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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recombinant human tissue-type plasminogen activator (rt-PA), a relatively clot-specific fibrinolytic agent, represents a novel and promising approach to thrombolytic therapy of pulmonary embolism. Therefore, the efficacy and safety of peripheral intravenous rt-PA therapy were assessed in 47 patients with angiographically documented pulmonary embolism. The drug regimen was 50 mg over 2 hours followed by repeat angiography and, if necessary, an additional 40 mg over 4 hours. By 6 hours, 44 of the 47 patients had angiographic evidence of clot lysis that was slight (n = 5), moderate (n = 12) or marked (n = 27). Among the 34 patients with pulmonary hypertension before treatment (mean pulmonary artery pressure exceeding 17 mm Hg), the pressure decreased from 43/17 (mean 27) to 31/13 (mean 19) mm Hg (p less than 0.0001). Fibrinogen decreased 33% from baseline at 2 hours and 42% from baseline at 6 hours. There were two major complications that required surgical control of bleeding: hemorrhage from a pelvic tumor and mediastinal tamponade in a patient 8 days after coronary artery bypass surgery. The initial results demonstrate that, among selected patients, peripheral intravenous rt-PA can rapidly and, for the most part, safely lyse pulmonary embolism within 6 hours.
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PMID:Thrombolytic therapy of acute pulmonary embolism: current status and future potential. 311 62

To determine if pulmonary perfusion was improved in acute pulmonary embolism after therapy with recombinant human tissue-type plasminogen activator (rt-PA), lung scans were obtained before and a mean of 22 hours after therapy in 19 patients. The posttherapy lung scans were compared with baseline, pretherapy scans with use of two semiquantitative methods--an anteroposterior view method, similar to that used in the Urokinase Pulmonary Embolism Trial, and a segmental method that emphasized pulmonary anatomy. There was an improvement in the defect score from 0.35 to 0.14 (P less than .01) when the anteroposterior view method was used and from 0.37 to 0.16 (P less than .01) when the segmental method was used. These encouraging results in the early posttherapy period suggest that rt-PA is especially effective in improving regional perfusion after pulmonary embolism and that a larger controlled trial of therapy with rt-PA for acute pulmonary embolism should be performed. Scoring lung scans with a segmental method is feasible and appropriate for present-day lung scan technique and should be considered in future studies.
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PMID:Pulmonary perfusion after rt-PA therapy for acute embolism: early improvement assessed with segmental perfusion scanning. 312 66

Eight centers participated in a study in which intrapulmonary and intravenous administration of recombinant tissue-type plasminogen activator (rt-PA) were compared in 34 patients with acute massive pulmonary embolism. All patients received intravenous heparin in a bolus of 5,000 IU followed by 1,000 IU/hr. After 50 mg rt-PA given over 2 hr the severity of embolism, determined from pulmonary angiograms, declined by 12% in the intrapulmonary drug group (p less than .005) and 15% in the intravenous drug group (p less than .005); mean pulmonary arterial pressure fell from 31 +/- 7 to 22 +/- 6 mm Hg (p less than .005) and from 31 +/- 12 to 21 +/- 9 mm Hg (p less than .005) in the respective groups. After a further 50 mg given over 5 hr (22 patients), the angiographically determined severity of embolism had decreased by 38% from baseline in the intrapulmonary drug group and by 38% in the intravenous drug group. The mean pulmonary arterial pressure further declined to 18 +/- 7 and 12 +/- 5 mm Hg in the respective groups. Fibrinogen levels dropped to 48% of baseline after 50 mg and to 36% of baseline after 100 mg rt-PA. Some degree of bleeding at puncture and/or operation sites was noted in 16 patients, including four who required a transfusion of two or more units of blood and had been operated on an average of 7.5 days (range 2 to 13) before thrombolytic treatment was started.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intravenous and intrapulmonary recombinant tissue-type plasminogen activator in the treatment of acute massive pulmonary embolism. 312 91

