Loss of Small Vessel Volume Fraction as a Marker for Pulmonary Hypertension in COPD

Abstract

SESSION TITLE: Pulmonary Hypertension SESSION TYPE: Original Investigation Poster PRESENTED ON: Wednesday, November 1, 2017 at 01:30 PM - 02:30 PM PURPOSE: Pulmonary hypertension develops in a subset of subjects with COPD, and when present is accompanied by increasing morbidity and mortality. Early diagnosis, prognostication and selection of subjects that may benefit from pulmonary vasodilatory therapy remains challenging. In prior work it has been shown that smokers show evidence of pulmonary vascular pruning in 3D reconstruction of the pulmonary vasculature. In this study we examine changes to the pulmonary vascular tree in patients with COPD and pre-capillary pulmonary hypertension proven by right heart catheterization (PAH). METHODS: A retrospective database query of subjects with diagnosis of COPD and PH possessing ct angiograms yielded approximately 200 subjects. From these, 21 subjects with non-elevated PCWP (<15mmHg), PH (elevated PVR and mPAP) and FEV1/FVC of less than 70% by PFT were selected. Of these, seven had 1mm cuts appropriate for reconstruction. A cohort of 15 subjects having undergone right heart catheterization, imaging and exercise testing with no evidence of cardiopulmonary disease was used as control subjects. Vascular reconstruction was performed as previously described. Small vessel volume fraction, defined as the vascular volume in small vessels (less than 5mm2 in cross-sectional area) divided by total vascular volume, was used to measure pruning. Association was tested using a two-tailed t-test, assuming unequal variances. RESULTS: Seven patients (Age 65.7±10.5) with COPD (FEV1pp 61.7±6.8%) were identified with precapillary PAH (mPAP 45±14.3mmHg; PVR 8.6±6WU; mPCWP 10.8±2.2mmHg, max 14mmHg). Fifteen subjects (Age 46 ; mPAP 15mmHg; PVR 1.1 WU; mPCWP 9mmHg) were used as controls. Subjects with PAH and COPD had significant proximal dilation and distal loss of vasculature, which was quantified by dividing the volume in small vessels (defined as those with cross sectional area of less than 5mm2 ) by the total volume of the vasculature detected. Small vessel volume fraction in the COPD group was lower (0.37 ± 0.12) as compared to control subjects (0.55 ±0.11) with a p-value of 0.006 for the comparison. CONCLUSIONS: The vascular pruning previously described in smokers is quantifiable from CT angiography in subjects with precapillary pulmonary arterial hypertension in the context of significant COPD burden. CLINICAL IMPLICATIONS: Measurement of pulmonary vascular morphology in smokers may be useful in detecting and subtyping the extent of pulmonary vascular disease in smokers. DISCLOSURE: The following authors have nothing to disclose: Farbod Rahaghi, Viviana Paz, James Ross, Raúl San José Estépar, George Washko, Franck Rahaghi Image processing techniques for reconstruction of the vasculature used are currently in exploratory stage and appropriate only for research purposes.