title: 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) identification of determinants explaining the persistence of tricuspid insufficiency after atrial septal defect closure, and (2) evaluation of functional capacity of patients with persistent mild tricuspid insufficiency.
  
  
  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 insufficiency (2/4) compared to 19 patients (76%) with no or minimal tricuspid insufficiency ( 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 insufficiency were significantly older than those with no or minimal tricuspid insufficiency (P = 0.042). At rest, no differences in right heart configuration, mean pulmonary artery pressure or right ventricular function were found. At peak exercise, mean pulmonary artery pressure was significantly higher in patients with mild persistent tricuspid insufficiency (P = 0.026). Peak oxygen uptake was significantly lower in patients with mild persistent tricuspid insufficiency (P = 0.019).
  
  
  CONCLUSIONS
  Mild tricuspid insufficiency 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 insufficiency, functional capacity was more reduced. Mild tricuspid insufficiency could be a marker of subclinical persistent pressure load on the right ventricle.
authors.affiliation: Dept. of Cardiology, University Hospitals Leuven, Belgium.
authors.forename: Pieter
authors.initials: P
authors.lastname: De Meester
authors.forename: Alexander
authors.initials: A
authors.lastname: Van De Bruaene
authors.forename: Paul
authors.initials: P
authors.lastname: Herijgers
authors.forename: Jens-Uwe
authors.initials: JU
authors.lastname: Voigt
authors.forename: Luc
authors.initials: L
authors.lastname: Vanhees
authors.forename: Werner
authors.initials: W
authors.lastname: Budts
mesh_terms: D000328:Adult; D000367:Age Factors; D001530:Belgium; D006348:Cardiac Surgical Procedures / Q000009:adverse effects* / Q000379:methods; D025401:Echocardiography, Stress / Q000379:methods; D005080:Exercise Test / Q000379:methods; D005260:Female; D006344:Heart Septal Defects, Atrial / Q000601:surgery*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011183:Postoperative Complications / Q000175:diagnosis* / Q000453:epidemiology / Q000503:physiopathology; D011379:Prognosis; D011651:Pulmonary Artery / Q000000981:diagnostic imaging / Q000503:physiopathology; D018570:Risk Assessment; D012307:Risk Factors; D016896:Treatment Outcome; D014262:Tricuspid Valve Insufficiency / Q000175:diagnosis* / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology