Abstract 14941: Increased Prevalence of Pulmonary Artery Hypertension and Deterioration of Right Ventricular Function after Chronic Right Ventricular Apical Pacing
Purpose: There is little information on the impact of right ventricular apical (RVA) pacing on the prevalence of pulmonary artery hypertension (PAH) and right ventricular (RV) function. This study aimed to investigate if elevated pulmonary artery systolic pressure (PASP) and impaired RV function developed in patients with preserved ejection fraction and without preexisting PAH after chronic RVA pacing during long-term follow up.
Methods: This prospective study enrolled 46 patients (mean age: 67±11years, 29 males) with symptomatic bradycardia and no evidence of PAH (PASP <35mmHg) who received RVA pacing. Patients who had LV ejection fraction <45% or had history of heart failure, persistent atrial fibrillation and pulmonary disease were excluded. Echocardiography was done at baseline and 1 year. PASP was calculated from the maximal velocity of tricuspid regurgitation and estimated right atrial pressure. Peak systolic (S') and peak diastolic velocity (E') at tricuspid annulus were measured by pulse-wave tissue Doppler imaging (TDI). Tricuspid annular displacement, peak systolic (Sm) and peak early diastolic (Em) myocardial velocities in basal and mid segments of RV free wall were measured by color-coded TDI. Mean velocity of two segments was calculated.
Results: The mean percentage of cumulative ventricular pacing during one year was 97.1%. In the whole group, PASP increased significantly at 1 year follow up when compared with baseline. PASP >35mmHg occurred in 10 patients (21.7%) at 1 year after chronic RVA pacing. TDI showed significant reduction in tricuspid annular displacement, S' & E' at tricuspid annulus and Sm & Em at RV free wall reflecting impairment of RV function (Table).
Conclusions: During chronic RVA pacing, elevated PASP and impaired RV function were detected in patients with preserved ejection fraction and without preexisting PAH. There is an increased risk of developing PAH even in patients without preexisting PAH before implantation.
- © 2010 by American Heart Association, Inc.