title: Determinants of cardiopulmonary functional improvement after transcatheter atrial septal defect closure in asymptomatic adults.
abstract: OBJECTIVE
  We sought to evaluate the course of cardiopulmonary function after transcatheter atrial septal defect (ASD) closure and to identify the physiopathologic mechanisms leading to this change.
  
  
  BACKGROUND
  Conflicting reports exist on cardiopulmonary functional improvement in asymptomatic adults after transcatheter closure of a secundum ASD.
  
  
  METHODS
  Thirty-two consecutive adults (13 males; age 42.6 +/- 16.7 years) underwent maximal cardiopulmonary exercise testing and transthoracic echocardiography both on the day before and six months after transcatheter ASD closure. Mean pulmonary artery pressure, pulmonary to systemic flow ratio (Qp/Qs), and ASD diameter were measured before closure.
  
  
  RESULTS
  Peak oxygen uptake (Vo(2)) (p < 0.001), peak oxygen pulse (p = 0.0027), and vital capacity (p = 0.0086) improved after ASD closure, although peak heart rate did not. A significant correlation was found between peak Vo(2) improvements and Qp/Qs (p = 0.0013). Left ventricular ejection fraction (LVEF) (p < 0.0001) and left ventricular end-diastolic diameter (LVEDD) (p < 0.0001) significantly increased after six months, although left ventricular end-systolic diameter did not. Right ventricular long- and short-axis dimensions decreased (both p < 0.0001). Peak Vo(2) and of peak oxygen pulse improvements correlated to both LVEF (p = 0.0009 and 0.0019, respectively) and LVEDD (p < 0.0001 and 0.032, respectively) increments. The decrease of both long- and short-axis right ventricular dimensions positively correlated to both LVEF and LVEDD improvements. The improvement in LVEF correlated to Qp/Qs (p = 0.0026).
  
  
  CONCLUSIONS
  Transcatheter ASD closure leads to a significant improvement in cardiopulmonary function within six months, via an increase in peak oxygen pulse. An increase in both left ventricular stroke volume and cardiac output due to a positive ventricular interaction is the mechanism leading to improved peak Vo(2).
authors.affiliation: Pediatric Cardiology and Adult Congenital Unit, Bologna, Italy. alessandro5574@iol.it
authors.forename: Alessandro
authors.initials: A
authors.lastname: Giardini
authors.forename: Andrea
authors.initials: A
authors.lastname: Donti
authors.forename: Roberto
authors.initials: R
authors.lastname: Formigari
authors.forename: Salvatore
authors.initials: S
authors.lastname: Specchia
authors.forename: Daniela
authors.initials: D
authors.lastname: Prandstraller
authors.forename: Gabriele
authors.initials: G
authors.lastname: Bronzetti
authors.forename: Marco
authors.initials: M
authors.lastname: Bonvicini
authors.forename: Fernando M
authors.initials: FM
authors.lastname: Picchio
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D004452:Echocardiography; D005080:Exercise Test; D017079:Exercise Tolerance; D005260:Female; D006344:Heart Septal Defects, Atrial / Q000503:physiopathology* / Q000601:surgery*; D006801:Humans; D008297:Male; D008875:Middle Aged; D019919:Prosthesis Implantation / Q000379:methods*; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000502:physiology