Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Data on the feasibility, safety, and clinical outcome of intracoronary stenting in acute myocardial infarction (AMI) are limited. This study examined the immediate angiographic results and the early and late outcomes in 32 patients who had stenting during AMI. Coronary angiograms recorded at the time of stenting were reviewed with quantitative measurements obtained on the "target" coronary lesion before and after stenting. Immediate angiographic success was achieved in 30 patients (94%). The minimal luminal diameter increased from 0.36 +/- 0.37 to 2.58 +/- 0.41 mm (p<0.0001). Two patients died in the hospital. Of the remainder, none had reinfarction or required bypass surgery, whereas 2 required repeat coronary angioplasty for recurrent ischemia. Although thrombus at the infarct-related coronary lesion was initially detected in 41% of the patients, its presence was not associated with adverse procedural outcome. Only 1 patient had persistent thrombus after stenting, which resolved with intracoronary urokinase. At a mean follow-up of 6.1 +/- 4.1 months, there was 1 additional cardiac death, and no patient had AMI or required repeat coronary angioplasty or bypass; among the 29 survivors, 86% were free of angina. Thus, intracoronary stenting of the infarct-related artery in the setting of AMI is associated with excellent immediate angiographic success and a favorable clinical outcome, and remains an option even in the presence of thrombus.
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PMID:Usefulness of intracoronary stenting in acute myocardial infarction. 871 34

Recently occluded saphenous vein grafts (SVG) contain abundant thrombus. Distal embolization and myocardial infarction often occur when recanalization of such SVG is attempted. In 80 patients with occluded SVG, we employed transcatheter devices to lyse, compress or extract thrombus. Primary treatment for these SVG was performed in the following manner; PTCA 29, intragraft urokinase 12, TEC atherectomy 39. Following urokinase or atherectomy, adjunctive PTCA was performed to diminish the residual stenosis. All patients had class III or IV angina. Clinically, SVG occlusions were 3 days to 3 months old. TIMI flow was grade 0, and occlusion length was greater than 6 cm for all SVG. Each strategy resulted in a similar procedure success rate. However, when used as a primary treatment, TEC may be associated with lower rates of distal embolization and myocardial infarction.
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PMID:PTCA, thrombolysis or atherectomy: rational treatment of recently occluded saphenous vein grafts. 871 2

This report describes the successful treatment of totally occluded aortocoronary saphenous vein grafts with percutaneous transluminal extraction atherectomy (TEC) in three patients with severe angina and high reoperative surgical risk. The method presented here may provide an alternative to overnight urokinase infusion or repeat surgery in high risk patients.
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PMID:Extraction atherectomy for the recanalization of totally occluded aortocoronary saphenous vein grafts. 871 87

Patients with coronary artery disease and severe angina pectoris refractory to conventional medical treatment (beta blockers, nitrates, calcium antagonists) and without the option for invasive revascularization procedures represent an increasing clinical problem. For these patients, chronic-intermittent urokinase therapy has been developed. Twenty patients received 500,000 IU urokinase as intravenous bolus injection 3 times a week over a period of 12 weeks. The average reduction in anginal symptoms in 19 patients was 74%, from 23.5 +/- 10.8 to 5.2 +/- 4.8 events/week (p < 0.001); 1 patient was excluded from further treatment because of an increase of > 66% in anginal events. Fibrinogen decreased by 34% from 370 +/- 57 to 244 +/- 44 mg/dl (p < 0.001), the rheological parameters plasma viscosity by 6.1% from 1.39 +/- 0.04 to 1.31 +/- 0.03 mPas (< 0.001), and red blood cell aggregation by 18% from 13.9 +/- 2.4 to 11.2 +/- 2.2 (p < 0.001). Exercise tolerance increased by 51%. Average ST-segment depression decreased from 0.16 +/- 0.10 to 0.12 +/- 0.09 (p < 0.01). After 12 weeks of follow-up, angina pectoris and fibrinogen levels were still significantly reduced compared with baseline values. Chronic-intermittent urokinase therapy represents an effective anti-ischemic and antianginal approach in patients with refractory angina pectoris and end-stage coronary artery disease. Improvement of rheological blood properties and thrombolytic effects are likely therapeutic mechanisms.
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PMID:Chronic-intermittent urokinase therapy in patients with end-stage coronary artery disease and refractory angina pectoris--a pilot study. 882 21

