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)

Fibrinolysis has opened up a new avenue in the treatment of acute myocardial infarction (AMI). In principle, the rate of reperfusion depends on the type of compound used, the mode of administration and the time between onset of symptoms and the beginning of treatment. With intracoronary streptokinase the reperfusion rate is of the order of 85%. Intravenous urokinase administered as a bolus results in a reopening rate of 50-60%; a similar rate of reperfusion is achieved with rt-PA as infusion, while i.v. streptokinase produces about 50% reopened coronary vessels. The final infarct size is decreased in 70% of patients if fibrinolysis is initiated within 2.5 hours after the onset of symptoms and followed by reopening of the occluded vessel. This results in a lowering of in-hospital mortality, which in various studies is of the order of 45-60%.- Bearing in mind the contraindications, fibrinolysis should be initiated within 3 hours. Hemodynamic improvement by a decrease of infarct size may also be achieved beyond 3 hours in large anterior myocardial infarctions and in posterior infarctions with cardiogenic shock. Early initiation of thrombolysis is of major importance in improving left ventricular function and lowering mortality following acute myocardial infarction. Therefore, prehospital thrombolytic therapy should be considered. - In the postinfarction phase coronary angiography is indicated in patients with angina at rest, stable angina of ECG signs of ischemia. In this situation transfer to a specialized cardiology division for possible percutaneous transluminal angioplasty is indicated. - Reocclusion after successful thrombolysis occurs in 20-30%, and it is therefore important to avoid reinfarction to improve the long term prognosis after AMI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Fibrinolysis in acute myocardial infarct]. 332 20

The authors report a fifty-year-old woman with acute inferior myocardial infarction in whom left atrial mobile thrombus was found by echocardiography. They believe this to be the first echocardiographic documentation of such a thrombus after acute myocardial infarction. The combination of the stagnant flow in the left atrium due to atrial ischemia, the low output state due to left ventricular dysfunction, and the hemoconcentric tendency from use of diuretics might have played a role in the present thrombus formation. The thrombus was safely lysed without complication after intravenous urokinase.
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PMID:Transient left atrial mobile thrombus in acute myocardial infarction--a case report. 334 6

A 36-year-old man with thoracic outlet syndrome, admitted to the hospital with digital ischemia from subclavian artery thrombosis and distal embolization, was given intra-arterial urokinase. Thrombus in the subclavian artery was lysed successfully and peripheral emboli were partially cleared, resulting in relief of digital symptoms. Although surgical decompression and vascular reconstruction at the thoracic outlet may be necessary, this technique provides a means of recanalizing small distal vessels.
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PMID:Treatment of a case of thromboembolism resulting from thoracic outlet syndrome with intra-arterial urokinase infusion. 335 71

Human arteries and veins contract with hypoxia and deprivation of substrate provoked by increasing calcium inflow into the cell and reduced energy. Such spasm may be eliminated by phosphoenolpyruvate which loads up the cell's energy, blocking glycogen reduction at the same time. Reperfusion will then guarantee a sufficient energy stroke. Therapy should pursue the following steps: 1. Phosphoenolpyruvate infusion (1 X 10(-6) up to 1 X 10(-3) gm/ml in tyrodes solution pH 7.3) into the arterial branch, proximal and distal to the injury. 2. Subsequent treatment with vasodilating drugs and rheologically active substances. 3. Failed therapy after more than three hours warm ischemia could be due to autolytic processes and requires resection of the affected vessel. 4. The imbalance of the thrombolytic system with the so-called no reflow phenomenon could be due to a plasminogen activator's inhibitor released during hypoxia. Such cases may reasonably be treated by urokinase or by streptokinase plasminogen complex.
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PMID:[Vascular spasms in microsurgery]. 362 68

