title: Hypercoagulable state after thrombolytic therapy in patients with acute myocardial infarction (AMI) treated with streptokinase.
abstract: Fibrinogen activity was studied in 70 patients with AMI who were treated with an intravenous infusion of SK (800,000 U/30 min or 1.5 mill U/60 min). Patients received a continuous infusion of heparin after thrombolytic therapy was completed. 800,000 U and 1.5 mill U SK recanalized infarct-related arteries at a rate of 78%. Early re-infarction occurred in 6% in each group. Upon admission to the hospital patients showed a hypercoagulable state that may be related to an elevated level of fibrinogen and HMW fibrinogen (70.5 +/- 2 vs 65 +/- 2% in patient and normal plasmas, respectively) that changed to a transitory hypercoagulable state indicated by decreased fibrinogen levels after SK treatment. Forty-eight hours after SK, a new fibrinogen hyperfunction, related to an increase in fibrinogen level and especially HMW synthesized fibrinogen (82 +/- 1 or 81 +/- 1%, 800,000 and 1.5 mill U SK, respectively) was observed, which was neutralized by heparin therapy (1,660 U/h with continuous infusion). The elevated levels of fibrinogen (363 +/- 21 vs 240 +/- 8 mg/dl in patient and normal plasmas, respectively) and HMW fibrinogen (70 +/- 3% with both SK hypercoagulable state that is not neutralized by the heparin dose were compared with those whose arteries recanalized. The former group had a higher concentration of fibrinogen (197 +/- 31 vs 147 +/- 18 mg/dl), HMW fibrinogen (78 +/- 0.5 vs 74 +/- 0.3%, respectively), and FPA (130 +/- 3 vs 6 +/- 4 pmol/ml) and more extensive fibrin gel formation kinetics (gelation rate 3.3 +/- 1.4 vs 1.1 +/- 0.2 OD/s x 10(-4), respectively) than the second group. The hypercoagulable state found in patients with acute myocardial infarction undergoing thrombolytic therapy may be related mainly to the progression of HMW fibrinogen and fibrinogen levels.
authors.affiliation: Research Center, La Fe Hospital, Valencia, Spain.
authors.forename: V
authors.initials: V
authors.lastname: Vila
authors.forename: E
authors.initials: E
authors.lastname: Regañón
authors.forename: J
authors.initials: J
authors.lastname: Aznar
authors.forename: V
authors.initials: V
authors.lastname: Lacueva
authors.forename: M
authors.initials: M
authors.lastname: Ruano
authors.forename: B
authors.initials: B
authors.lastname: Laiz
mesh_terms: D000328:Adult; D000368:Aged; D001777:Blood Coagulation / Q000187:drug effects*; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis*; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy* / Q000517:prevention & control; D012008:Recurrence; D013300:Streptokinase / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D013917:Thrombin / Q000032:analysis
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D005340:Fibrinogen; D006493:Heparin; D013300:Streptokinase; D013917:Thrombin