Increased pulmonary artery pressures during exercise are related to persistent tricuspid regurgitation after atrial septal defect closure

Abstract

Objective Although closure of an atrial septal defect type secundum often normalizes right heart dimensions and pressures, mild tricuspid insufficiency might persist. This study aimed at (1) identifi cation of determinants explaining the persistence of tricuspid insuffi ciency after atrial septal defect closure, and (2) evaluation of functional capacity of patients with persistent mild tricuspid insuffi ciency.Methods and results Twenty-five consecutive patients (age 42 ± 17 y) were included from the outpatient clinic of congenital heart disease at the University Hospitals of Leuven. All underwent transthoracic echocardiography, semi-supine bicycle stress echocardiography and cardio-pulmonary exercise testing. Six patients (24%) had mild tricuspid insuffi ciency (2/4) compared to 19 patients (76%) with no or minimal tricuspid insuffi ciency (≤ 1/4) as assessed by semi-quantitative colour Doppler echocardiography. Mann-Whitney U and Fisher’s exact tests were performed where applicable. Patients with persistent mild tricuspid insuffi ciency were signifi cantly older than those with no or minimal tricuspid insuffi ciency (P = 0.042). At rest, no diff erences in right heart confi guration, mean pulmonary artery pressure or right ventricular function were found. At peak exercise, mean pulmonary artery pressure was signifi cantly higher in patients with mild persistent tricuspid insuffi ciency (P = 0.026). Peak oxygen uptake was signifi cantly lower in patients with mild persistent tricuspid insuffi ciency (P = 0.019).Conclusions Mild tricuspid insuffi ciency after atrial septal defect repair occurs more frequently in older patients and in patients with higher mean pulmonary artery pressure at peak exercise. In patients with mild tricuspid insuffi ciency, functional capacity was more reduced. Mild tricuspid insuffi ciency could be a marker of subclinical persistent pressure load on the right ventricle.