Search

A comparison of the effects of two regimens of urokinase infusion not associated to heparin and of continuous heparin infusion was made assessing the rate of emboli and arterial hypoxemia resolution in patients with acute pulmonary embolism. Twenty-nine patients with acute pulmonary embolism, each one diagnosed by means of perfusion lung scan and selective pulmonary arteriography, were admitted to the study and randomly allocated to three treatment groups: A, 10 patients, urokinase: 800,000 CTA units/day for three days followed by oral anticoagulants; B, 9 patients, heparin: mean daily dose 30,000 units for seven days followed by oral anticoagulants; C, 10 patients, urokinase: 3,300,000 CTA units in 12 hours followed by oral anticoagulants. Pulmonary lung scan and PaO2st (PaO2 standardized to PaCO2 of 40 mmHg) were repeated at 1, 3, 7, and 30 days in all the groups of treatment. The mean daily rate of improvement, assessed from both the perfused lung segments and the PaO2st increment, in group C was highest in the first 24 hours and lowest from the first to the third day of treatment. However, from the third to the seventh day of treatment and onwards the mean daily rate of improvement was roughly the same in all the groups. After one month, lung perfusion and the PaO2st had considerably improved, but had not attained full recovery in any of the treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Dissolution of pulmonary emboli with heparin and urokinase is ascribed, respectively, to anticoagulation and fibrinolysis. Since truly independent assessment of these effects in man is lacking, we administered each drug alone. Fibrinogen and plasminogen plasma levels and the resolution of pulmonary emboli were measured in three randomized groups of 10 patients each: groups A and C infused with small repeated doses of urokinase and a large single dose of urokinase, respectively, and group B who received heparin. After 6 h of treatment, fibrinogen fell in all the groups, while, after 12 h, remained equally reduced in groups A and B and declined further in group C. Plasminogen behaved similarly. Up to 60 h, statistical analysis showed that these effects were related to timing and amounts of urokinase and heparin infusion. These observations suggest that heparin may induce a lytic state. As to signs of pulmonary emboli resolution, no differences between groups were found in lung perfusion and gas exchange recovery at any time (from 1 day to 1 year) and in pulmonary artery pressure reduction at 1 week. The greater angiographic and scintigraphic recovery observed with urokinase, versus heparin alone, after 1 day of treatment in the Urokinase Pulmonary Embolism Trial may be ascribed to a synergistic effect with urokinase of heparin administered during the diagnostic work-out. The indications of heparin and urokinase should be evaluated in the light of these results.