Published reports suggest that 30% to 50% of patients experiencing a pulmonary embolism (PE) have perfusion defects 6 to 12 months later [Cosmi B et al. Intern Emerg Med. 2011; Sanchez O et al. J Thromb Haemost. 2010; Nijkeuter M et al. Chest. 2006]. An increased risk of dyspnea and greater pulmonary artery pressure can accompany these residual perfusion defects [Sanchez O et al. J Thromb Haemost. 2010]. The PADIS-PE study [NCT00740883] was a randomized, double-blind, multicenter study conducted to determine the rate of residual perfusion defects and associated risk factors in patients who had experienced a single episode of unprovoked PE. The study results were presented by Olivier Sanchez, MD, PhD, Georges Pompidou European Hospital, Paris, France.

The study was conducted from 2007 to 2012 at multiple centers in France. Patients having their first unprovoked PE received 6 months of anticoagulation therapy, then underwent a lung ventilation/perfusion (V/Q) scan, echocardiography, and a leg ultrasound. Patients with a normal or near-normal V/Q lung scan at baseline were classified as having no perfusion defect, and those with a pulmonary vascular obstruction ≥ 10% were classified as having a perfusion defect. Patients were randomized to 18 months of warfarin treatment (n = 184) or placebo (n = 187), evaluated at 18 months, and followed for another 24 months. Risk factors associated with the presence of residual perfusion defects were identified using univariate and multivariate analyses of the patients’ baseline data.

PE was initially diagnosed via positive spiral computed tomography in 285 patients (77%) and via high-probability V/Q lung scan in 86 patients (23%). Proximal deep vein thrombosis and right ventricular dysfunction were diagnosed in 112 (30%) and 123 (33%) patients, respectively. A total of 234 patients received low-molecular-weight heparin (LMWH), 370 patients received vitamin K antagonists, 6 had fibrinolysis, and 1 patient was treated with rivaroxaban.

In this study, 124 patients (33%) had residual perfusion defects, 61 patients (16%) had residual deep vein thrombosis, and 95 (27%) had thrombophilia. The mean ± SD D-dimer level was 352 ± 459 µg/L. Univariate analysis indicated that patients with a perfusion defect were significantly older (66 vs 53 years; OR, 1.05; 95% CI, 1.03 to 1.06; P < .0001), and that significantly higher proportions of patients with a perfusion defect had chronic respiratory disease (39 vs 34%; OR, 2.77; 95% CI, 1.64 to 4.67; P < .001) and chronic cardiac disease (9 vs 4%; OR, 4.60; 95% CI, 1.39 to 15.2; P = .013). Independent risk factors for residual perfusion defects identified in the multivariate analysis included age > 65 years (OR, 3.28; 95% CI, 1.91 to 5.63; P < .0001), chronic respiratory disease (OR, 2.10; 95% CI, 1.12 to 3.93; P = .021), and right ventricular dysfunction at diagnosis (OR 1.96; 95% CI, 1.14 to 3.37; P = .014). Initial treatment with LMWH vs unfractionated heparin or pentasaccharide was associated with a decreased risk of residual perfusion defects (OR, 0.50; 95% CI, 0.29 to 0.86; P = .013).