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)

The author report the case of a 48 years old patient, admitted to hospital 3 hours and a half after an anterior myocardial infarct which was well tolerated. Coronary recanalization with urokinase-plasminogen removed the obstruction of the middle part of the anterior interventricular artery 1 hour and a half after the patient's arrival. Selective left coronary angiography demonstrated a narrow stenosis, in the order of 98%, in the proximal part of the AIV artery. Angioplasty was attempted immediately, in view of the ease with which the guide wire was passed through the initial thrombosis and the good haemodynamic tolerance. The residual stenosis was estimated to be 20% after the angioplasty and at the examination 48 hours later. The ECG on discharge from hospital showed a QS appearance in V1 to V3 with R in V4. An improvement in the ejection fraction (EF) and in the end-diastolic volumes was found: EF: 48% compared to 38%, EDV (cc/m2): 79 compared to 120. The clinical course at two months is very satisfactory, with no residual angina and a negative stress test. This special procedure, combining a double therapeutic catheterization, lasted 1 hour 50 minutes and allowed the progression of the myocardial infarction to be halted and also avoided a subsequent aorto-coronary graft operation.
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PMID:[Coronary angioplasty immediately after coronary recanalization in the acute phase of myocardial infarct]. 622 68

Early postinfarction angina implies an unfavorable prognosis. Most published information on this outcome represents data collected in the prethrombolytic era, in which definitions and populations differed considerably. Our purpose was to evaluate the incidence and importance of recurrent ischemia after administration of thrombolytic therapy. We studied patients enrolled in the Thrombolysis and Angioplasty in Myocardial Infarction studies. Patients were enrolled into 5 studies with similar entry criteria; 552 patients were treated with tissue plasminogen activator (t-PA), 293 were treated with urokinase, and 385 received both thrombolytic agents. Recurrent ischemia was defined as symptoms in association with electrocardiographic changes; reinfarction was defined as a reelevation of creatine kinase myocardial band isoenzyme in an appropriate clinical setting. Both recurrent ischemia and reinfarction occurred in 42 patients (3.4%), recurrent ischemia alone occurred in 226 (18%), whereas neither occurred in 964 (78%). Although baseline characteristics were similar among the 3 groups, in-hospital cardiac events (total 73 deaths, 253 heart failure episodes) were not: in-hospital mortality in patients with reinfarction was 21%; with recurrent ischemia, 11%; and with neither event, 4% (p < 0.0001). The in-hospital heart failure rate of patients with reinfarction was 50%; with recurrent ischemia alone, 31%; and with neither event, 17% (p < 0.0001). As expected, median in-hospital costs were highest in patients with reinfarction ($26,802), intermediate for those with recurrent ischemia alone ($18,422), and lowest in patients with neither event ($15,623). Recurrent myocardial ischemia after thrombolytic therapy is a frequent, important, and expensive adverse clinical outcome, making it a critical target for therapeutic intervention.
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PMID:Frequency, significance, and cost of recurrent ischemia after thrombolytic therapy for acute myocardial infarction. TAMI Study Group. 748 52

This study was designed to determine the safety and efficacy of extended, continuous infusion of urokinase plus stent deployment to treat older saphenous vein bypass grafts obstructed by both thrombus and atheromatous material. Thirty patients with angiographic evidence of thrombus and atheromatous material obstructing older vein grafts (mean age 8.3 years) underwent the combined interventions of urokinase infusion and stent deployment. The continuous infusion of urokinase was administered directly into each obstructed vein graft over a mean of 20.5 +/- 8.1 hours (median dose 2.2 +/- 0.7 million units). Stents were deployed at the sites of atheromatous obstruction either before (5 patients) or after (25 patients) infusion of urokinase. Twenty-eight of the 30 patients were successfully treated with the combined interventions (success rate 93.3%). In these 28 patients, percent diameter stenosis at the site of obstruction decreased from 86.0% to -0.2% and Thrombolysis in Myocardial Infarction trial flow increased from 1.0 to 2.5. Two patients (6.7%) developed stent thrombosis followed by myocardial infarction (1 with Q-wave infarction, 3.3%) and congestive heart failure. Minor complications included non-Q-wave myocardial infarction (5 patients, 16.7%) and access-site hemorrhage (5 patients, 16.7%). At 2-week follow-up, anginal symptoms were decreased in all 28 successfully treated patients. At 7.2 +/- 3.7-month follow-up, 5 of the 28 successfully treated patients (17.9%) had reacceleration of angina and angiographically documented restenosis at the site of stent deployment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety and efficacy of extended urokinase infusion plus stent deployment for treatment of obstructed, older saphenous vein grafts. 757 53

