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

We observed the changes of molecular markers for hemostatic activation in a patient with acute pulmonary embolism treated with 2 x 10(7) unit tissue plasminogen activator (t-PA). Blood samples were obtained before, just after, at 30 min, 1, 2, 6, and 24 hours after the infusion. Molecular markers included thrombin-antithrombin III complex (TAT), plasminogen-alpha 2 plasmin inhibitor complex (PIC), and thrombomodulin (TM). Marked elevation of TAT was observed from immediately after the t-PA infusion to 6 hours after, although it had been observed for only 1 hour in our previous report on the cases of acute myocardial infarction. PIC level was significantly increased during t-PA infusion but returned to almost baseline value 6 hours after the end of t-PA infusion. This finding was almost the same as the one previously reported concerning acute myocardial infarction cases. TM level increased throughout the evaluation, and remained so, even on the 7th day after t-PA infusion. Our present data revealed a clear difference between the reactive TAT increases after t-PA therapy in acute myocardial infarction cases and in acute pulmonary embolism cases. Our present data also revealed a prolonged elevation of TM during the acute period of pulmonary embolism. It is therefore necessary to keep an eye on the changes of molecular markers for hemostatic activation after t-PA therapy in acute pulmonary embolism.
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PMID:[The changes in molecular markers for hemostatic activation after t-PA therapy in case of pulmonary embolism]. 131 73

Over the past decade there has been an increasing use of thrombolytic agents in the treatment of coronary artery disease, pulmonary embolism, and thromboembolic strokes. The use of thrombolytic agents has been most successful in treating acute myocardial infarction. When treatment with intravenous streptokinase or tissue plasminogen activator (tPA) is initiated within the first 3 to 4 hours from the onset of symptoms, the rate of reperfusion ranges from 60% to 90%, as compared to a rate of 13% to 21% for placebo control. Both streptokinase and tPA have been extensively studied as therapies for acute myocardial infarction, and in general, a higher initial rate of reperfusion is achieved in tPA-treated patients than in streptokinase-treated patients, although the final arterial patency rate may not be different in the two groups due to a higher rate of reocclusion in the tPA-treated population. Furthermore, time dependency for efficacy from the onset of symptoms to the initiation of treatment is less for tPA than for streptokinase. However, the role of thrombolytic agents in the treatment of thromboembolic strokes is more experimental than clinical at the present time. Of all agents, tPA is the most promising and the most extensively studied. This paper will review the experimental data on the use of tPA in acute thromboembolic strokes as well as the existing clinical data on stroke reperfusion.
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PMID:The efficacy and safety of tissue plasminogen activator in acute ischemic strokes. 162 47

We employed a canine model of pulmonary embolism induced by radioactive blood clots to determine if low-molecular-weight heparin augments recombinant tissue plasminogen activator (rtPA)-induced thrombolysis. Following embolization, dogs were randomized: group 1 dogs received heparin; group 2 dogs received low-molecular-weight heparin; group 3 dogs received 1.5 mg/kg of rtPA over 45 minutes; group 4 dogs received rtPA 3 mg/kg over 45 minutes; and group 5 dogs received 1.5 mg/kg of rtPA plus low-molecular-weight heparin. Over three hours, little thrombolysis occurred in groups 1 and 2. In contrast, significant thrombolysis occurred in groups 3 to 5, 46 percent, 49 percent, and 46 percent, respectively (all p less than 0.01 compared with groups 1 and 2). We conclude that there is an upper limit to the dose-thrombolytic rate relationship with rtPA, and that low-molecular-weight heparin does not augment rtPA-induced thrombolysis.
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PMID:Effect of low-molecular-weight heparin on recombinant tissue plasminogen activator-induced thrombolysis in canine pulmonary embolism. 165 Jun 81

We employed a canine model of pulmonary embolism induced by injection of radioactive blood clots to investigate effects of changes in cardiac output (CO) on recombinant tissue plasminogen activator- (rtPA) induced pulmonary thrombolysis. Rate and extent of thrombolysis were assessed with a gamma camera. Eighteen dogs were studied. Emboli increased mean pulmonary arterial pressure and decreased CO from 2.6 to 1.9 l/min (P less than 0.001). Subsequently, dogs were randomly divided into three groups: group 1 received 0.5 mg/kg of rtPA over 30 min; 30 min before the same dose regimen of rtPA, in the six group 2 dogs, mean CO was increased to approximately 3.25 l/min by opening one systemic arteriovenous fistula; in the six group 3 dogs, before rtPA, mean CO was increased to approximately 4.5 l/min by opening two or three fistulas. After embolization, CO remained low in group 1; the mean 2-h time-averaged CO was 1.8 l/min. CO was much higher in groups 2 and 3 (3.3 and 4.6 l/min, respectively; both P less than 0.001 compared with group 1; and P less than 0.001, group 2 vs. group 3). Compared with group 1, corresponding to the increased flow in groups 2 and 3, rate and extent of pulmonary thrombolysis significantly increased. These results indicate that an increase in flow per se augments rtPA-induced pulmonary thrombolysis. Also, because thrombolysis was similar between groups 2 and 3, these results define an upper limit to the flow-thrombolytic relationship with rtPA.
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PMID:Effects of flow on recombinant tissue plasminogen activator-induced pulmonary thrombolysis. 175 68

The incidence of deep vein thrombosis (DVT) and pulmonary embolism was studied prospectively in patients undergoing elective total hip replacement. 96 patients were randomly allocated to receive either low molecular weight heparin (LMWH) or unfractionated heparin (UFH). All patients had bilateral phlebography and pulmonary perfusion/ventilation scintigraphy 10-12 days after surgery. The following fibrinolytic variables were analysed in plasma and related to thromboembolism: tissue plasminogen activator (t-PA) activity, t-PA antigen (t-PA Ag), plasminogen activator inhibitor (PAI-1) activity and PAI-1 antigen (PAI-1 Ag). No significant difference was found, regarding the fibrinolytic response to surgery, between patients treated with LMWH and UFH. The level of PAI-1 activity was significantly increased before operation in patients developing DVT as compared to non-DVT patients (p less than 0.03). Immediately after surgery and in the morning the first postoperative day the levels of PAI-1 activity, PAI-1 Ag and t-PA Ag were positively correlated to thromboembolism. PAI-1 activity was the only preoperative fibrinolytic variable correlated to thromboembolism.
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PMID:Impaired fibrinolysis and postoperative thromboembolism in orthopedic patients. 185 6

We employed a canine model of pulmonary embolism, induced by injection of autologous radiolabelled blood clots, to investigate effects of hydralazine and an increase in cardiac output per se on recombinant tissue plasminogen activator-induced thrombolysis. Emboli increased pulmonary artery pressure (PAP) and decreased CO from 2.7 to 1.8 L/min-1. Following embolization, dogs were randomly divided into three groups. Group 1 received .5 mg/kg of rtPA over 30 minutes. Group 2 received the same dose of rtPA and were pretreated with hydralazine to increase CO approximately 50 percent. In the group 3 dogs, CO was increased by opening a systemic A-V fistula. Following embolization, CO remained low in group 1, the mean 2 h time-averaged CO was 1.9 L/min-1. The CO was 2.9 and 3.1 L/min-1 in groups 2 and 3, respectively. Corresponding to the increased flow in groups 2 and 3, rate and extent of pulmonary thrombolysis significantly increased. These results indicate that an increase in CO augments rtPA-induced pulmonary thrombolysis.
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PMID:Effects of hydralazine and increased cardiac output on recombinant tissue plasminogen activator-induced thrombolysis in canine pulmonary embolism. 170 25

More than 10 years ago, thrombolytic therapy with urokinase and streptokinase for pulmonary embolism was found to have considerable advantages over standard heparin therapy. After the introduction of alteplase, a recombinant tissue plasminogen activator, further studies confirmed this benefit. However, thrombolytic therapy for pulmonary embolism has not gained universal acceptance, even though it now has U.S. Food and Drug Administration approval. Clear advantages of thrombolytic therapy over conventional heparin therapy are improved pulmonary capillary blood volume, accelerated clot lysis and accelerated pulmonary perfusion. Earlier reversal of right-sided heart failure, a lower incidence of recurrent pulmonary embolism, a reduced risk of chronic pulmonary hypertension and reduced mortality have been claimed as advantages, but these have not been adequately proved. A recent survey suggests that about half of all patients with pulmonary embolism are potential candidates for thrombolytic therapy. In a subset of patients with hemodynamic compromise, thrombolysis has definite advantages over heparin therapy.
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PMID:Thrombolysis for pulmonary embolism. 192 47

