Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 49 year-old woman with acute pulmonary thromboembolism and severe hemodynamic impairment was successfully treated with tissue-type plasminogen activator (r-TPA). She did not have previous pulmonary or cardiac diseases. Thirty days after immobilization of the right ankle, she had a sudden onset of dyspnea, epigastrial pain and syncope. As heparin therapy was unsuccessful, 90 mg of IV r-TPA was administered. There was rapid clinical and hemodynamic improvement of her condition. Pulmonary scanning one week later was normal and she was discharged without symptoms 12 days after the acute episode.
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PMID:[Treatment of pulmonary thromboembolism with extrinsic plasminogen activator. A case report]. 251 12

In a double-blind randomized trial involving five Sydney hospitals and the city ambulance paramedical service, 145 patients with a first evolving myocardial infarction and with onset of pain less than 2.5 (mean 1.9 +/- 0.5 [SD]) hr previously were allocated to intravenous infusion of 100 mg recombinant tissue-type plasminogen activator (rt-PA) or placebo over 3 hr. The groups at entry were similar. At assessment 21 days later, left ventricular ejection fraction measured both by contrast and radionuclide ventriculography was higher in the rt-PA compared with the placebo group (61 +/- 13%, n = 64, vs 54 +/- 14%, n = 62, contrast, 2p = .006; 52 +/- 13%, n = 66, vs 48 +/- 13%, n = 62 isotope, 2p = .08). This indicates limitation of myocardial infarction by rt-PA.
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PMID:Limitation of myocardial infarction by early infusion of recombinant tissue-type plasminogen activator. 313 Oct 40

The concepts of acute, potentially reversible coronary artery thrombosis and myocardial salvage by early coronary thrombolysis using pharmacologic agents and/or percutaneous transluminal coronary angioplasty have evolved rapidly since 1980. Broad, general application of these methods awaited clear data on efficacy and safety of proposed treatment regimens, and in May 1987 streptokinase was recommended for approval by the Food and Drug Administration for intravenous use in patients with acute myocardial infarction. A second, more promising drug, recombinant tissue-type plasminogen activator, was approved by the FDA in November 1987. Thrombolysis is now accepted therapy for patients with acute myocardial infarction. Rapid identification of the patient with acute myocardial infarction plays an important role in treatment, because thrombolytic therapy is maximally effective if begun within four hours of the onset of symptoms. Care must be taken in selecting patients for treatment to ensure that an acute myocardial infarction is in evolution and that a medical condition predisposing to hemorrhage is not present. Cost of treatment and risk of complications must be considered before initiating therapy. In many patients, thrombolytic therapy can be considered only the first step in treatment, because of the relatively frequent occurrence of reocclusion and reinfarction after initial thrombolysis. If cardiac catheterization, angioplasty, and open heart surgery facilities are not readily available, transfer to a tertiary care center is indicated for high-risk patients, such as those with large anterior infarction, vacillating pain, or previous myocardial infarction. Transfer is safe if carried out promptly by critical care transport teams experienced in cardiac care.
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PMID:Identification and transport of patients with acute myocardial infarction for thrombolytic therapy. 314 15

The plasminogen activator (PA) and plasminogen activator inhibitor (PAI) in synovial fluid (SF) of osteoarthritis (OA) were examined to clarify their pathophysiological roles in this disease. Three PAs with molecular weights of 90K, 55K, and 33K were found in the SF, but the 55K PA was dominant. Immunologically, both the 55K and 33K PA were u-PA, while the 90K PA was t-PA. The PAI reacted against both u-PA and t-PA, but the PAI activity against u-PA was much stronger. Urinary trypsin inhibitor (UTI) made a complex with the 55K PA and suppressed the PA activity. A clinical study in which UTI was injected into the joint space of OA (18 joints in 15 patients) revealed excellent (39%), good (16%), and fair (44%) results based on assessment of the pain, range of motion, ballottement and activity of daily living.
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PMID:Effect of urinary trypsin inhibitor on osteoarthritis. 314 65

