Right Ventricular Dysfunction and Remodeling in Chronic Obstructive Pulmonary Disease Without Pulmonary Hypertension

Objectives The aim of the present study was to elucidate right ventricular (RV) function and structure in patients with chronic obstructive pulmonary disease (COPD) without pulmonary hypertension (PH). Background There is little knowledge of RV function and remodeling in COPD without PH. Methods Thirty-four controls and 98 patients with COPD were included. The study patients were divided into 2 groups by right heart catheterization: no PH (mean pulmonary artery pressure [mPAP] <25 mm Hg) and PH (mPAP >= 25 mm Hg). The echocardiographic tissue Doppler imaging variables of RV isovolumic acceleration, peak systolic strain, and RV myocardial performance index were measured at the basal free wall, and RV wall thickness and RV internal dimension were measured in the RV outflow tract. Results The increases in RV wall thickness and RV dimension were more evident when comparing controls with the no PH group (3.5 +/- 0.5 mm to 5.5 +/- 1.0 mm [p < 0.01] and 1.5 cm +/- 0.2 to 2.0 +/- 0.5 cm [p < 0.01]) than comparing the no PH group with the PH group (5.5 +/- 1.0 mm to 6.6 +/- 1.1 mm [p < 0.01] and 2.0 cm +/- 0.5 to 2.1 +/- 0.3 cm [p = NS]), respectively. Similarly, RV isovolumic acceleration, performance index, and strain deteriorated significantly when comparing controls with the no PH group and comparing the no PH group with the PH group (p < 0.01). Significant correlations were observed between mPAP and RV isovolumic acceleration, performance index, strain, and RV wall thickness (p < 0.01). RV impairment and increased RV wall thickness and RV dimensions were present even at slight elevations of mPAP (18 +/- 3 mm Hg) in the no PH group. Conclusions The present study showed that impaired RV systolic function, hypertrophy, and dilation were present even at a slight increase of mPAP, which indicates an early impact on RV function and structure in patients with COPD. RV isovolumic acceleration, performance index, and strain could detect subclinical disease and separate controls from those with no PH. (C) 2013 by the American College of Cardiology Foundation