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 RESULTS: Seventeen 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/m(2) at rest vs. 52.8 ± 8.8 mL/m(2) 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/m(2), 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/m(2), 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/m(2), 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). CONCLUSION: Percutaneous 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.
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 RESULTS: Seventeen 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/m(2) at rest vs. 52.8 ± 8.8 mL/m(2) 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/m(2), 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/m(2), 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/m(2), 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). CONCLUSION: Percutaneous 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.
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