The troublesome sequelae of pulmonary embolism (PE) and deep vein thrombosis (DVT) justify an aggressive therapeutic approach. Results of anticoagulation in patients with DVT have shown that a significant percentage of patients have no clot resolution and may progress to develop the postphlebitic syndrome. Lytic therapy has been more effective, with patients showing improvement within 24 h of treatment. This approach has also been found to compare favorably with anticoagulation in the treatment of PE. Preliminary research also suggests a potential role for recombinant human tissue-type plasminogen activator to resolve PE.
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PMID:Fibrinolytic therapy for deep vein thrombosis and pulmonary embolism. 313 Oct 6

Thrombolysis with tissue plasminogen activator (tPA) has been used to treat myocardial infarction and pulmonary embolism in humans. This plasminogen activator may also be useful in treating certain strokes. We infused tPA or saline in rabbits 15 minutes after selective internal carotid artery embolization with 18-hour aged autologous clot. By serial angiography, the tPA-treated group demonstrated rapid angiographic reperfusion of the occluded vascular territory in 7 of 8 animals, whereas none of 6 saline controls did. None of the animals in either group developed macroscopic cerebral hemorrhage. Both groups showed cerebral infarction, predominantly in the territory of the occluded vessel; the extent of infarction did not differ between tPA-treated animals and controls. Early tPA therapy can allow reperfusion of occluded cerebral arteries safely and effectively in a rabbit cerebral embolization model.
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PMID:The safety and angiographic efficacy of tissue plasminogen activator in a cerebral embolization model. 313 92

Pulmonary embolism is diagnosed 120,000 times yearly in the United States and contributes to 30,000 deaths. This probably represents an underestimate of incidence because massive acute pulmonary embolism may often result in rapid and therefore unexplained death in the absence of autopsy confirmation. The innovative and judicious use of thrombolytic agents by emergency department and paramedical ambulance personnel may lead to a decreased mortality for this disease. Clinical studies are necessary to determine if the cardiopulmonary compromise associated with massive pulmonary embolism can be rapidly reversed through thrombolysis and whether that reversal will lead to increased survival. The use of thrombolytic agents will gain favor only if their risk:benefit and cost:benefit ratios are acceptable. We discuss the results of using first- and second-generation thrombolytic agents in the treatment of pulmonary embolism and review the encouraging data that have emerged from our studies with recombinant tissue-type plasminogen activator (tPA). This agent has relative fibrin specificity and may provide therapeutic advantages over the conventional thrombolytic agents, urokinase and streptokinase, particularly when the latter are administered in the currently recommended dose schedules for treatment of pulmonary embolism.
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PMID:Acute pulmonary embolism treated with thrombolytic agents: current status of tPA and future implications for emergency medicine. 314 20

We assessed the efficacy and safety of peripheral intravenous recombinant human tissue-type plasminogen activator (rt-PA) in 47 patients with angiographically documented pulmonary embolism (PE). We administered 50 mg/2 h and, if necessary, an additional 40 mg/4 h. By 6 hours, 94% of the patients had angiographic evidence of clot lysis that was slight in 5, moderate in 12, and marked in 27 patients. Among the 34 patients with pulmonary hypertension prior to treatment, average pulmonary artery pressure decreased from 43/17 (27) to 31/13 (19) mm Hg (P less than 0.0001). The average lung scan perfusion defect decreased from 37% before therapy to 16% (P less than 0.01) after therapy among the 19 patients who had pre- and post-treatment lung scans. Of 7 patients with pre- and post-treatment imaging and Doppler echocardiograms, hypokinetic right ventricular wall movement (mild in 1, moderate in 2, and severe in 4) normalized in 5 and improved to mild hypokinesis in 2. Right ventricular diameter decreased from 3.9 +/- 1.0 to 2.0 +/- 0.5 cm (P less than 0.005). Fibrinogen decreased 33% from baseline at 2 h and 42% from baseline at 6 h. However, patients with the greatest degree of angiographic clot lysis at 2 h had a preponderance of fibrinogenolysis over fibrinolysis, demonstrated by a lower ratio of cross-linked fibrin degradation products to fibrin(ogen) degradation products (0.14 +/- 0.09 vs. 0.54 +/- 0.82) (P less than 0.04). Among selected patients, peripheral intravenous rt-PA is associated with rapid lysis of PE, improved pulmonary perfusion, and improved right ventricular function.
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PMID:Tissue plasminogen activator and acute pulmonary embolism. 314 83

