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)

The effectiveness of intracoronary urokinase infusion as an adjunct to percutaneous transluminal coronary angioplasty (PTCA) was studied in 50 patients who underwent angioplasty for complex coronary narrowings or had thromboembolic complications during PTCA (29 [58%] men, 3 [6%] stable and 37 [74%] unstable angina, and 16 [32%] prior coronary bypass surgery). The primary indications for intracoronary urokinase infusion were intracoronary thrombus in 27 patients (54%), distal coronary embolization in 9 (18%), and abrupt reclosure in 14 (28%). Urokinase was infused in a mean (+/- standard deviation) dosage of 399,000 +/- 194,000 IU (range 150,000 to 1,000,000) at an average rate of 5,000 to 20,000 IU/min. Angiographic success was achieved in 43 patients (86%). Complications included the need for urgent bypass surgery in 3 patients, Q-wave myocardial infarction in 2, and non-Q-wave myocardial infarction in 12 (8 of whom had peak creatine kinase less than twice the upper normal limit). The incidence of myocardial infarction was significantly higher in patients with vein grafts (69%) than in those with PTCA of native vessels (14%). Two patients died (1 massive gastrointestinal necrosis 24 hours after angioplasty, and 1 after urgent bypass surgery). Mean (+/- standard deviation) fibrinogen levels were 355 +/- 73 mg/dl before urokinase infusion, and 361 +/- 70, twelve hours afterward. Three patients had local bleeding, but no transfusions were needed. It is concluded that intracoronary urokinase is a safe and effective adjunct to PTCA in patients with associated thrombi and may improve the success rate in angioplasty complicated by thrombus formation.
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PMID:Intracoronary urokinase as an adjunct to percutaneous transluminal coronary angioplasty in patients with complex coronary narrowings or angioplasty-induced complications. 172 68

Although thrombolytic agents were discovered nearly 60 years ago, it is only within the past decade that the clinical use of these agents has revolutionized the treatment of acute myocardial infarction. There are four currently available agents approved for use in treatment of myocardial infarction: streptokinase, urokinase, tissue plasminogen activator, and anistreplase. Although each of these agents works in a unique fashion, the common end point of therapy is the dissolution of a fibrin clot by the conversion of plasminogen to plasmin. A number of clinically measurable end points have been used to determine the effectiveness of these agents in the treatment of acute myocardial infarction, including mortality, reperfusion, patency, left ventricular function, left ventricular volumes, and quantitative creatine kinase isoenzyme analysis. Secondary end points have included bleeding and stroke, as well as recurrent ischemic events. Numerous clinical studies have demonstrated the effectiveness of all of these agents in achieving the desired end points and comparative studies, including several large-scale trials, have failed to differentiate among these agents with regard to efficacy. Newer dosing regimens for currently available thrombolytic agents, as well as new thrombolytic agents, are currently under active investigation and will be the subject of intense research over the next few years. Despite the lack of consensus as to which agent is superior, it is clear that thrombolytic therapy for acute myocardial infarction is the treatment of choice.
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PMID:Thrombolytic therapy: then and now. 191 23

The clinical features of acute non-Q wave myocardial infarction (NQMI) with R wave regression and no ST segment depression are distinct from those of acute Q wave myocardial infarction (QMI). NQMI patients showed ST segment elevation at admission, and significantly earlier regression of the ST segment elevation and appearance of coronary T waves were observed compared to QMI patients. In addition to the significantly lower level of mean peak serum creatine kinase activity and the significantly lower incidence of pump failure during the acute phase, the incidences of in-hospital mortality and multivessel disease were significantly lower in the NQMI patients. With respect to acute-phase coronary angiographic features within 48 h after the onset, the rate of spontaneous opening of infarct-related vessels was significantly higher in the NQMI patients. Thirteen of the 19 NQMI patients responded to urokinase infusion. These facts suggest that transient, intermittent or incomplete obstruction may favor this type of NQMI over QMI, and that thrombus might be an important factor in the pathogenesis of this type of NQMI.
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PMID:Coronary angiographic features within 48 hours from onset of non-Q wave myocardial infarction with R wave regression and no ST segment depression. 211 28