The aim was to investigate circulating E-selectin and Intercellular Adhesion Molecule-1 (ICAM-1) in acute myocardial infarction. Our study was carried out in 80 patients, 40 hospitalized for acute myocardial infarction (AMI), 20 suffering from chronic stable angina and 20 healthy control subjects. Samples of venous blood were taken from all patients at the moment of hospitalization and after 2, 4, 6, 8, 10, 12 and 24 hours from the thrombolytic treatment (AMI + urokinase) or conventional therapy (AMI + nitroglycerin), for the dosage of creatinine kinase (CK) and adhesion molecules. The CK was determined by means of a Hitachi 901 automatic analyser using an enzymatic method (reagents Boheringer-Biochemia, Germany). Soluble E-selectin (sE-selectin) and soluble ICAM-1 (sICAM-1) were measured in the serum using a specific immunoassay (British Biotechnology Products). The serum levels of Tumor Necrosis Factor (TNF-alpha) were evaluated using an immunoenzymatic assay to quantitate the serum levels of the cytokine (British Biotechnology Products). Patients with acute myocardial infarction (AMI) had increased serum levels of soluble E-selectin (sE-selectin; AMI + urokinase = 312 +/- 20 ng/ml; AMI + nitroglycerin = 334 +/- 15 ng/ml) and soluble ICAM-1 (sICAM-1; AMI + urokinase = 629 +/- 30 ng/ml; AMI + nitroglycerin = 655 +/- 25 ng/ml) compared to both patients with chronic angina (sE-selectin = 67 +/- 10 ng/ml; sICAM-1 = 230 +/- 20 ng/ml) and healthy control subjects (sE-selectin = 53 +/- 15 ng/ml; sICAM-1 200 +/- 16 ng/ml). Furthermore patients with acute myocardial infarction also had increased serum levels of Tumor Necrosis Factor (TNF-alpha = 309 +/- 10 pg/ml; control subjects = 13 +/- 5 pg/ml). Thrombolytic therapy with urokinase (1,000,000 IU as an intravenous bolus for 5 minutes, followed by an infusion of an additional 1,000,000 IU for the following two hours) succeeded in producing reperfusion and reduced the serum levels of sE-selectin (52 +/- 13 ng/ml) and sICAM-1 (202 +/- 31 ng/ml). In contrast patients not eligible for thrombolytic therapy and therefore treated with conventional therapy (a continuous i.v. infusion of nitroglycerin at the dose of 50 mg/die) did not show any significant reduction in both sE-selectin and sICAM-1 throughout the study. 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:Thrombolytic therapy with urokinase reduces increased circulating endothelial adhesion molecules in acute myocardial infarction. 882 73

Besides the thrombolytic therapy several adjuvant therapeutic measures were identified which significantly improve the prognosis of patients with acute myocardial infarction (AMI). These measures include the treatment by means of acetylsalicylic acid (ASA), beta-blockers and ACE inhibitors. Early administration of ASA and beta-blockers are indicated in all patients with AMI who have no contraindications for this therapy. They are especially the patients with manifest heart failure or asymptomatic left ventricular dysfunction who benefit from ACE inhibitors. The effectivity of routine administration of other medicaments such as anticoagulants, nitrates, calcium channel blockers and magnesium, have not been convincingly proved. However, some selected patients with AMI can benefit from these medicaments. Intravenous administration of heparin is unambiguously justified only in thrombolysis with t-PA. Thrombolyses with streptokinase, urokinase, and anistreplase are justified only at high risk of thromboembolic complications. Their prevention and therapy include also the necessity to restrict the administration of pelentan. The use of nitrates is indicated in patients with AMI in case of sustaining stenocardia, arterial hypertension and manifest heart left ventricular failure. Until the definitive standpoint is gained regarding the effect of magnesium in patients with AIM, its administration remains especially indicated in cases of arterial hypertension, tachycardiac disturbances of the heart rhythm and states of assumed or proved hypomagnesiemia. In AMI cases when magnesium is used in order to protect the patient from reperfusion lesion, it must be administered prior to the reperfusion therapy. An intensive research in the field of therapeutical measures in patients with AMI still continues. It is certain that it will soon bring further knowledge which will in turn improve the prognosis and quality of life of patients with AMI. (Tab. 4, Ref. 133.)
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PMID:[Adjuvant therapy in patients with acute myocardial infarct]. 892 11

Interventions that modify lipid metabolism and blood coagulation have been shown to favourably influence the natural course of coronary artery disease in terms of the primary prevention and treatment of acute cardiovascular events. Various findings suggest that such interventions may also preserve and enhance myocardial perfusion in the chronic stage of the disease. Long-term intermittent urokinase therapy was developed for patients with end-stage coronary artery disease and refractory angina pectoris. A dose of 500,000 IU of urokinase given intravenously as a bolus three times a week for of 12 weeks reduced symptoms by 70% and was accompanied by objective improvements in myocardial perfusion and an increase of ergometric exercise capacity. The possible therapeutic mechanisms of long-term intermittent urokinase therapy-improvement of rheological blood properties mediated by fibrinogen reduction, thrombolysis of non-occlusive subclinical thrombi, and regression of atherosclerotic plaques-are discussed in the context of other antithrombotic approaches.
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PMID:Antithrombotic treatment in stable coronary syndromes: long-term intermittent urokinase therapy in end-stage coronary artery disease and refractory angina pectoris. 903 88

