UNSTABLE ANGINA - TISSUE-PLASMINOGEN ACTI VATOR INHIBITOR AND OTHER HEMOSTATIC FACTORS IN PATIENTS TREATED WITH ORAL ASPIRIN OR INTRAVENOUSHEPARIN

In order to assess the influence of oral aspirin (165 mg/day) and intr avenous infusion of heparin (1000 U/h) on fibrinolysis in unstable ang ina we determined plasminogen activator inhibitor (PAI) activity and p lasma contents of fibrinogen, antithrombin III, protein C on admission and on day 3 of treatment in a subgroup of 51 patients (25 aspirin, 2 6 heparin) from double blind randomized comparative trial of aspirin a nd i.v. heparin. Initial PAI activity was lower in the aspirin group p resumably 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 hepa rin- and aspirin- treated patients, respectively. Fibrinogen level inc reased 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 antithrombi n 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 hepari n caused changes in hemostatic parameters which may be interpreted as profibrinolytic action. Changes of PAI are unlikely related to antithr ombotic treatment and probably reflect its diurnal and <<acute phase>> fluctuations.