Fibrinolysis of 19 patients who developed CVI after deep vein thrombosis was examined. Mean age of patients at the first thrombosis was 31.8 years. For testing fibrinolysis fibrinogen, plasminogen, AP, ECLT, with venous occlusion were determined. In 10 patients t-PA and PAI-1 activities were also measured and plethysmography was carried out. For screening blood coagulation abnormalities of TCT count, PT, APTT, TT, AT III, protein C were tested. The common abnormality was the decreased fibrinolysis. Patients had been on coumarin for 6.14 years before entering the study. Under coumarin treatment 6 patients had relapsed DVT, 4 had crural ulcer and CVI deteriorated in 8 patients. Therefore we added fibrinolysis increasing PPS to coumarin. PPS dose was individually determined by PPS loading test (150-500 mg). Mean observation time with the combined treatment was 2.92 years. Clinical check up and fibrinolysis test were carried out every 6 months. Clinical improvement occurred in 13 patients, (decrease of swelling, pain etc). Two out of 4 patients with stasis ulcer experienced complete healing; in 1 the ulcer territory diminished in size. Maximum venous outflow improved in 7 patients, 3 patients were non-responders. We observed an increase of fibrinolysis in 10 patients. Venous occlusion enhanced the fibrinolysis increasing effect of PPS. The activity reached its maximum by the first control. The fibrinolysis increase and the clinical improvement do not always run parallel, therefore other effects of PPS as the reason for being beneficial in CVI must be considered (antiinflammatory, ect.). Combination of coumarin and PPS seems to be an effective therapy in CVI with decreased fibrinolysis.
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PMID:[Management of chronic venous insufficiency with the combination of coumarin (Syncoumar) and oral pentosan polysulfate (PPS, SP 54) (preliminary report)]. 767 12

Adjunctive therapy for acute myocardial infarction should include aspirin, beta-adrenergic blocking agents, and, in most patients, consideration of the use of angiotensin-converting enzyme inhibitors, especially if left ventricular function is reduced. Heparin has an important adjunctive role in enhancing early vessel patency in patients who receive tissue-type plasminogen activator and in decreasing the frequency of reocclusion of an infarct-related artery during any thrombolytic therapy. Heparin must also be administered to all patients who undergo primary angioplasty. Intravenously administered nitroglycerin and orally administered nitrates are probably most effective in patients with symptomatic ischemia. Calcium channel blockers and prophylactic antiarrhythmic agents are not indicated for most patients with acute myocardial infarction. Currently, insufficient evidence is available to recommend the widespread use of intravenously administered magnesium sulfate in the setting of acute myocardial infarction. In patients with ischemic pain, judicious intravenous administration of morphine can provide relief. Use of warfarin sodium should be reserved for patients at risk for left ventricular mural thrombus. Although the use of lipid-lowering agents after myocardial infarction has been controversial, recent studies have demonstrated the importance of such therapy for secondary prevention of death and morbidity.
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PMID:Adjunctive therapy in the management of patients with acute myocardial infarction. 773 Dec 56

The demonstration that the vast majority of acute transmural myocardial infarctions are caused by an occlusive thrombus in the coronary artery, together with the concept that myocardium can be salvaged for a period of time after the onset of such occlusion, has heralded a new era of management of this disorder. This involves an aggressive interventional approach aimed at restoring coronary artery patency early while decreasing myocardial oxygen demands. Abundant data show that coronary flow can be reestablished using either intravenous chemical thrombolytic agents (tissue-type plasminogen activator and streptokinase), percutaneous transluminal coronary angioplasty, or coronary artery bypass grafting. Conjunctive aspirin or heparin therapy (or both) is effective in maintaining vessel patency once perfusion is restored. Myocardial oxygen demand can be reduced, where feasible, by pharmacotherapy and control of the patient's associated pain and anxiety. The beta-adrenergic blockers and nitrates are particularly suitable in this regard, and angiotensin-converting enzyme inhibitors favorably affect infarct expansion and ventricular remodeling. With such an approach, infarct size can be reduced, leading to improved left ventricular function--the prime determinant of morbidity and mortality in patients with acute infarction. The in-hospital mortality has fallen from about 30% three decades ago to less than 8% in many coronary care units.
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PMID:Early interventions in the management of acute uncomplicated myocardial infarction. 786 52

