Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
 10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six cases of post-embolic chronic cor pulmonale are presented. All six were treated with thrombolytic agents (4 with streptokinase, 2 with urokinase), and in only one case was improvement maintained at the end of one year. Two patients underwent a disobliterative procedure of the pulmonary artery, together with ligation of the inferior vena cava. One of these operations was unsuccessful, and the other had a successful outcome, as confirmed by objective assessment with angiography, scintigraphy and haemodynamic studies. The literature is reviewed at this stage. It was found that the fibrinolytic agents had some chance of working only if the condition was less than a few months old. One major drawback to surgical disobliteration that cannot be foreseen before operation is the presence of thromboses at the arteriolar level in subjects whose main arteries are already blocked proximally. Nervertheless it is possible to obtain good results by surgery, and the operation is worth attempting in young subjects, given the poor prognosis of the untreated condition.
Arch Mal Coeur Vaiss 1975 Nov
PMID:[Chronic pulmonary artery thrombosis. Therapeutic modality. Apropos of 6 cases]. 81 83

The effects of thrombolytic therapy in acute myocardial infarction are related exclusively to coronary arterial reperfusion. This is the main factor which influences myocardial salvage, the conservation of left ventricular function and, ultimately, the reduction in mortality. From the beginning of the 80s, the patency (or reperfusion) rate was arbitrarily assesses at 90 minutes. However, arterial reperfusion is a progressive phenomenon and the patency rate in a population of acute myocardial infarctions varies with time. Depending on the thrombolytic agent and the rate of administration, the patency increases at a variable rate attaining a plateau at the 4th-6th hour, the maximal patency being obtained between the 24th to the 48th hour. Therefore, assessing patency at the 90th minute of thrombolytic therapy is an approximate and relatively inaccurate method of assessing the efficacy of a given thrombolytic agent. When evaluating a thrombolytic drug administered at a certain dosage, the rate of reperfusion and the value and precocity of the plateau phase must be taken into account. The respective performances of different thrombolytics in terms of arterial patency are comparable. Nevertheless, the rate of reperfusion with Streptokinase given at the dose of 1.5 million i.v. in 60 minutes is lower than that obtained with more recent thrombolytic drugs. Streptokinase also appears to be less active on chronic thrombi. The late patency rate after the 24th hour is over 90% with nearly all thrombolytic drugs but it would seem to be less with rt-PA because of a higher reocclusion rate associated with this particular agent. The study of reocclusion requires control coronary angiography between the 24th and 72nd hour (7th day in some studies). The prevalence of this complication is influenced by several factors, especially the severity of residual stenosis after thrombolysis and the grade of perfusion obtained after the treatment: secondary reocclusion is significantly lower with long-acting and non-fibrin specific thrombolytic agents. It is approximately 2 to 5% with APSAC, Streptokinase and pro-urokinase, and two to three times greater with rt-PA. Finally, the use of more powerful antiplatelet drugs than those currently available and of specific anti-thrombin agents could reduce the rate of secondary reocclusion. Associations of thrombolytic agents, the development of thrombolytic chimera and new thrombolytic molecules could improve the efficacy of thrombolytic therapy in terms of capacity of reperfusion and tolerance, especially with respect to haemorrhagic complications.
Arch Mal Coeur Vaiss 1992 May
PMID:[Arterial permeability, objective of thrombolytic therapy]. 153 Apr 9

Five thrombolytic agents have been used in the acute phase of myocardial infarction: streptokinase, recombinant tissue plasminogen activator (rt-PA) and its acyl enzyme (APSAC), urokinase and pro-urokinase. Experience with the latter two agents is much more limited. The antigenicity, biological half-life, fibrino-specificity and cost are important parameters to be taken into account when choosing a therapeutic agent. The doses expressed in different units or in milligrams vary with the product used. Large scale clinical trials have not shown improved efficacy of new thrombolytic agents. The role of associated treatments, aspirin and/or heparin and their respective doses, the timing of their administration are also important elements in the evaluation of efficacy judged by the frequency of coronary recanalisation and early reocclusion. The haemorrhagic risk is difficult to assess and seems more related to heparin therapy than the prescription of aspirin. Mutants of rt-PA obtained by genetic engineering and other new thrombolytics are currently under evaluation to try and obtain new, more effective and safer thrombolytic agents.
Arch Mal Coeur Vaiss 1992 May
PMID:[Elements of choice of thrombolytic agents in myocardial infarction]. 153 Apr 14

