AIMS: To investigate the early clinical and physiological consequences of relieving chronic right ventricular (RV) volume overload with percutaneous pulmonary valve implantation (PPVI). METHODS AND RESULTS: We selected 17 patients (age 21.2 +/- 8.7 years), from a total of 125 who underwent PPVI, because they had important pulmonary regurgitation (PR) [regurgitant fraction > 25% on magnetic resonance (MR)] and an echocardiographic gradient < 50 mmHg across the RV outflow tract. Cardiopulmonary exercise testing, tissue Doppler and MR were performed before and within 3 months of PPVI. Following PPVI, PR (40.7 +/- 7.3 to 4.1 +/- 6.1%, P < 0.001) and RV end-diastolic volume fell (115.4 +/- 33.1 to 98.9 +/- 32.0 mL/m(2), P = 0.001); effective RV stroke volume increased (34.3 +/- 7.8 to 44.4 +/- 9.3 mL/m(2), P < 0.001). Left ventricular end-diastolic volume (66.6 +/- 18.0 to 73.4 +/- 16.5 mL/m(2), P = 0.014), stroke volume (38.4 +/- 11.1 to 46.4 +/- 10.2 mL/m(2), P = 0.001) and ejection fraction (57.8 +/- 8.1 to 63.5 +/- 5.2 mL/m(2), P = 0.001) increased. Pulmonary artery diastolic pressure (8.9 +/- 4.5 to 12.5 +/- 5.2 mmHg, P = 0.041) and mitral E/Ea increased (from 9.0 +/- 2.0 to 11.6 +/- 3.1, P = 0.003). Patients felt better, but standard measures of exercise capacity were unchanged. CONCLUSION: PPVI relieves PR and restores compensatory cardiac performance. The lack of improvement in exercise parameters suggests that, in contrast to pressure overload, the contractile reserve of chronically volume-overloaded myocardium is limited.
AIMS: To investigate the early clinical and physiological consequences of relieving chronic right ventricular (RV) volume overload with percutaneous pulmonary valve implantation (PPVI). METHODS AND RESULTS: We selected 17 patients (age 21.2 +/- 8.7 years), from a total of 125 who underwent PPVI, because they had important pulmonary regurgitation (PR) [regurgitant fraction > 25% on magnetic resonance (MR)] and an echocardiographic gradient < 50 mmHg across the RV outflow tract. Cardiopulmonary exercise testing, tissue Doppler and MR were performed before and within 3 months of PPVI. Following PPVI, PR (40.7 +/- 7.3 to 4.1 +/- 6.1%, P < 0.001) and RV end-diastolic volume fell (115.4 +/- 33.1 to 98.9 +/- 32.0 mL/m(2), P = 0.001); effective RV stroke volume increased (34.3 +/- 7.8 to 44.4 +/- 9.3 mL/m(2), P < 0.001). Left ventricular end-diastolic volume (66.6 +/- 18.0 to 73.4 +/- 16.5 mL/m(2), P = 0.014), stroke volume (38.4 +/- 11.1 to 46.4 +/- 10.2 mL/m(2), P = 0.001) and ejection fraction (57.8 +/- 8.1 to 63.5 +/- 5.2 mL/m(2), P = 0.001) increased. Pulmonary artery diastolic pressure (8.9 +/- 4.5 to 12.5 +/- 5.2 mmHg, P = 0.041) and mitral E/Ea increased (from 9.0 +/- 2.0 to 11.6 +/- 3.1, P = 0.003). Patients felt better, but standard measures of exercise capacity were unchanged. CONCLUSION:PPVI relieves PR and restores compensatory cardiac performance. The lack of improvement in exercise parameters suggests that, in contrast to pressure overload, the contractile reserve of chronically volume-overloaded myocardium is limited.
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