Chronic thromboembolic pulmonary hypertension (CTEPH) comprises organizing thrombotic obstructions in the pulmonary arteries by nonresolving thromboemboli, formation of fibrosis and remodeling of pulmonary blood vessels. Surgical pulmonary endarterectomy (PEA) is the therapy of choice for patients with surgically accessible CTEPH, which leads to a profound improvement in hemodynamics, functional class and survival. Selecting the candidates that will benefit from surgery is still a challenging task. Criteria for surgical suitability have been described but the decision-making for or against surgical intervention remains still subjective. The optimal characterization of the reciprocal contribution of large vessel and small vessel disease in the elevation of pulmonary vascular resistance is crucial for the in-
COMMENTARY ON HOT ARTICLESWe read with great interest the recent article by Toshner et al [1] describing the analysis of pressure decay curve after pulmonary arterial occlusion (between the moment of occlusion and the pulmonary artery occluded pressure, PAOP) to test if the occlusion technique distinguished small from large vessel disease in chronic thromboembolic pulmonary hypertension (CTEPH).Pulmonary endarterectomy (PEA) of major, lobar, and segmental pulmonary arteries branches is the mainstay of therapy for patients with CTEPH. The best surgical results are achieved with complete endarterectomy and early postoperative reduction of pulmonary vascular resistance (PVR) to < 500 dyn.s.cm -5[2,3] . The cause of residual pulmonary hypertension in most cases is from concomitant small vessel disease, with three possible scenarios: (1) predominant obstructions of small subsegmental elastic pulmonary arteries; (2) classic pulmonary
FIELD OF VISION
18March 26, 2013|Volume 5|Issue 3|