The early intravenous administration of thrombolytic agents in the acute phase of myocardial infarction induces reperfusion of the artery responsible for the necrosis, thereby limiting the size of the infarct and preserving the left ventricular systolic function with consequent reduction of short- or long-term mortality. With the exception of urokinase, these effects have been demonstrated with all thrombolytic agents used so far, including streptokinase, plasminogen tissue activator and anistreplase. Owing to its special pharmacokinetic properties, the latest thrombolytic agent, formerly known as APSAC (anisoylated plasminogen streptokinase activator complex), provides a high arterial reperfusion rate with a low percentage of reocclusion. As a result, the mean size of the infarct is reduced by 31 per cent (36% in the case of anterior infarct), and the left ventricular systolic function is highly significantly preserved.
Arch Mal Coeur Vaiss 1990 Feb
PMID:[Effect of thrombolytic agents on infarct size and left ventricle systolic function in myocardial infarction]. 210 44

The records of 5 neonates with systemic arterial thrombosis (aortic in one case, peripheral in four cases) were reviewed. Fibrinolysis was performed with urokinase administered by infusion (1,000 to 4,000 U/kg/h). This treatment was combined with heparin therapy in 4 cases. Thrombosis was due to various causes: umbilical arterial catheter (1 case), disorders of supraventricular rhythm in utero (1 case), aneurysm of the ductus arteriosus with dysplastic aortic arch vessels (2 cases); one of these patients also had myocardiopathy. No cause could be found in a premature child weighing 1,300 g. The presenting symptoms of systemic arterial thrombosis are ischaemia of the extremities and suppression of peripheral pulses; heart failure with arterial hypertension is frequent. In our series the diagnosis was confirmed by doppler-ultrasonography in one case and by angiography in three cases (angiography in the left ventricule with foramen ovale, or umbilical aortography). Treatment with urokinase lasted 1.5 to 7 days. In 2 children the initial dosage had to be increased as there was no clinical improvement. Four children were completely cured; the fifth child, who had left renal thrombosis, shows slight functional impairment of the left kidney. There were no haemorrhagic complications. The fibrinolytic treatment with urokinase of systemic arterial thrombosis in the newborn is effective and has few drawbacks.
Arch Mal Coeur Vaiss 1989 May
PMID:[Treatment with urokinase of systemic arterial thrombosis in the newborn infant]. 250 Jan 1

MATERIALS AND METHODS Between 1981 and 1985, 78 iliocaval thrombi were treated by aggressive therapy: 52 surgical thrombectomies were performed by a femoral approach associated, depending on the case, with a caval approach; and 26 iliofemoral thrombi were lysed according to a protocol in which urokinase and plasminogen were used over a 48-h period. Subsequent functional evaluation was based on clinical scoring (0 to 9 points) taking into account functional impairment, edema and trophic disorders. Patency of trunks and the deep valvular state were assessed by Doppler examination and plethysmography. RESULTS In the surgical group, 3 early deaths occurred, only one of which could be attributed to an embolic course. Six weeks after surgery the rate of recurrence of iliac thrombosis was 50% (25% postoperative + 25% secondary). Beyond this period, there were no recurrences of thrombosis. There was a direct, statistically significant relation between the degree of iliac patency and the realization of an ideal thrombectomy on a nonadherent fresh clot. The functional results, assessed after four and a half years of follow-up, are satisfactory (score less than 3) in 80% of patients. The poor results with venous claudication or varicose ulcer all occurred in the case of massive persistent thrombi of the femoral confluence. Valve lesions were signaled in 46% of patients by a massive backflow in orthostatism. In the medical group, a major hemorrhagic complication occurred under urokinase therapy in 11% of patients, including one for whom it was fatal. Sixty percent of patients showed immediate radiological improvement allowing partial or total freeing of a venous confluence. The functional results after 4 years of follow-up were nondisabling in 85% of patients. No leg ulcers were detected. Late iliac patency was low (26%), whereas at the femoral level almost all of the thrombi which remained after lysis became patent again spontaneously. Valve failure was found in 37% of patients. Both groups had very similar late functional results despite rather different anatomical conditions. The iliac patency rate was higher in the surgical group (50% vs 26%), but plethysmographic study showed that in case of therapeutic failure devalvulation was greater after surgery (46% vs 37%).
J Mal Vasc 1989
PMID:[Thrombectomy or thrombolysis in the treatment of proximal phlebitis. Functional long term results]. 258 85