Apart from the relevance of disorders of lipid metabolism for the clinical and morphological progression of coronary artery disease, coronary thrombosis has received increasing attention in recent years. It is undoubtedly the decisive factor in the pathogenesis of acute coronary syndromes, which is underlined by the therapeutic success of various antithrombotic interventions. Furthermore coronary thrombosis is regarded to be a key factor for morphological disease progression also in stable coronary syndromes, which eventually may lead to critical limitation of myocardial perfusion. This is caused by the formation of subclinical coronary thrombi, which either undergo endogenous lysis or become morphologically fixed as they are incorporated into the plaque. Besides local factors, systemic disturbances of hemostasis and endogenous thrombolysis are of relevance. The concept of thrombotic progression of coronary thrombosis is supported by data on the reduction of morphological disease progression or antiischemic effectiveness of anti-thrombotic interventions like aspirin, low-molecular weight heparin and low-dose intermittent urokinase therapy. Percutaneous transluminal coronary angioplasty results in deep mechanical injury of the vessel wall, which is accompanied by secondary coronary thrombosis in the majority of the cases, not necessarily leading to abrupt vessel closure. Particularly, dilatation of primary thrombus as it has been described as the substrate of the culprit lesion in unstable coronary syndromes, promotes release of thrombin and activation of platelets, which in turn furthers the proliferative processes in the pathogenesis of restenosis. Even though data on the reduction of the rate of restenosis by the use of platelet aggregation inhibitors like aspirin, ticlopidin and dipyridamole have not consistently supported this concept, the EPIC. Study has shown that even in patients with stable angina pectoris clinical restenosis rate may be reduced by a platelet-IIb/IIIa-antagonist.
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PMID:[Significance of coronary thrombosis for chronic myocardial ischemia]. 917 23

Long-term intermittent urokinase therapy has been developed for patients with severe coronary artery disease and refractory angina pectoris. This therapeutic approach is predominantly effective at the microcirculatory level based on a combination of rheologic and fibrinolytic effects; furthermore, plaque regression seems to be a possible mechanism. Patients with refractory angina pectoris are characterized by severe coronary artery disease without a therapeutic option for conventional revascularization procedures, only slight impairment of left ventricular systolic function and hyperfibrinogenemia, which results in further enhancement of myocardial ischemia due to microcirculatory impairment of blood flow. In this article data on the anti-ischemic effectiveness as well as first results on the impact of this therapeutic approach on hemodynamics are described. A dose-response study, which compared 3 x 50,000 IU with 3 x 500,000 IU urokinase three times a week over a treatment period of 12 weeks demonstrated subjective as well as objective antiischemic effectiveness. Only patients who were treated with 500,000 IU per injection achieved marked increases in exercise capacity, while some patients in the low-dose group presented even with a deterioration of exercise performance. First hemodynamic studies could not show marked changes of systolic parameters, either at rest or during exercise. But a decrease of pulmonary capillary wedge pressure at rest after treatment with 500,000 IU per injection indicates an improvement of diastolic function as a result of enhanced myocardial perfusion. Echocardiographic measurements of transmitral Doppler flow in 21 patients with end-stage coronary artery disease demonstrated normalization of early and late diastolic filling rates in most cases. These changes were accompanied by a reduction of clinical signs of heart failure. Long-term intermittent urokinase therapy is a valuable approach as it not only improves quality of life during the actual treatment period but by the persistence of therapeutic effects following the cessation of therapy.
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PMID:[Chronic intermittent urokinase therapy: anti-ischemic and hemodynamic effects]. 917 24

Symptomatic end-stage arterial disease in coronary artery or peripheral arterial occlusive disease represents an increasing clinical problem as cardiovascular mortality in these patient groups has declined due to improved secondary prevention. While in peripheral arterial occlusive disease amputation with subsequent life-long physical disability is the major problem, patients with end-stage coronary artery disease and refractory angina pectoris repeatedly report to the emergency ward with the clinical symptoms of unstable coronary syndromes, but myocardial infarction is generally ruled out. For these patients long-term intermittent urokinase therapy has been developed as an alternative treatment modality. Potential mechanisms for clinical effectiveness include improvement of rheological blood properties, thrombolysis of non-occluding arterial thrombi and possibly plaque regression. In coronary artery disease urokinase is applied as an intravenous bolus injection of 500,000 IU urokinase three times a week over a period of 12 weeks. This leads to a marked reduction of fibrinogen by about 35% and of clinical symptoms by around 70% accompanied by a reduction of exercise-induced myocardial ischemia. In observational studies in patients with peripheral arterial occlusive disease injections of 500,000 IU of urokinase were usually given daily for a shorter time period of three to four weeks with a clinical success rate, defined as a cessation or marked reduction of rest pain and/or salvage of a limb, of around 50%. Given the state of critical ischemia in both entities of atherosclerotic disease, long-term intermittent urokinase therapy represents a promising antiischemic approach. In particular in patients with peripheral arterial occlusive disease randomized controlled trials with prolonged treatment periods, which are likely to improve clinical results, are warranted.
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PMID:Low-dose intermittent urokinase therapy in chronic symptomatic end-stage arterial disease--clinical relevance for patients with coronary artery disease or peripheral arterial occlusive disease. 918 59


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