Kuper’s November E-shift

Question 1 What is the utility of Echo for a pt with established submassive PE?

Although, the pt with submassive PE (ie hemodynamically stable) is going to be receiving heparin regardless, an echo is a very good thing to get after the diagnosis has been made as it helps to risk stratify your pt. Mortality after submassive PE is linked to several things that could be elucidated on echo. RV strain leads to a two-fold increase in mortality¹ while RV thrombus increases 3 month mortality to 29 vs 14%². Following that logic that you should risk stratify PE pts they also should have a LE duplex scan since the presence of DVT has a hazard ratio of 2.01 for mortality at 3 months. That being said, I’m not sure if they need to stay in the department for either one of these scans.  

¹ ten Wolde M, Söhne M, Quak E, et al. Prognostic value of echocardiographically assessed right     ventricular dysfunction in patients with pulmonary embolism. Arch Intern Med 2004; 164:1685.

²Torbicki A, Galié N, Covezzoli A, et al. Right heart thrombi in pulmonary embolism: results from the International Cooperative Pulmonary Embolism Registry. J Am Coll Cardiol 2003; 41:2245.

 

Question 2 What is the role of thrombolytics in a submassive PE?

This question is complicated, I’m going to break it up into two discrete pt populations to make it manageable.

2a. A pt with submassive PE and RV dysfunction

The PEITHO trial tackled this question and showed that thrombolytics did improve pt outcome initially. Compared with heparin alone, thrombolysis resulted in a reduction in the primary endpoint of death or hemodynamic decompensation at seven days (6 versus 3 percent; OR 0.44, 95% CI: 0.23-0.87). However this improvement came at a cost with 2% vs 0.2% of pts had an ICH. Major bleeding was also reported 11% of pts older than 75 vs 0.6% in the heparin group. Importantly at 30 days there was no difference in mortality 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). I take away from this that we need to further risk stratify tenectaplase recipients before we start giving thrombolytics for RV dysfunction.

Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med 2014; 370:1402.

            2b. A pt with a large clot burden

The MOPETT trial addressed this, the randomized pts with a large clot burden defined as computed tomographic pulmonary angiography demonstrating >70 percent involvement with embolism in ≥2 lobar arteries or main pulmonary arteries or by a high probability ventilation/perfusion scan showing ventilation/perfusion mismatch in ≥2 lobes. The study used smaller doses of thrombolytics than previous using 100mg for pt >50kg or 0.5mg/kg for pt <50 kg. They found that:

• Lower rates of pulmonary hypertension (57 versus 16 percent)
• Lower pulmonary artery systolic pressures at 28 months (43 ± 6 versus 28 ± 7 mmHg)
• Faster resolution of pulmonary hypertension (50 ± 6 mmHg versus 51 ± 7 mmHg on admission; 43 ± 6 mmHg versus 28 ± 7 mmHg at 28 months)
• Similar rates of bleeding (0 percent in each group), recurrent PE (5 versus 0 percent), and mortality (5 versus 1.6 percent)

Criticism of this trial centers around the fact that <25% of the participants had any signs of RV strain (so possible a less severe cohort than the PEITHO trial). Also, only 121 pts were enrolled in the study so it needs to be done on a larger scale.

Sharifi M, Bay C, Skrocki L, et al. Moderate pulmonary embolism treated with thrombolysis (from the “MOPETT” Trial). Am J Cardiol 2013; 111:273.