Patients with unstable angina, refractory to intensive medical therapy, are at high risk for developing thrombotic complications, such as recurrent ischemia, myocardial infarction and coronary occlusion during coronary angioplasty. As both platelet aggregation and/or thrombus formation play an important role in this ongoing ischemic process, a monoclonal platelet GPIIb/IIIa receptor antibody (c7E3) or thrombolytic therapy (alteplase) might be able to modify the clinical course and underlying coronary lesion morphology. To evaluate whether alteplase or c7E3 could influence the incidence of complications, we randomized 36 and 60 patients, respectively to alteplase or placebo, or c7E3 or placebo. All patients exhibited dynamic ECG changes and recurrent pain attacks, despite maximal tolerated medical therapy. Patients were randomized in both studies after initial angiography had demonstrated a culprit lesion amenable for angioplasty. After study drug infusion quantitative angiography was repeated and angioplasty performed. Recurrent ischemia during study drug infusion occurred in 5, 6, 9 and 16 patients from the alteplase, placebo, c7E3 and placebo group, respectively. Major events defined as death, myocardial infarction or urgent intervention occurred in 7, 3, 1 and 7 patients, respectively. Two patients died: one in the alteplase group and one in the placebo group from the c7E3 study. The first patient due to retroperitoneal hemorrhage, the second as a result of recurrent infarction. Qualitative angiography showed resolution of clots in the c7E3 group only, while the same group of patients showed in 20% an improvement in TIMI flow grade, without deterioration in any patient from this group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Correlation between clinical course and quantitative analysis of the ischemia related artery in patients with unstable angina pectoris, refractory to medical treatment. Results of two randomized trials. The European Cooperative Study Group. 787 57

Tumor necrosis factor alpha (TNF-alpha) is a cytokine that affects endothelial cells' function by changing their antithrombotic potential to a net procoagulant effect. Only a few data have so far been reported for the pathophysiologic role of TNF in vascular diseases in the involvement of microvessels and/or macrovessels and a prothrombotic state. In the present study the authors evaluated plasma TNF (and interleukin-1) levels in 20 patients with chronic arterial obstructive disease (CAOD) with intermittent claudication and 10 CAOD patients with more severe disease (pain at rest/skin ulcers). In addition, they studied 10 patients with Raynaud's phenomenon (RP), suspected to be secondary to a collagen disease. The control group consisted of 20 subjects matched for sex and age with the three groups of patients. TNF levels were assayed by enzyme-linked immunosorbent assay. The antigen levels of von Willebrand factor (vWF), tissue plasminogen activator (t-PA), and its inhibitor (PAI) were also determined as markers of release from the endothelium, while the fragment 1 + 2 of prothrombin (F1 + 2) and thrombin-antithrombin III (TAT) complexes were assessed as indexes of systemic thrombin generation. TNF levels were significantly higher in both groups of CAOD patients than in controls or RP patients, and the same was true for vWF. t-PA was significantly higher only in the CAOD subjects with more severe disease. No differences among groups were seen in PAI antigen/activity or thrombin generation. When data were corrected for age, TNF no longer differentiated CAOD patients from controls and RP subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma levels of tumor necrosis factor and endothelial response in patients with chronic arterial obstructive disease or Raynaud's phenomenon. 798 28

Previous studies have reported that some patients presenting with unstable angina are found at coronary angiography to have no critical coronary stenosis. This study evaluated the clinical presentation and arteriographic findings in patients enrolled in the Thrombolysis in Myocardial Ischemia (TIMI-IIIA) trial, which assessed the effect of tissue-type plasminogen activator added to conventional therapy on the coronary arteriographic findings in patients presenting with ischemic pain at rest. Three hundred ninety-one patients were enrolled in the TIMI-IIIA trial and underwent coronary arteriography within 12 hours of enrollment. Fifty-three patients (14%) had no luminal diameter stenosis of a major coronary artery of > or = 60% on the baseline arteriogram. Compared with patients with unstable angina with an identifiable culprit lesion, patients without critical coronary obstruction were more likely to be women and non-white and less likely to have ST-segment deviation on the presenting electrocardiogram. Arteriography in such patients revealed no visually detectable coronary stenosis in half of the group; the remaining patients had noncritical coronary narrowing (i.e., < 60% luminal diameter stenosis) without morphologic features (ulceration or thrombus) suggestive of unstable or active coronary plaque. Nearly one third of the patients without critical coronary stenosis had impaired angiographic filling, suggesting a possible pathophysiologic role for coronary microvascular dysfunction. These patients with unstable angina and no critical coronary obstruction had an excellent short-term prognosis; 2% died or had myocardial infarction compared with 18% of patients with critical obstruction.
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PMID:Clinical and arteriographic characterization of patients with unstable angina without critical coronary arterial narrowing (from the TIMI-IIIA Trial). 807 33


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