Determinants of cardiopulmonary functional improvement after transcatheter atrial septal defect closure in asymptomatic adults

OBJECTIVES 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) under-went 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 VO2) (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 VO2 improvements and Qp/Qs (p = 0.0013). Left ventricular ejection fraction (LVEF) (p < 0.0001) and left ventricular end-diastolic diameter (LVEDD) (1) < 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 VO2 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 VO2. (C) 2004 by the American College of Cardiology Foundation.