Poster session 4

Background: The purpose of this study was to assess right ventricular (RV) function in patients with chronic obstructive pulmonary disease (COPD) with and without pulmonary hypertension (PH) using three-dimensional speckle tracking echocardiography (3DSTE) and compare 3DSTE parameters with conventional RV function indexes.\udMethods: Thirty-two patients with COPD and thirty-two healthy subjects were studied. Twelve patients had PH confirmed by right heart catheterization (mean pulmonary artery pressure >25mmHg). Twenty patients had normal pulmonary artery pressures. Standard 2D measurements (tricuspid annulus excursion -TAPSE-, fractional area change -RVFAC-) and mitral and tricuspid tissue-Doppler annular velocities were obtained. RV 3D volumes, and RV global and regional ejection fraction (3DRVEF) were determined. Peak systolic velocities and strain were measured in the LV and RV free-wall segments. Respiratory function tests were performed (FEV1/VC = forced expiratory volume in one second / vital capacity; DLCO/VA = carbon monoxide diffusion lung capacity per unit of alveolar volume).\udResults: Global free-wall RV longitudinal strain (GFW-RVLS) and 3DRVEF were significantly lower compared to controls both in patients with PH (p<0.0001 and p=0.0003 respectively) and without PH (p<0.001 and p<0.005 respectively). Both GFW-RVLS and 3DRVEF correlated similarly with mean pulmonary artery pressure (r=0.62 and r=0.64; p=0.004 for both) and with pulmonary vascular resistance (r=0.65 and r=0.67; p=0.003 for both). No correlation was observed between RV and LV strain parameters. A significant relationship was shown between GFW-RVLS and DLCO/VA (r=0.72, p<0.005), and GFW-RVLS and FEV1/VC (r=0.75, p<0.001).\udConclusions: RV 3D and 3DSTE parameters were abnormal in COPD patients compared to normals and had a higher association with COPD severity compared to standard RV function measurements. RV deformation changes did not appear to be a consequence of LV dysfunction. Detection of RV systolic impairment, even in the absence of pulmonary hypertension, suggests that RV myocardial damage in COPD cannot be blamed solely to pressure overload