The white clot syndrome or heparin associated thrombocytopenia and thrombosis (WCS or HATT) (26 cases).

The Authors report a new iatrogenic complication of preventive or curative standard heparinotherapy. This so called "white clot syndrome" or "Heparin associated thrombocytopenia and thrombosis" is an anatomico-clinical entity characterized by severe, multiple, recurrent, arterial and/or venous thromboembolic accidents which are sometimes fatal. They appear, paradoxically, under heparin treatment and are concomitant with thrombocytopenia (generally less than 100 10(9)/l). Antiplatelet immunoallergic phenomena, via type IgG antibodies, induced by heparin, are the most commonly admitted in physiopathology; however they remain controversial. Treatment of "WCS" includes urgent suppression of standard heparin, administration of antivitamin K, or the new generation of low molecular weight heparin. This series presents 26 cases of HATT treated by LMWH (CY 216 CHOAY). Severe complications must be surgically cured. Prevention of WCS or HATT is mandatory by the systematic survey of platelet count during heparinotherapy.

[Treatment of acute pulmonary embolism with urokinase compared with the combination plasminogen-urokinase. Apropos of 67 cases]. / Traitement de l'embolie pulmonaire aiguë par urokinase comparée à l'association plasminogène-urokinase. A propos de 67 cas.

Sixty-seven patients with recent acute pulmonary embolism (within 5 days) and an angiographic deficit of over 30% were included in a randomised study designed to compare the efficacy of the associations of urokinase-heparin (Group I) and lysyl-plasminogen-urokinase-heparin (Group II). Plasminogen was administered as an intravenous bolus of 150 microkatal units at the beginning of the urokinase infusion, the dosage of which was set at 2 700 000 IU over 24 hours. Both groups received anticoagulant doses of heparin. The efficacy of treatment was judged by early revascularisation on pulmonary angiography performed during the 24 hours after the end of treatment and by changes in the parameters of fibrinolysis and its inhibitors. The clinical features of the two groups were comparable but the angiographic changes were more pronounced in Group I (deficit: 68.5 +/- 10.4% vs 62.3 +/- 10.9%, p less than 0.02). Treatment had to be stopped before the 24th hour in 4 cases (3 early deaths and 1 severe haemorrhage). The average revascularisation was 30.5 +/- 6.8% in Group I and 38.3 +/- 31.1% in Group II (NS). The alpha-2-antiplasmins were lower (NS) in Group II as were the fibrinogen levels (p less than 0.01 at the 12th and 24th hour) whilst the plasminogen levels and surface of fibrin plateaux were higher (p less than 0.01 at the 6th hour and p less than 0.05 at the 12th hour, respectively). These results show that moderate doses of urokinase associated with heparin are effective in the treatment of acute pulmonary embolism.(ABSTRACT TRUNCATED AT 250 WORDS)

[Treatment by urokinase of myocardial infarction and threatened infarction. Randomised study of 120 cases]. / Le traitement par l'urokinase des infarctus du myocarde et syndromes de menace. Etude randomisée de 120 cas]

Two randomized series of 60 cases of myocardial infarction or menace syndrome have been treated at the acute stage, one by Heparin alone, the other by the combination Urokinase-Heparin. The average dosage was 300 mg Heparin in the first series, of 2,700,000 CTA units of Urokinase combined with 240 mg of Heparin in the second series. After the first 24 hours, equal heparinization was performed in both series up to the third week. Significantly different results were obtained in the two series. They favour Urokinase and concern: -- the disappearance time of pain, -- the course of the arrhythmias and of cardiac failure, -- the regression or limitation of the necrosis q waves and the lesion areas on the electrocardiogram. Finally the 30th-day overall mortality was 13% in the Heparin series and 3% in the myocardial infarction on the way of constitution, or which have done so for less than 24 hours.