Thrombolytic therapy decreases mortality in patients with acute myocardial infarction and is now widely used in such patients. The choice of which thrombolytic agent to use in such patients, either streptokinase or recombinant tissue plasminogen activator (rt-PA), is based on regional preferences. The standard dose of streptokinase is 1.5 million units over 60 min, and the dose of rt-PA that is commonly used is 100 mg over 3 h. Experiments in animals have demonstrated that rt-PA produces continuing thrombolysis after it is cleared from the circulation and that thrombolysis is both increased and accelerated and bleeding is reduced when rt-PA is administered over a short time period. Based on these studies, there have been a number of recent trials examining alternative dosage regimens for rt-PA (bolus, front-loaded, and accelerated) in patients with myocardial infarction. To date, there is no convincing evidence that such regimens are superior to the more traditional rt-PA regimen. Future randomized trials will determine whether attempts to optimize rt-PA regimens will result in more efficacious treatment regimens. Interest in the use of thrombolytic therapy for patients with acute pulmonary embolism has been rekindled. The traditional 12- to 24-h regimens of streptokinase and urokinase are not optimal because of their logistic complexity and associated hemorrhagic complications. Clinical studies have demonstrated that rt-PA, 100 mg over 2 h, is an effective thrombolytic agent in patients with acute pulmonary embolism. In a recent double-blind trial in patients with acute pulmonary embolism, rt-PA, 0.6 mg/kg infused over 2 min, improved pulmonary perfusion. This bolus regimen is attractive because it is simple to administer. Future studies will compare the relative efficacy and safety of these two rt-PA regimens in patients with acute pulmonary embolism.
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PMID:Bolus, front-loaded, and accelerated thrombolytic infusions for myocardial infarction and pulmonary embolism. 200 9

A canine model of pulmonary embolism, induced by injection of autologous radioactive blood clots, was used to investigate principles of thrombolysis in pulmonary embolism. One study compared recombinant tissue plasminogen activator (rtPA) with heparin in the treatment of pulmonary embolism. This study also compared the efficacy of rtPA (1 mg/kg) given over 15 min (rtPA15) to the same total dose infused over 90 min. Compared with heparin, both rtPA regimens induced marked pulmonary thrombolysis. During drug infusion, the rate of thrombolysis was increased 2-fold with rtPA15. A 2nd canine study investigated the physiologic mechanism of the decrease in pulmonary artery pressure with rtPA. The pattern of hemodynamic improvement with rtPA indicated that pulmonary thrombolysis predominantly occurred in partially, rather than totally, obstructed vascular units. A 3rd canine study compared rtPA and high-dose urokinase (UK) in treatment of pulmonary embolism. Both rtPA regimens were superior to UK in inducing pulmonary thrombolysis and improving pulmonary hemodynamics. Most recently, the effects of flow dynamics on rtPA-induced pulmonary thrombolysis were investigated, and it was demonstrated that an increase in cardiac output markedly enhanced rtPA-induced pulmonary thrombolysis. Most likely, the increase in cardiac output increased thrombolysis by enhancing delivery of rtPA to thrombus in partially obstructed vascular units.
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PMID:Principles of thrombolysis in pulmonary embolism. 200 13

Acute and subacute deep venous thrombosis can be followed by two serious complications: pulmonary embolism feared in the early stadium and the postthrombotic syndrome (PTS) as a late complication. After a lapse of months and years there might appear a complete or incomplete recanalization, but the valves of the veins will be destroyed. Therefore it is understandable to strive first an active therapy as thrombectomy or thrombolysis to remove thrombosis. There will be released a physiological tissue plasminogen activator from the endothelium of the vein increasing a local fibrinolytic activity. But it is not strong enough to reopen the occlusion within a few days. This is only possible adding exogenous activators as streptokinase, urokinase and recently rt-PA. Heparin is well known at low-dose subcutaneously for thrombosis prophylaxis. The high doses of heparin infusion intravenously with 30-40,000 units daily are used "therapeutically" inhibiting growth-promotion of the thrombus and reducing the incidence of pulmonary embolism markedly. In respect of a postthrombotic syndrome (oedema, leg ulcers) it needs the evaluation of the early and follow up late results and the analysis of efficiency and risk of the two models of treatment. It was necessary comparing the success rate of reopening of the occluded veins after some days and follow up 5 or 6 years in clinical studies. The reopening rate in thrombolysis was about 3 times higher than in heparin therapy. But in contrast bleeding was 3 times lower in heparin therapy. For the long term follow up, physical examination, doppler-sonography phlebodynamometry and vein occlusion plethysmography were assessed. The acute intervention, regarding treatment, turned out to be the crucial prognostic parameter. Syndromes and clinical findings did indeed correlate quite well with the outcome of fibrinolytic treatment. Postthrombotic syndrome was rare in cases with complete patency. In cases where patency was only partially or not at all achieved, postthrombotic syndrome was present to a higher degree the more central and the more extensive the remaining thrombus was. In deep venous thrombosis of the lower extremity thrombolytic therapy is recommended mostly to younger patients with acute, the popliteal and the femoral vein including thrombosis, except of contraindications. More over in each of an individual case it has to be decided whether the aggressive or conservative therapy is to prefer.
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PMID:[The treatment of deep venous thrombosis. Thrombolysis vs heparin]. 209 22


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