***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    ***EXAMPLES*** 
    Input: Pulmonary embolism has frequently been chosen for trials of thrombolytic therapy , not only because of its importance to public health , but also because the effects of therapy on the embolus can be readily appreciated by the use of pulmonary angiography , hemodynamics , and lung scans . Moreover , this lesion is theoretically the most attractive potential indication for thrombolytic agents , because its pathophysiologic effects are attributable to right heart strain rather than less reversible tissue necrosis , and because the emboli are usually in previously healthy vessels with ready access to a systemically administered lytic agent . The disadvantages of study ing this lesion are its high sudden death rate , which leaves only less severe cases for study , and the demonstration that spontaneous fibrinolytic activity itself may result in the clearing of the pulmonary arterial tree . 2 , 3 Clinical trials have been carried out with both streptokinase and Dissolution of pulmonary emboli with heparin and urokinase is ascribed , respectively , to anticoagulation and fibrinolysis . Since truly independent assessment of these effects in man is lacking , we administered each drug alone . Fibrinogen and plasminogen plasma levels and the resolution of pulmonary emboli were measured in three r and omized groups of 10 patients each : groups A and C infused with small repeated doses of urokinase and a large single dose of urokinase , respectively , and group B who received heparin . After 6 h of treatment , fibrinogen fell in all the groups , while , after 12 h , remained equally reduced in groups A and B and declined further in group C. Plasminogen behaved similarly . Up to 60 h , statistical analysis showed that these effects were related to timing and amounts of urokinase and heparin infusion . These observations suggest that heparin may induce a lytic state . As to signs of pulmonary emboli resolution , no differences between groups were found in lung perfusion and gas exchange recovery at any time ( from 1 day to 1 year ) and in pulmonary artery pressure reduction at 1 week . The greater angiographic and scintigraphic recovery observed with urokinase , versus heparin alone , after 1 day of treatment in the Urokinase Pulmonary Embolism Trial may be ascribed to a synergistic effect with urokinase of heparin administered during the diagnostic work-out . The indications of heparin and urokinase should be evaluated in the light of these results BACKGROUND The role of fibrinolytic therapy in patients with intermediate-risk pulmonary embolism is controversial . METHODS In a r and omized , double-blind trial , we compared tenecteplase plus heparin with placebo plus heparin in normotensive patients with intermediate-risk pulmonary embolism . Eligible patients had right ventricular dysfunction on echocardiography or computed tomography , as well as myocardial injury as indicated by a positive test for cardiac troponin I or troponin T. The primary outcome was death or hemodynamic decompensation ( or collapse ) within 7 days after r and omization . The main safety outcomes were major extracranial bleeding and ischemic or hemorrhagic stroke within 7 days after r and omization . RESULTS Of 1006 patients who underwent r and omization , 1005 were included in the intention-to-treat analysis .  Death or hemodynamic decompensation occurred in 13 of 506 patients ( 2.6 % ) in the tenecteplase group as compared with 28 of 499 ( 5.6 % ) in the placebo group ( odds ratio , 0.44 ; 95 % confidence interval , 0.23 to 0.87 ; P=0.02 ) . Between r and omization and day 7 , a total of 6 patients ( 1.2 % ) in the tenecteplase group and 9 ( 1.8 % ) in the placebo group died ( P=0.42 ) . Extracranial bleeding occurred in 32 patients ( 6.3 % ) in the tenecteplase group and 6 patients ( 1.2 % ) in the placebo group ( P<0.001 ) . Stroke occurred in 12 patients ( 2.4 % ) in the tenecteplase group and was hemorrhagic in 10 patients ; 1 patient ( 0.2 % ) in the placebo group