Since Ca++-overloading is a major problem after myocardial reperfusion we studied the effects of Diltiazem on the left ventricular diastolic function in the early days following coronary thrombolysis. Twelve patients who had myocardial reperfusion by intracoronary urokinase in acute myocardial infarction were admitted to the study. Previous infarct, cardiogenic shock or late thrombolysis (greater than 4 h from symptoms onset) were exclusion criteria. All subjects were evaluated at control cardiac catheterization 5-8 days after the acute ischemia. Simultaneous left ventricular angiography and high-fidelity pressure recordings by means of a tip-micromanometer and angiographic catheter were performed at rest and after intravenous Diltiazem administration (16 mg over 2' + 0.008 mg/Kg/min). Indexes of myocardial relaxation and early ventricular filling were impaired at rest but improved significantly after Diltiazem (Tab. II). Isovolumic relaxation period fell from 92 +/- 8 msec to 77 +/- 12 msec (p less than .01), T constant of isovolumic pressure decay decreased from 61 +/- 7 msec to 55 +/- 7 msec (p = ns), first-third of filling rate increased from 64 +/- 7% to 79 +/- 6% (p less than .01). On the other hand, indexes of left ventricular compliance were altered after coronary reperfusion (left ventricular end-diastolic compliance 17 +/- 13 mmHg-1. 10(-3), modulus of chamber stiffness .045 +/- .008) but but did not change after calcium-blocker therapy. In conclusion, post-thrombolysis diastolic function is severely impaired at rest, probably because of raised intracellular Ca++ and delayed asynchronous relaxation. Diltiazem improves energy-dependent early diastole, but does not affect ventricular compliance.
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PMID:[Hemodynamic effects of diltiazem in the subacute stage of myocardial infarct treated by thrombolysis]. 365 3

Sixty-two patients hospitalized for recent angiographically documented arterial occlusion in the legs (46 femoropopliteal arteries and 16 grafts) benefited from local fibrinolytic therapy delivered at the site of the occlusion with a No. 4F or No. 5F catheter. This therapy combined a continuous urokinase (UK) infusion of 1000 U/kg/hr and a lysyl plasminogen (LYS-PLG) infusion of 15 mukat every 30 minutes. Angiographically confirmed lysis was obtained in 77% of the cases. Five percent of the patients had major and 8% had minor groin hematomas. Only two patients had concentrations of fibrinogen as low as 100 mg/dl. Intravascular infusion of UK and LYS-PLG is as effective as streptokinase but produces lower systemic fibrinolysis. However, local fibrinolysis remains a potentially hazardous procedure (10% suffered major complications) and must only be applied to patients with severe ischemia and little or no possibility of surgical intervention.
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PMID:Local thrombolysis in peripheral arteries and bypass grafts. 365 85

In order to investigate the role of coronary thrombosis as a precipitating factor of acute myocardial infarction (AMI), we examined coronary angiographic findings in 89 patients with AMI taken within 24 hours of the onset and in 42 patients with prolonged angina attack of impending myocardial infarction (impending MI) taken within 50 hours of the last angina attack. Furthermore, in the patients with impending MI, the effects of intracoronary and intravenous thrombolytic therapy and anticoagulant therapy used to prevent impending MI from developing into AMI, were also studied. (1) In 72 of 89 patients (81%) with AMI, coronary thrombi were detected angiographically. The thrombi were detected most frequently (88%) in angiographs taken within 3 hours of onset. (2) In 23 of 42 patients with impending MI, coronary thrombi were detected angiographically. In 6 patients with coronary thrombi who underwent intracoronary thrombolysis during angina attack, occlusive coronary thrombi in ischemia-related vessels were the observed, and recanalization by thrombolysis with intracoronary urokinase infusion relieved chest pain and improved ECG changes. (3) The incidence of AMI in 42 patients with impending MI who were treated with intracoronary and intravenous thrombolytic therapy and anticoagulant therapy was significantly less than in the conventional therapy group (80 patients) (11.9% vs. 27.5%; p less than 0.05). In 4 of 5 patients with developing AMI, coronary thrombi were detected angiographically in the acute phase of impending MI. These results indicate that coronary thrombosis plays an important role not only in the precipitation of impending MI but also in the development of impending MI to AMI.
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PMID:Pathogenesis of impending myocardial infarction and acute myocardial infarction: clinical and angiographic evaluation of coronary thrombosis as a precipitating factor. 372 81

Thirty-five patients hospitalized for recent angiographically documented arterial occlusion in the legs (27 femoropopliteal arteries and eight grafts) benefited from local fibrinolytic therapy delivered at the site of the occlusion with a 4- or 5-F catheter. This therapy combined a continuous urokinase (UK) infusion of 1,000 U/kg/hour and a lysyl plasminogen (LYS-PLG) infusion of 15 microkatals every 30 minutes. Angiographically confirmed lysis was obtained in 85% of the cases. Only 3% of the patients had major and 6% had minor groin hematomas. Only two patients had concentrations of fibrinogen as low as 100 mg/dl. Intravascular infusion of UK-LYS-PLG is as effective as streptokinase. Its excellent tolerance makes it a good alternative in the treatment of acute ischemia in the lower limbs.
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PMID:Acute peripheral arterial and graft occlusion: treatment with selective infusion of urokinase and lysyl plasminogen. 394 77

