Open AccessImpaired Exercise Capacity following Atrial Septal Defect Closure: An Invasive Study of the Right Heart and Pulmonary Circulation
Author(s) -
Santos Mário,
Systrom David,
Epstein Stephen E.,
John Anitha,
Ruiz George,
Landzberg Michael J.,
Opotowsky Alexander R.
Publication year - 2014
Publication title -
pulmonary circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.791
H-Index - 40
ISSN - 2045-8940
DOI - 10.1086/678509
Subject(s) - medicine , asymptomatic , cardiology , vascular resistance , hemodynamics , cardiac index , stroke volume , vo2 max , cardiac output , blood pressure , heart rate
Patients with early repair of an isolated atrial septal defect (ASD) are expected to have unremarkable right ventricular (RV) and pulmonary circulation physiology. Some studies, however, suggest persistent functional impairment. We aimed to examine the role of abnormal RV and pulmonary vascular response to exercise in patients who had undergone ASD closure. Using a previously published data set, we reviewed invasive exercise cardiopulmonary testing with right‐sided hemodynamic data for 12 asymptomatic patients who had undergone ASD closure. The 5 (42%) patients with impaired maximal oxygen uptake ( V ̇ o 2max ) were older and exhibited a lower peak cardiac index (5.6 ± 0.8 vs. 9.0 ± 1.2 L/min/m 2 ; P =. 005) because of abnormal stroke volume augmentation (+3.2 ± 3.9 vs. +17.4 ± 10.2 mL/m 2 ; P =. 02). While all resting hemodynamic variables were similar, patients with lowV ̇ o 2max tended to have abnormal total pulmonary vascular resistance change during exercise (+11% ± 41% vs. ?28% ± 26%; P =. 06) and had a steeper relation between mean pulmonary arterial pressure and cardiac index (5.8 ± 0.6 vs. 2.2 ± 0.1 L/min/m 2 ; P =. 02). The increase in peak mean RV power during exercise was also significantly lower in the impaired‐ V ̇ o 2max patients (4.7 ± 1.6 vs. 7.6 ± 2.1 J/s; P =. 04). As described in the original study, despite normal resting hemodynamics, a subset of asymptomatic patients with repaired ASD had diminished exercise capacity. Our analysis allows us to conclude that this is due to a combination of abnormal pulmonary vascular response to exercise and impaired RV function.