had a stroke , which was hemorrhagic ( P=0.003 ) . By day 30 , a total of 12 patients ( 2.4 % ) in the tenecteplase group and 16 patients ( 3.2 % ) in the placebo group had died ( P=0.42 ) . CONCLUSIONS In patients with intermediate-risk pulmonary embolism , fibrinolytic therapy prevented hemodynamic decompensation but increased the risk of major hemorrhage and stroke . ( Funded by the Programme Hospitalier de Recherche Clinique in France and others ; PEITHO EudraCT number , 2006 - 005328 - 18 ; Clinical Trials.gov number , NCT00639743 . ) Background — Clinical predictors for fatal pulmonary embolism ( PE ) in patients with venous thromboembolism have never been studied . Methods and Results — Using data from the international prospect i ve Registro Informatizado de la Enfermedad TromboEmbolica venosa ( RIETE ) registry about patients with objective ly confirmed symptomatic acute venous thromboembolism , we determined independent predictive factors for fatal PE . Between March 2001 and July 2006 , 15 520 consecutive patients ( mean age±SD , 66.3±16.9 years ; 49.7 % men ) with acute venous thromboembolism were included .  Symptomatic deep-vein thrombosis without symptomatic PE was observed in 58.0 % ( n=9008 ) of patients , symptomatic nonmassive PE in 40.4 % ( n=6264 ) , and symptomatic massive PE in 1.6 % ( n=248 ) . At 3 months , the cumulative rates of overall mortality and fatal PE were 8.65 % and 1.68 % , respectively . On multivariable analysis , patients with symptomatic nonmassive PE at presentation exhibited a 5.42-fold higher risk of fatal PE compared with patients with deep-vein thrombosis without symptomatic PE ( P<0.001 ) . The risk of fatal PE was multiplied by 17.5 in patients presenting with a symptomatic massive PE . Other clinical factors independently associated with an increased risk of fatal PE were immobilization for neurological disease , age > 75 years , and cancer . Conclusion — PE remains a potentially fatal disease . The clinical predictors identified in the present study should be included in any clinical risk stratification scheme to optimally adapt the treatment of PE to the risk of the fatal outcome The role of low-dose thrombolysis in the reduction of pulmonary artery pressure in moderate pulmonary embolism ( PE ) has not been investigated . Because the lungs are very sensitive to thrombolysis , we postulated that effective and safe thrombolysis might be achieved by a lower dose of tissue plasminogen activator . The purpose of the present study was to evaluate the role of this " safe dose " thrombolysis in the reduction of pulmonary artery pressure in moderate PE . During a 22-month period , 121 patients with moderate PE were r and omized to receive a " safe dose " of tissue plasminogen activator plus anticoagulation ( thrombolysis group [ TG ] , n = 61 patients ) or anticoagulation alone ( control group [ CG ] , n = 60 ) . The primary end points consisted of pulmonary hypertension and the composite end point of pulmonary hypertension and recurrent PE at 28 months . Pulmonary hypertension and the composite end point developed in 9 of 58 patients ( 16 % ) in the TG and 32 of 56 patients ( 57 % ) in the CG ( p < 0.001 ) and 9 of 58 patients ( 16 % ) in the TG and 35 of 56 patients ( 63 % ) in the CG ( p < 0.001 ) , respectively . The secondary end points were total mortality , the duration of hospital stay , bleeding at the index hospitalization , recurrent PE , and the combination of mortality and recurrent PE . The duration of hospitalization was 2.2 ± 0.5 days in the TG and 4.9 ± 0.8 days in the CG ( p < 0.001 ) . The combination of death plus recurrent PE was 1 ( 1.6 % ) in TG and 6 ( 10 % ) in the CG ( p = 0.0489 ) . No bleeding occurred in any group , and despite a positive trend in favor of a " safe dose " thrombolysis , no significant difference was noted in the rate of individual outcomes of death and recurrent PE when assessed independently . In conclusion , the results from the present prospect i ve r and omized trial suggests that " safe dose " thrombolysis is safe and