The degree of platelet activation and damage in 15 cases with acute myocardial infarction (AMI) receiving thrombolytic therapy and 15 cases with AMI receiving anticoagulant therapy were studied in vivo and in vitro by using specific monoclonal antibodies (SZ-51 & S12) against alpha-granule membrane protein 140 (GMP-140). Clinical indexes and myocardial enzyme changes in the two groups of patients were also observed. The results showed that the number of GMP-140 molecules on platelet surface and the concentration of GMP-140 in plasma were increased before treatment. The number of GMP-140 molecules on platelet surface began to decrease on the 1st day and returned to baseline on the 7th day after treatment. The concentration of GMP-140 in plasma reached a peak on the 1st day, began to fall on the 2nd day and returned to baseline on the 3rd day after treatment. There were no significant differences in the dynamic changes of number of GMP-140 molecules on platelet surface and the concentration of GMP-140 in plasma between groups of thrombolytic therapy and anticoagulant therapy. In vitro experiment showed that the thrombolytic medicine urokinase neither activated platelets nor inhibited platelet activation induced by thrombin. Significantly greater reperfusion rate and earlier appearance of CK and CK-MB peaks were found in the thrombolytic than in the anticoagulant group. LVEF determined by echocardiography, rate of return of ST segments to baseline and alleviation rate of chest pain were significantly greater and complications of AMI (ventricular fibrillation, left ventricular failure and angina) were less in the group receiving thrombolytic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Dynamic observation of alpha-granule membrane protein 140 during the treatment of thrombolytic and anticoagulant therapy in patients with acute myocardial infarction]. 758 6

Patients with aged saphenous vein grafts and recurrent symptoms of angina are being seen with increasing frequency [Bourassa: J Am Coll Cardiol 17:1081-1083, 1991]. The treatment of these patients remains a dilemma. Direct balloon angioplasty is frequently complicated by distal embolization and early restenosis [Aureran and Gruentzig: Am J Cardiol 53:953-954, 1984]. There is evidence that thrombus plays a significant role in this occlusive process [Hartmann et al.: J Am Coll Cardiol 18:1517-1523, 1991]. Prolonged intragraft urokinase infusion with a new multiside hole infusion catheter debulks thrombus and permits balloon angioplasty without the usual complications.
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PMID:Prolonged intragraft urokinase with a new infusion wire: improved short-term results. 814 30

To resolve the question of whether coronary thrombolysis for acute myocardial infarction is more effective in patients with or in those without chronic preinfarction angina, we retrospectively analyzed cineventriculograms in 54 patients with the first anterior Q-wave myocardial infarction during the chronic stage of myocardial infarction. Patients were divided into 2 groups according to the presence (group A, n = 24) or absence (group B, n = 30) of chronic preinfarction angina. In group A, 16 had either intracoronary (n = 6) or intravenous (n = 10) coronary thrombolysis with urokinase within 6 h after the onset of acute myocardial infarction. In group B, 11 had either intracoronary (n = 4) or intravenous (n = 7) coronary thrombolysis within 6 h after the onset of acute myocardial infarction. Global left ventricular ejection fraction and regional wall motion in infarct areas were evaluated quantitatively. In group A, the percentage of systolic segment shortening in infarct areas was 20 +/- (SD) 16% in patients with thrombolytic therapy and 17 +/- 15% in those with conventional therapy (p = NS). By contrast, in group B, the regional wall motion in infarct areas was significantly (p < 0.01) better in patients with thrombolytic therapy compared to those with conventional therapy (13 +/- 10 vs. 3 +/- 8%). Thus, patients without chronic preinfarction angina might benefit from coronary thrombolysis, while in those with preinfarction angina the beneficial effect of thrombolytic therapy may be relatively limited.
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PMID:Comparative efficacy of thrombolytic therapy for acute myocardial infarction in patients with and without chronic preinfarction angina. 826 93

