[Unstable angina: tissue-type plasminogen activator inhibitor and other hemostatic factors in aspirin and intravenous heparin administration].

In order to assess the influence of oral aspirin (165 mg/day) and intravenous infusion of heparin (1000 U/h) on fibrinolysis in unstable angina we determined plasminogen activator inhibitor (PAI) activity and plasma contents of fibrinogen, antithrombin III, protein C on admission and on day 3 of treatment in a subgroup of 51 patients (25 aspirin, 26 heparin) from double blind randomized comparative trial of aspirin and i.v. heparin. Initial PAI activity was lower in the aspirin group presumably due to later admissions of these patients during the day. By day 3 activity of PAI increased from 13.5 +/- 2.0 to 18.2 +/- 1.93 U/ml, p = 0.018, and from 17.8 +/- 1.83 to 20.2 +/- 2.44 U/ml, ns, in heparin- and aspirin-treated patients, respectively. Fibrinogen level increased from 3.34 +/- 0.15 to 3.95 +/- 0.18 g/l, p < 0.001, and from 3.36 +/- 0.17 to 3.94 +/- 0.17 g/l p = 0.003 in aspirin and heparin groups, respectively. Protein C level was unchanged. A decrease in antithrombin III observed in heparin group (from 115 +/- 3.2% to 98 +/- 3.4%, p < 0.001) reflected specific action of the drug. Neither aspirin no heparin caused changes in hemostatic parameters which may be interpreted as profibrinolytic action. Changes of PAI are unlikely related to antithrombotic treatment and probably reflect its diurnal and "acute phase" fluctuations.