Evaluation of pulmonary artery pressure and resistance by pulsed Doppler echocardiography in patients with end-stage renal disease on dialysis therapy

Abstract

BackgroundPulmonary hypertension (PH) is one of the most important comorbidities in patients undergoing hemodialysis (HD). The goal of the present work is to determine the possible etiologic factors for its occurrence. MethodsThe prevalence of PH was estimated by Doppler echocardiography in a cohort of 100 patients aged 49.3±13.9years on regular HD. Mean pulmonary artery pressure was estimated from pulmonary acceleration time by Mahan’s regression equation. Pulmonary vascular resistance and pulmonary capillary wedge pressure were calculated. We focused on the effect of HD on left and right ventricle diastolic and systolic function. Right ventricle systolic function was assessed by tricuspid annular systolic excursion and pulsed Doppler myocardial performance index. Since impaired endothelial function was postulated as an underlying cause of PH, we studied the effects of HD on brachial artery endothelial function. ResultsThe current study found that pulmonary hypertension was prevalent in 70% of patients on dialysis. Left atrium diameter, left ventricle mass indexed to body surface area, and mitral E/E′ were increased in the dialysis group (4.4±0.2cm, 126.5±24.6g/m2, and 16.9±4.4, respectively, p<0.001 for all). Pulmonary artery systolic pressure was positively correlated to duration of dialysis and negatively correlated to glomerular filtration rate (p<0.001 and r=−0.991). Pulmonary vascular resistance was significantly increased in dialysis patients (1.9±0.2 Wood units vs. 1.2 Wood units in controls, p<0.001). Endothelial dysfunction, defined as brachial artery flow mediated dilatation <6%, was found in 46% of dialysis group. ConclusionIncreased pulmonary artery systolic pressure in the HD population could be attributed to left atrium dilatation and left ventricle diastolic dysfunction. Pulmonary vascular resistance was significantly increased in dialysis group. This might be explained by impaired endothelial nitric oxide synthesis that not only caused systemic vasoconstriction but also affected the pulmonary vasculature.