The benefit and risk of prehospital thrombolysis for acute myocardial infarction (AMI) were evaluated in a double-blind randomized trial. Patients presenting less than 4 hours after symptom onset received 2 million units of urokinase as an intravenous bolus either before (group A, n = 40) or after (group B, n = 38) hospital admission. The mean time interval from onset of symptoms to thrombolytic therapy was 85 +/- 51 minutes in group A and 137 +/- 50 minutes in group B (p less than 0.0005). In 91% of the patients, thrombolytic therapy was administered less than 3 hours after symptom onset. Complication rates during the pre- and in-hospital period were low and did not differ between groups. Three patients died (1 in group A, 2 in group B) from reinfarction 7 to 14 days after admission. Left-sided cardiac catheterization before discharge revealed a patency rate in the infarct-related artery of 61% in group A and 67% in group B (difference not significant). Global left ventricular function and regional wall motion at the infarct site did not differ significantly between group A and B (ejection fraction 51 +/- 10%, n = 28 vs 53 +/- 14%, n = 28; wall motion -2.3 +/- 1.3 vs -2.2 +/- 1.1 standard deviation, respectively). Also, peak creatine kinase did not differ significantly (838 +/- 634 U/liter in group A vs 924 +/- 595 U/liter in group B). Prehospital thrombolysis using a bolus injection of urokinase has a low risk when performed by a trained physician with a mobile care unit. The saving of 45 minutes in the early stage of an acute infarction through prehospital thrombolysis did not appear to be important for salvage of myocardial function.
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PMID:Prehospital thrombolysis in acute myocardial infarction. 225 87

Early appearance of positive findings on a technetium-99m pyrophosphate scan has been shown to be associated with the presence of a reperfused acute myocardial infarction (AMI). Early technetium-99m pyrophosphate imaging was performed by emission computed tomography to evaluate reperfusion and to test the feasibility of estimating infarct size soon after coronary reperfusion based on acute positive tomographic findings. Twenty-seven patients with transmural AMI who were treated with intracoronary urokinase infusion followed by percutaneous transluminal coronary angioplasty underwent pyrophosphate imaging 8.7 +/- 2.1 hours after the onset of AMI. None of the 8 patients in whom reperfusion was unsuccessful had acute positive findings. Of 19 patients in whom reperfusion was successful, 17 had acute positive findings (p less than 0.001). In these 17, tomographic infarct volumes were determined from reconstructed transaxial images. The threshold for areas of increased pyrophosphate uptake within the infarct was set at 60% of peak activity by the computerized edge-detection algorithm. The total number of pixels in all transaxial sections showing increased tracer uptake were added and multiplied by a size factor and 1.05 g/cm3 muscle to determine infarct volume. The correlations of tomographic infarct volumes with peak serum creatine kinase (CK) levels (r = 0.82) and with cumulative release of CK-MB isoenzyme (r = 0.89) were good. Moreover, the time to positive imaging was significantly shorter than that to peak CK level (8.5 +/- 2.3 vs 10.4 +/- 2.2 hours, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early estimation of acute myocardial infarct size soon after coronary reperfusion using emission computed tomography with technetium-99m pyrophosphate. 282 91

Twelve patients with acute transmural myocardial infarction (AMI) were treated with percutaneous transluminal coronary angioplasty (PTCA) following intracoronary thrombolysis using urokinase, and underwent technetium-99m stannous pyrophosphate (Tc-99m-PPi) imaging 9.2 +/- 2.1 hours after the onset of chest pain. The imaging was performed with emission computed tomography (ECT). Compared to planar imaging, this allowed more accurate detection of small myocardial infarcts and accurate measurements of infarcts irrespective of their location was also made. Early Tc-99m-PPi images were obtained to test the hypothesis that an early, abnormal Tc-99m-PPi image suggest successful reperfusion. The results were presented for two groups of patients: three with unsuccessful reperfusion (Group A) and nine with successful reperfusion (Group B). Eight of the nine patients with successful reperfusion had positive acute Tc-99m-PPi images. On the contrary, all the three patients for whom reperfusion failed had negative acute Tc-99m-PPi images. We also examined the feasibility of estimating infarct size using positive Tc-99m-PPi images in patients with successful reperfusion during the early phase of AMI. The Tc-99m-PPi uptake score (Tc-US) was used to measure infarct size in this study. Areas of increased Tc-99m-PPi uptake within myocardial infarcts were threshold at 60% of the peak activity. The Tc-US of each patient was obtained to sum the scores of all myocardial segments using a scoring system with a maximum score of 108. Using this method, Tc-US ranged from 2 to 39. The correlation of Tc-US with the peak serum creatine kinase level was significant (r = 0.91).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Evaluation of coronary reperfusion for acute myocardial infarction by emission CT using technetium-99m pyrophosphate]. 296 42

