: F
authors.initials: F
authors.lastname: Bär
authors.forename: J
authors.initials: J
authors.lastname: Meyer
authors.forename: J
authors.initials: J
authors.lastname: van de Loo
mesh_terms: D001780:Blood Coagulation Tests; D003326:Coronary Circulation / Q000187:drug effects*; D003328:Coronary Thrombosis / Q000097:blood / Q000188:drug therapy*; D004311:Double-Blind Method; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism*; D006470:Hemorrhage / Q000097:blood / Q000139:chemically induced*; D006487:Hemostasis / Q000187:drug effects; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy*; D011994:Recombinant Proteins; D012008:Recurrence; D013300:Streptokinase / Q000008:administration & dosage / Q000009:adverse effects; D015912:Thrombolytic Therapy; D014568:Urokinase-Type Plasminogen Activator / Q000008:administration & dosage* / Q000009:adverse effects; D014654:Vascular Patency / Q000187:drug effects / Q000502:physiology
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D011994:Recombinant Proteins; D005340:Fibrinogen; D013300:Streptokinase; D014568:Urokinase-Type Plasminogen Activator; C067551:saruplase