The purpose of this study is the retrospective evaluation of the treatment of 196 cases of pulmonary embolism. Therapeutic attitude was standardized. Intravenous heparin followed early on by oral anticoagulants remains the basic treatment of the majority of patients (74%). This treatment could be associated with: (1) Fibrinolysis with urokinase bolus at the time of massive pulmonary embolism with clinical and hemodynamic signs of shock (14%). No severe hemorrhagic complication was observed. 2) Inferior vena caval interruption in case of contraindications or failure of anticoagulation (29%). Only one death was observed in this study.
J Mal Vasc 1989
PMID:[Therapeutic approach to pulmonary embolism]. 277 95

The authors report a case of percutaneous dilatation of a coronary artery performed immediately after a mild myocardial infarction and complicated by occlusive thrombosis without dissection, despite a presumably effective anticoagulant treatment. A second dilatation resulted in rapid recanalization of the artery, but recurrent thrombosis developed at the site of dilatation. The thrombotic process was controlled with an intracoronary infusion of urokinase and higher doses of intravenous heparin, but only after a long delay (80 minutes). This case suggests that in similar circumstances one must wait long enough before referring the patient to a surgical unit for emergency aorto-coronary bypass.
Arch Mal Coeur Vaiss 1988 Mar
PMID:[Late effect of intracoronary urokinase. Apropos of a case of recurrent coronary thrombosis after angioplasty]. 296 26

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)
Arch Mal Coeur Vaiss 1986 Apr
PMID:[Treatment of acute pulmonary embolism with urokinase compared with the combination plasminogen-urokinase. Apropos of 67 cases]. 309 Sep 61

Seventy seven cases of severe pulmonary embolism (Miller index greater than 13 points) including 61 acute (under 5 days) and 16 subacute episodes, underwent continuous haemodynamic monitoring during treatment with either urokinase 2 000 U/kg/h for 24 hours with heparin (Group I: 18 patients), or urokinase 4 500 U/kg/h for 12 hours without heparin (Group II: 47 patients), or with streptokinase 2 00 000 U over 10 hours (Group III: 12 patients). Efficacy was defined as greater than 20% improvement of Miller index at control angiography after 48 hours (Group I: 10 patients, Group II: 31 patients, Group III: 8 patients). In the 49 patients (63%) with good results, the Miller index fell by about 50% with a significant increase in cardiac index (20%) from the 12th hour. There was a concomitant fall in pulmonary systolic arterial pressure (35%). In the 28 patients (37%) with partial improvement a 20% increase in cardiac index and an 18% fall in pulmonary systolic arterial pressure were observed only in the high dose urokinase group, despite incomplete pulmonary revascularisation demonstrating the vasodilator effect of this protocol. Fibrinolysis was repeated in the patients with incomplete results or a Miller index of over 13 points, leading to improvement in 78% of patients. Accelerated lysis of pulmonary embolism leads to rapid normalisation of haemodynamic parameters and improves the prognosis of massive pulmonary embolism by reducing the number of recurrences and the mortality rate (4%).
Arch Mal Coeur Vaiss 1986 Apr
PMID:[Hemodynamic course during fibrinolysis in severe pulmonary embolism]. 309 Sep 62


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