To evaluate the role of selective intra-arterial low-dose thrombolytic therapy (SILDT) as an alternative to the surgical management of acute arterial occlusion, the hospital records of 40 patients who underwent 43 SILDT treatments with either streptokinase (36) or urokinase (7) between December 1979 and March 1984 were reviewed. Twenty-eight patients underwent 30 treatments (group 1) for native arterial occlusion and 12 patients underwent 13 treatments (group 2) for prosthetic or autogenous graft occlusions. Therapy was deemed successful if subsequent surgical therapy was obviated. In group 1, SILDT was successful in 13 of 28 (45%) patients with 12 of 25 lower extremity occlusions and one of three upper extremity occlusions. Successful lysis in the native artery occlusion group fell into three categories: five patients were successfully treated for arterial thrombosis complicating percutaneous transluminal angioplasty (PTA); four patients required PTA after complete lysis revealed an underlying arterial stenosis; and only three required no further therapy after SILDT. SILDT failed in all three patients with the aortoiliac occlusions. Eleven patients with femoral artery occlusions and unsuccessful SILDT required six bypass procedures, three amputations, one embolectomy, and one PTA. In group 2 only 3 of 14 treatments (21%) were successful. Bypass revision was not possible in 11 patients and all required amputation. Systemic fibrinolysis was seen in 20 (59%) of 34 patients with available data. Neither fibrinogen levels nor fibrin degradation products predicted the occurrence of complications. Minor complications occurred in 18 of 43 (43%) treatments; small hematomas at the catheter entry site were most common. Minor complications occurred in 20 of 43 treatments (44%) and included severe local hemorrhage (four), distant bleeding (three), pulmonary embolism (four), myocardial infarction (three), unmasking of an aortoduodenal fistula (one), and clot migration requiring emergency thrombectomy (four). SILDT is most effective in acute arterial thrombosis complicating arteriography or percutaneous angioplasty. It may play a role in the patient in whom thrombolysis can reveal an underlying stenosis amenable to percutaneous angioplasty. This experience shows SILDT to be of limited value in the management of prosthetic autogenous graft occlusions. Finally, thrombolytic therapy is associated with significant morbidity and mortality rates and requires cautious monitoring to detect arterial thrombus migration, worsening tissue ischemia, venous thromboembolism, intracerebral hemorrhage, and local or systemic bleeding.
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PMID:Thrombolytic therapy for acute arterial occlusion. 396 60

Macroscopic hemorrhagic infarction was studied in 14 autopsied hearts with selective coronary thrombolysis (SCT) after acute myocardial infarction (AMI). In all patients urokinase, 240,000 - 720,000 units, had been selectively injected into ischemia-related coronary artery at 2 - 7 hours after the onset of AMI. The degree of stenosis after SCT was 90 - 99% in 13 patients and 100% in one patient. According to the duration of illness at death, the 14 patients were classified into 3 stages; stage I: 4 - 9 hours; stage II: 15 hours to 11 days; stage III: 19 days to 12 months. Three hearts in stage I had no macroscopic hemorrhage. In stage II, marked and diffuse hemorrhage in the infarct area was macroscopically evident in 6 of 7 hearts. In a stage II patient, extravasation of contrast medium into the myocardium was found at 3 hours after the onset of AMI. In stage III, 4 hearts had massive fibrosis or granulation in the left ventricular wall without macroscopic hemorrhage. Cardiac rupture was seen in 4 of 10 patients from stages I and II. It is concluded that macroscopic bleeding appears in most patients with AMI treated with coronary thrombolysis. In the majority of cases, the hemorrhage increases gradually after SCT and becomes macroscopically definite approximately 15 hours after the onset of AMI. Rarely, massive bleeding appears earlier. Hemorrhagic infarction is replaced by massive fibrosis after approximately 2 weeks.
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PMID:Macroscopic hemorrhagic infarction following selective coronary thrombolysis in acute myocardial infarction. 403 86


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