A 72-year-old female, who had received medication for hypertension and angina pectoris was hospitalized with complaining of an abrupt dyspnea. Roentgenogram of the chest revealed no abnormal findings except cardiac enlargement. An electrocardiogram showed overloading of the right ventricle. Arterial blood gas analysis of room air showed 55.4 mmHg of PaO2, 25.5 mmHg of PaCO2 and 7.30 of PH, respectively. Acute and massive pulmonary embolism was diagnosed by an emergent pulmonary arteriography. Despite intensive treatment such as infusion of urokinase and heparin for four days, thrombus was still detected in the left main pulmonary artery by a transesophageal echocardiography. By the result of ineffective conservative therapy, embolectomy was performed under cardiopulmonary bypass. However mechanical respiratory support was required for a long time due to the right heart failure, she is doing well for a year after the operation.
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PMID:[Acute massive pulmonary embolism--report of a case]. 845 37

Balloon dilation of saphenous vein graft (SVG) occlusions has a lower success rate than angioplasty of native coronary arteries. To improve this outcome, a new therapy for chronic total SVG occlusions was developed. In three aortocoronary bypass graft patients with class III-IV angina and chronic occlusion of the SVGs to the left anterior descending artery (age of occlusions: 2-24 wk, age of graft 1-13 yr), standard recanalization was achieved with a guide wire and intracoronary urokinase infusion (0.5-1.0 million unit bolus followed by 100,000 IU/hr for 11-24 hr; mean infusion time: 19.7 hr). In each patient, a residual focal stenosis (average 82.5%) was successfully dilated and stented (single 4.0 mm Palmaz-Schatz in two patients and a 3.5 mm Strecker stent in the other). All patients had complete relief of symptoms and no sequelae. During a mean 7.7 mon follow-up, 6-mon arteriographic evaluation in two patients showed minimal intra-stent narrowing (26% and 34%). In the Strecker stent patient, the device proved too small for the vein graft, leading to an 89% stent stenosis found on follow-up arteriography at 5 mon. The stent was redilated successfully with a 5% residual narrowing. After urokinase recanalization of chronic total SVG occlusions, intravascular stents may improve the long-term results seen with conventional SVG angioplasty.
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PMID:New treatment approach for chronic total occlusions of saphenous vein grafts: thrombolysis and intravascular stents. 849 75

Coronary spasm was observed in two sisters. Neither of them had significant atheromatous stenosis in the coronary arteries. The 41-year-old elder sister presented with resting morning angina. The stress electrocardiogram showed marked depression of the ST-segment in precordial leads. Diffuse vasospasm in the left anterior descending artery was induced by the intracoronary administration of acetylcholine. The 38-year-old younger sister suffered from acute inferior myocardial infarction after taking methylergonovine following an abortion. Emergent coronary angiography disclosed a thrombus in the proximal right coronary artery which was dissolved with intracoronary administration of urokinase. There was no residual stenosis in the culprit vessel. Although the sisters do have risk factors for coronary spasm, an inherited factor may contribute to the mechanism of the spasm.
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PMID:Coronary spasm in two sisters. 851 Mar 17

It has been suggested that leukocyte adhesion mechanisms play a key role in experimental myocardial infarction. We have recently shown that E-selectin, an adhesion molecule belonging to the selectin family, is involved in the pathogenesis of experimental myocardial ischemia. We investigated the circulating levels of E-selectin, studied as a marker of endothelial dysfunction, in acute myocardial infarction. Our study was carried out in 60 patients, 20 hospitalized for acute myocardial infarction, 20 suffered from angina pectoris and 20 healthy control subjects. Patients with acute myocardial infarction had increased serum levels of soluble E-selectin (sE-selectin = 255 +/- 12 ng/ml) compared to both patients with angina pectoris (sE-selectin = 51 +/- 14 ng/ml). Thrombolytic therapy with urokinase (1,000,000 IU as an intravenous bolus in 5 min, followed by producing reperfusion and reduced the serum levels of sE-selectin (71 +/- 19 ng/ml). Our results confirm previous experimental data and indicate that adhesion mechanisms supporting leukocyte-endothelium interaction may also be operative in human acute myocardial infarction.
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PMID:Soluble E-selectin levels in acute human myocardial infarction. 865 56


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