Thrombolytic therapy leads to a more rapid rate of resolution ofpulmonary embolic obstruction then standard therapy withheparin. This has been documented by angiography [1–3], lungscans [1,2,4,5], and echocardiography [4]. This being true, whyisn’t thrombolytic therapy indicated in all patients with pul-monary embolism (PE)?There are two major drawbacks of thrombolytic therapy ascomparedtoheparin:increasedmajorbleedingcomplicationsandincreased cost. Given these two disadvantages, thrombolytictherapy could only be recommended if it was shown to decreasethemortalityormorbidity ofpulmonaryembolism (PE).Despitenearly four decades of study, thrombolytic therapy has not beenshown to decrease the mortality or the morbidity of acute PE.Effect of thrombolytic therapy on the mortalityof haemodynamically stable PE patientsAs shown in Table1, there has been one randomized clinicaltrial comparing urokinase to heparin [1] and five trials compar-ing rt-PA to heparin [3–7]. The mortality in the 316 patientstreated with heparin in these trials (4.1%), was not significantlydifferent than the 4.6% mortality in the 305 patients treated witha thrombolytic agent.TheprincipalcauseofdeathinpatientswithPEwhoarehemo-dynamically stable when therapy is begun is recurrent PE [8].Therefore, thrombolytic therapy would decrease the mortalityof hemodynamically stable PE patients only if it decreased therate of recurrent PE. In studies where recurrent PE has beendocumented by follow-up lung scans or pulmonary angiograms,there has been no difference between patients treated withthrombolytics or heparin [1,3,6,7]. Given the available data,it would not be appropriate to recommend thrombolytic therapyfor PE patients who are hemodynamically stable, for whom themortality with heparin therapy is less than 5% [9].However, it has been shown that a subset of PE patients whoare hemodynamically stable, thosewho have echocardiographicevidence of right ventricular dysfunction (RVD), have a highermortality than those without RVD. In three reports [10–12] themortality of PE in 167 patients without shock, but with RVDwas 4% compared to 0.9% in 216 patients without RVD. In areport from a multicenter registry, Konstantinides et al. [13]reported the mortality of 719 PE patients who were hemody-namically stable. The mortality in those with RVD was 10%,compared to 4.1% in those without RVD. This increasedmortality in patients with evidence of RV dysfunction hasled to recommendations for thrombolytic therapy in this subsetof patients [7,13,14]. Given that approximately 50% of all PEpatients have RV dysfunction [4], the efficacy of this recom-mendation needs to be validated.Effect of thrombolytic therapy on the mortality ofhaemodynamically stable PE patients with rightventricular dysfunctionHamel et al. [15] reported data on the treatment of PE from aregistry in France. In this report, 153 consecutive patients withmassive PE were treated with heparin or thrombolytic therapydepending on the decision of the treating physician in this non-randomized observational study. Sixty-four patients treatedwith thrombolytic therapy were matched by echocardiographicevidence of RV dysfunction with 64 patients treated withheparin. In addition to comparable echocardiographic findings,the two groups were evenly matched by age, lung-scan findings,and the presence of associated cardiac and pulmonary disease.The mortality in the 64 patients treated with thrombolytics was6%; there were no deaths in those treated with heparin. The rateof recurrent PE was the same in both groups. These results donot support the use of thrombolytic therapy in PE patients withRVD who are hemodynamically stable.The first randomized clinical trial of heparinvs. thrombolytictherapy (alteplase) in PE patients with echocardiographic evi-dence of right ventricular dysfunction without shock wasreported by Konstantinides et al. [7]. The mortality in 118patients randomized to receive alteplase plus heparin (3.4%)was not significantly different than the mortality in 138 patientsreceiving heparin alone (2.2%). However, in-hospital death wasnot the primary end point in this important study. The primaryend point was in-hospital death or ‘clinical deterioration re-quiring an escalation of treatment.’ Escalation of treatmentoccurred in 24.6% of heparin patients, compared to 10.2% of