Impact of reduction in right ventricular pressure and/or volume overload by percutaneous pulmonary valve implantation on biventricular response to exercise: An exercise stress real-time CMR study

Abstract

Aims To assess the impact of relief of pulmonary stenosis (PS) and pulmonary regurgitation (PR) by percutaneous pulmonary valve implantation (PPVI) on biventricular function during exercise stress.Methods and resultsSeventeen patients, who underwent PPVI for PS or PR, were included. Magnetic resonance imaging was performed at rest and during supine exercise stress pre-and within 1-month post-PPVI, using a radial k-t SENSE real-time sequence. In patients with PS (n 9), there was no reserve in right ventricular (RV) ejection fraction (EF) in response to exercise prior to PPVI (48.2 ± 12.1 at rest vs. 48.4 ± 14.8 during exercise, P 0.87). Post-PPVI, reserve in RVEF in response to exercise was re-established (53.4 ± 15.0 at rest vs. 59.6 ± 17.3 during exercise, P 0.003) with improvement in left ventricular stroke volume (LVSV) (45.4 ± 6.2 mL/m2 at rest vs. 52.8 ± 8.8 mL/m2 during exercise, P 0.001). In patients with PR prior to PPVI (n 8), LVSV during exercise increased (43.0 ± 8.5 vs. 54.3 ± 6.6 mL/m2, P < 0.001) due to reduction in PR fraction during exercise (29.2 ± 5.2 vs. 13.6 ± 6.1, P < 0.001). After PPVI, LVSV increased from rest to exercise (48.4 ± 8.8 vs. 57.2 ± 8.1 mL/m2, P < 0.001) due to improved RVEF (45.5 ± 8.3 vs. 50.4 ± 6.9, P 0.001). There was a significantly higher increase in LVSV at exercise from pre-to post-PPVI in PS patients than in PR patients (ΔLVSV 8.2 ± 4.1 vs. Δ2.9 ± 4.1 mL/m2, P 0.01). The reduction in the RV outflow tract gradient correlated significantly with the improvement in LVSV during exercise (r-0.73, P < 0.001). ConclusionPercutaneous pulmonary valve implantation in patients with PS leads to restoration of reserve in RVEF during exercise stress. In patients with PR, SV augmentation improves only mildly post-PPVI. Improvement in SV augmentation during exercise stress after PPVI is dependent mainly on afterload reduction. © 2012 The European Society of Cardiology All rights reserved.