Serum creatinine kinase MB isoenzyme time-activity curves are useful for the assessment of coronary reperfusion after acute myocardial infarction. The purpose of this study was to compare serum creatine kinase MB catalytic activity with mass concentration for the determination of coronary reflow after therapeutic thrombolysis. Creatine kinase MB mass was determined immunoenzymometrically. Creatinine kinase MB catalytic activity concentration was determined by electrophoresis. Serum was collected every 4 hours for 96 hours in two groups of myocardial infarction patients: A (n = 10), urokinase induced reperfusion; B (n = 10), conventional therapy without urokinase. Peaks of mass and activity occurred at similar times in groups A and B. Both were significantly earlier in the urokinase treated patients. The maximal rate of increase of creatine kinase MB (based on either mass or catalytic activity) was threefold greater in the urokinase group. There are no important differences between the behaviour of creatine kinase measured as catalytic concentration or as mass concentration. Mass concentration is therefore equally useful as an indicator of coronary reperfusion.
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PMID:Comparison of catalytic activity and mass concentration of serum creatine kinase MB isoenzyme in the detection of coronary reperfusion in acute myocardial infarction after therapeutic thrombolysis. 304 4

Myocardial ischemia was induced by formation of an occlusive thrombus in the left anterior circumflex artery (LCX) in open chest dogs. The myocardial salvage by the fibrin specific recombinant single-chain urokinase-type plasminogen activator (r-scu-PA) alone and in combination with the oxygen radical scavenger human superoxide dismutase of recombinant origin (r-HSOD) was investigated. The three experimental groups were: group I (n = 4) did not receive any treatment after LCX thrombosis; in group II (n = 9) at 100 min after LCX thrombosis r-scu-PA (20 micrograms.kg1.min-1 i.v. for 30 min) was infused; dogs in group III (n = 8) received concomitant treatment with r-scu-PA and r-HSOD (10 mg.kg1 i.v. for 60 min). Percent of left ventricle at risk did not differ between the groups. Infarct size as percent of the risk zone was 45.3 +/- 8.0 in group I, 25.3 +/- 3.7 in group II (a less than or equal to 0.05 vs group I) and 14.9 +/- 3.2 in group III (a less than 0.05 vs group II). Incidence of reperfusion arrhythmias and increase in plasma creatine kinase were significantly diminished by r-HSOD when compared to dogs receiving r-scu-PA only. There were no significant differences in hemodynamic parameters between the groups. No changes in plasma fibrinogen were observed in r-scu-PA treated dogs. In conclusion, the combined treatment with r-scu-PA and r-HSOD yielded a significantly higher myocardial salvage versus thrombolytic treatment alone in a canine LCX thrombosis model.
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PMID:Enhanced myocardial salvage by combined treatment with recombinant single-chain urokinase-type plasminogen activator and recombinant human superoxide dismutase in a canine coronary thrombosis model. 336 72

The objectives of thrombolytic therapy in acute myocardial infarction are to restore coronary artery patency, salvage myocardium, reduce infarct size, and facilitate coronary artery repair. Urokinase and streptokinase are the two most frequently used thrombolytic agents. Both dissolve thrombi by converting circulating plasminogen, an inert precursor, into plasmin. One possible advantage of urokinase and streptokinase over new clot-specific agents is that the former have systemic fibrinolytic effects. This reduces blood viscosity and prevents other thrombi from forming. Angiography is the most objective technique for assessing reestablished arterial patency, but being invasive, it present disadvantages. Noninvasive criteria for coronary reperfusion include lowering of elevated ST-segments, shifting creatine kinase isoenzyme MB curves, and the appearance of reperfusion arrhythmias. Techniques for assessing myocardial salvage include thallium uptake, assessment of wall motion and myocardial thickening, ejection fraction, and positron emission tomography to assess infarct size. The role and appropriate timing of coronary artery repair after thrombolytic therapy are being studied.
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PMID:Objectives of thrombolytic therapy in acute myocardial infarction. 363 Nov 13

Kinetics of the catalytic activities of creatine kinase (CK;EC 2.7.3.2) for three CK-3 and two CK-2 isoforms in serum were studied in 20 patients with myocardial infarction randomly assigned to receive either intracoronary urokinase (group A) or conventional therapy (group B). The temporal characteristics of isoform changes described were (a) time at which the isoform activities are significantly greater than initial values, (b) maximal rate (Ka) at which isoforms are released into blood, (c) time lag from onset of pain until maximum activity value, (d) peak value of each serum isoform, and (e) rate (Kd) at which each isoform is cleared from serum. Thrombolytic treatment induced earlier peak times in group A: for CK-3(3), 7.4 vs 20.0 h; for CK-3(2), 11.6 vs 24.8; for CK-3(1), 18.6 vs 34.3; for CK-2(2), 9.1 vs 17.8; and for CK-2(1), 11.8 vs 26.8 (numbers given are medians; for all isoforms, P less than 0.05). Ka values were at least twofold greater and the first increase was significantly earlier in the urokinase group. Consequently, the ratio for CK-3(3) to CK-3(1) activities peaked significantly earlier in group A. Isoform peak activities and Kd were not significantly different between the two groups.
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PMID:Isoforms of creatine kinase isoenzymes in serum in acute myocardial infarction after intracoronary thrombolysis. 367 76


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