In the control group of the Moderate Pulmonary Embolism Treated With Thrombolysis (MOPETT) trial, the mean pulmonary artery systolic pressure (PASP) decreased from 51 to 43 mm Hg within 28 months, yet 57% of the patients were deemed to have pulmonary hypertension (PH) because their PASPs had remained ≥40 mm Hg. There are several explanations for this. First, in the calculation of PASP using the modified Bernoulli equation, we introduced the concept of right atrial/left atrial dimension ratio as a determinant of right atrial pressure. Consequently and in contrast to conventional calculations, which assign empiric values of 5 to 10 mm Hg for right atrial pressure, not infrequently, we assigned values of 15 to 18 mm Hg, thereby leading to higher PASPs. Second, the cumulative prevalence of pulmonary disease and active smoking status was higher in the control group. Third, most PASP values were clustered around the 40 mm Hg dichotomous cut-off point for defining PH. Hence, had this cutoff been increased by only a few mm Hg, a sharp decrease in the prevalence of PH would have resulted. Last, the patients were quite symptomatic and possibly sicker than in other studies, which had shown lower values of PASP.

In response to the other questions raised by Sehgal and Agarwal, we offer the following: The patients were adequately anticoagulated, and no difference was noted between the 2 groups in this respect. We did not analyze patients on the basis of the severity and type of pulmonary disease. The presence of diastolic dysfunction as determined by transvalvular spectral Doppler velocity waveforms in patients with interpretable tracings (excluding those with arrhythmias such as atrial fibrillation) was similar between the 2 groups, about 80%. As noted by Pengo et al, the frequency of PH after pulmonary embolism may be much higher than expected. Because the status of PASP before pulmonary embolism is not usually known, the increase in pressure after PE may still be within the normal range (and not reach the threshold to be considered PH), although for that particular patient, a definite adverse increase has occurred. What is clear is that the decrease in PASP at midterm follow-up from that at the time of pulmonary embolism is less in patients not receiving thrombolysis, whether one wants to consider this final pressure as indicative of PH.