effective in the treatment of moderate PE , with a significant immediate reduction in the pulmonary artery pressure that was maintained at 28 months BACKGROUND The effect of alteplase versus heparin in pulmonary embolism has not been studied extensively with serial pulmonary angiograms . OBJECTIVES The aim of this r and omized , open trial was to evaluate the efficacy and safety of alteplase followed by heparin , versus heparin alone , in 36 patients with angiographically documented pulmonary embolism . METHODS Twenty patients were allocated r and omly to a 2-h infusion of alteplase ( 10 mg bolus , then 90 mg over 2 h ) followed by heparin ; the other 16 patients were given intravenous heparin at a continuous infusion rate of 1,750 IU/h . RESULTS The vascular obstruction , assessed by the Miller index at pulmonary angiography , decreased significantly in alteplase-treated patients ( p less than 0.01 ) from a baseline of 28.3 + /- 2.9 to a value of 24.8 + /- 5.2 2 h after the start of infusion ; in the heparin group there was no change ( from 25.3 + /- 5.3 to 25.2 + /- 5.4 ) . Mean pulmonary artery pressure decreased significantly from a baseline of 30.2 + /- 7.8 mm Hg to 21.4 + /- 6.7 in the alteplase group and increased in the heparin group ( from 22.3 + /- 10.5 to 24.8 + /- 11.2 mm Hg ) . For a subset of patients , lung scans were performed at baseline and on days 7 and 30 . There were no differences between the two groups in the follow-up lung scans , but there were significant decreases from the baseline values . Bleeding occurred in 14 of 20 alteplase-treated patients and in 6 of 16 in the heparin group ( p = NS ) . There were three major bleeding episodes in the alteplase group and two in the heparin group . Two patients died after fibrinolysis ( one of acute renal failure after cardiac tamponade and one of cardiac arrest after cerebral hemorrhage ) and one patient in the heparin group died of recurrent pulmonary embolism . CONCLUSIONS Alteplase result ed in a greater and faster improvement of the angiographic and hemodynamic variables compared with heparin . However , the high frequency of bleeding observed with alteplase in this trial suggests that patients should be carefully selected before thrombolytic therapy is given AIMS To assess the role of cardiac troponin T ( cTnT ) levels on admission using a new , highly sensitive assay ( hsTnT ) in the risk assessment of normotensive patients with acute pulmonary embolism ( PE ) . METHODS AND RESULTS We prospect ively studied 156 consecutive normotensive patients with confirmed PE . The prognostic value of hsTnT at baseline was compared with the conventional cTnT troponin assay and with N-terminal pro-brain natriuretic peptide concentrations . Long-term follow-up was available for 153 patients ( 98.1 % ) . Highly sensitive troponin T values ranged from 0.001 to 357.2 pg/mL [ median 27.2 ( 25th-75th percentile 9.4 - 69.4 ) pg/mL ] . Overall , 100 patients ( 64 % ) had hsTnT > or = 14 pg/mL. Baseline hsTnT was higher in patients with an adverse 30-day outcome ( > or = 1 : death , need for catecholamines , endotracheal intubation , or cardiopulmonary resuscitation ) compared with an uncomplicated course [ 71.7 ( 35.5 - 117.9 ) vs. 26.4 ( 9.2 - 68.2 ) pg/mL ; P = 0.027 ] . The cut-off value of 14 pg/mL showed an excellent prognostic sensitivity and negative predictive value ( both 100 % ) . In comparison , as many as 50 % of the patients with an adverse early outcome would have been misclassified as low risk by cTnT ( cut-off 0.03 ng/mL ) . Logistic regression indicated a two-fold increase in the risk of an adverse outcome for each increase of hsTnT by 1SD of the natural logarithm ( P = 0.037 ) . Patients with elevated hs 
    Output:
    
Thrombolytic therapy reduces total mortality , PE recurrence , and PE-related mortality in patients with acute PE .
The decrease in overall mortality is , however , not significant in haemodynamically stable patients with acute PE .
Thrombolytic therapy is associated with an increase of major and fatal or intracranial haemorrhage