Pulmonary embolism remains a challenging problem in diagnosis and management for the emergency physician. Although its clinical presentation is protean and often ambiguous, risk stratification can be accomplished based on the predictive power of a limited number of physical and historical characteristics. Ventilation-perfusion lung scanning occupies a central position in the work-up of suspected PE; however, evidence exists that it may be misused by many physicians. A low probability V-Q scan does not exclude the diagnosis of PE. Patients with other than normal- or high-probability patterns of pulmonary ventilation and perfusion on lung scanning require further investigation. Noninvasive venous studies are useful when indicative of proximal deep venous thrombosis, but are normal in many patients with acute PE. Heparin remains the standard of treatment for most patients with PE. Vena cava filters effectively reduce the incidence of recurrent PE in patients with contraindications to anticoagulation. Thrombolytic therapy offers potential advantages in the treatment of patients with shock due to their PE. Case reports of PE treated with tissue-type plasminogen activator, a new thrombus-specific fibrinolytic agent, are encouraging but preliminary.
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PMID:Pulmonary embolism. 328 Mar 1

Early attempts to treat thromboembolic disorders focused on the prevention of thrombus formation, along with the prevention of extension and/or embolization of an existing thrombus. Antithrombotic therapy for these conditions included intravenous and oral anticoagulants and later antiplatelet agents, all of which remain in use today. Subsequent research sought a thrombolytic agent that could lyse a clot directly. Intravenously administered streptokinase and urokinase were found to act on the inactive proenzyme plasminogen to produce the active enzyme plasmin that could safely and effectively lyse fresh fibrin clots. These agents have proved effective for the treatment of myocardial infarction and pulmonary embolism, as well as peripheral arterial and venous thromboembolic conditions. Recent efforts have been directed toward a search for clot-specific agents that would avoid the systemic lytic state associated with the use of urokinase and streptokinase. Three clot-specific plasminogen activators are currently being evaluated: recombinant tissue-specific plasminogen activator, anisoylated streptokinase plasminogen activator complex, and pro-urokinase.
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PMID:Historical overview of antithrombotic and thrombolytic therapy. 330

Three patients with karyotype XYY who had presented with deep vein thrombosis and leg ulcers (plus pulmonary embolism in two of them) were investigated for: (1) androgens (plasma testosterone measurement, testosterone oestradiol binding globulin (TeBG) assay, GnRH 50 micrograms test), and (2) haemostasis by fibrinolysis tests (euglobulin lysis time and area, antigenic plasminogen activator assay before and after 10 min venostasis). Full evaluation of haemostasis failed to demonstrate the presence of circulating anticoagulant or of antithrombin III, protein C and protein S deficiencies. One patient had neither hormonal nor fibrinolytic abnormality. The other two patients shared some clinical features with male hypogonadism (gynoid morphotype in both, hypotrophy of the testes in one, gynaecomastia in the other). They also had hormonal disorders ("over-response" to the GnRH test in one case, elevated TeGB in the other case) and abnormalities of fibrinolysis (poor response to venostasis, high baseline level of plasminogen activator). Response to venostasis became normal after 3 months of treatment with percutaneous dihydrosterone 125 mg per day in the two patients with initially poor response. The mechanism of venous pathology in XYY subjects is discussed. A genetic defect not involving the fibrinolysis system is possible since fibrinolysis was normal in one patient; however, abnormal fibrinolysis may have been responsible for the venous pathology in the other 2 patients. The role played by abnormalities of fibrinolysis in the pathogenesis of deep vein thrombosis and leg ulcers is recalled, and the possible implication of these abnormalities in patients with XYY karyotype is emphasized.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Post-phlebitic leg ulcers and XYY karyotype: fibrinolysis and androgenic function tests. Apropos of 3 cases]. 343 47


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