Background The incidence of pulmonary hypertension (PH) after an episode of acute pulmonary embolism (PE) is thought to be up to 4%. The incidence of persistent clot without PH is less clear. We evaluated the incidence of persistent perfusion defects in patients followed up after PE and assessed the impact on pulmonary arterial pressure measured by echocardiography.
Methods The clinical pathway for outpatient follow-up of patients with PE includes a nuclear medicine ventilation-perfusion scan at 5 months post PE. When this is positive, an echocardiogram is requested to look for evidence of PH. A retrospective study of consecutive patients attending outpatient follow-up was carried out to determine the incidence of persistent perfusion defects and echocardiographic findings suggestive of PH.
Results Ninety-three patients were identified between February 2009 and July 2011 and their clinical data were studied retrospectively. 59 patients (63%) had persistent perfusion defects at 6 months. Of these 49 (83%) underwent echocardiography of which 12 had undetectable tricuspid regurgitation (TR). In the remaining 37, pulmonary artery systolic pressure (PASP) could be estimated from the TR velocity. Results are shown in Abstract S24 figure 1 and are skewed due to the presence of patients with PH. Median PASP (with IQR) was 32 mm Hg (26–39). The shaded area shows the 95% CIs for the normal PASP (28±9.8 mm Hg, mean ± 2SD). Fourteen patients had estimated PASP above the normal range. Six patients were investigated with cardiac catheterisation and two were found to have chronic thromboembolic pulmonary hypertension (CTEPH). Borderline patients were kept under observation.
Conclusions Although the number of patients with CTEPH was in the expected range, the incidence of persistent perfusion defects following PE was surprisingly high in our cohort. Many of these patients fall in to a grey zone with borderline elevated pressures on echocardiography. The long-term outcomes of these patients and the physiological implications of their persistent perfusion defects are yet to be established and require further evaluation.