Pulmonary homograft monocusp reconstruction of the right ventricular outflow tract: outcomes to the intermediate term.

BACKGROUND

There is limited information on longer-term outcomes of pulmonary homograft monocusp (PHM) reconstruction of the right ventricular outflow tract (RVOT).

METHODS

A retrospective review of 131 consecutive patients undergoing RVOT reconstruction with PHM was completed.

RESULTS

Median age was 7.6 months (range, 1 day to 14 years) and weight was 7.3 kg (range, 2 to 65 kg). Most patients (108 of 131; 82%) underwent repair for Tetralogy. After PHM, median duration of mechanical ventilation was 1 day (range, 0 to 89) and hospital stay was 6.5 days (range, 2 to 137). Hospital mortality was 2% (3 of 131) with 1 patient undergoing early replacement of PHM. Echocardiogram at hospital discharge demonstrated peak RVOT gradient of 16 mm Hg (range, 4 to 64 mm Hg); and pulmonary insufficiency was absent/trivial in 40%, mild in 42%, moderate in 16%, and severe in 2%. Follow-up is completed in 91% of hospital survivors at a median of 5 years (range, 1 to 12). There were 5 late deaths, with an actuarial survival of 96% +/- 3.7%, 94% +/- 4.6%, and 89% +/- 9.2% at 1 year, 5 years, and 10 years, respectively. There were 24 reinterventions, including 10 pulmonary valve replacements. Median time to valve replacement was 1.9 years (range, 0.4 to 4.6). Actuarial freedom from pulmonary valve replacement was 97% +/- 3.0%, 90% +/- 6.1%, and 85% +/- 10.3% at 1 year, 5 years, and 10 years, respectively. Echocardiogram at last follow-up demonstrated no increase in RVOT gradient compared with hospital discharge (16 mm Hg), but there was significant increase in pulmonary insufficiency (mild 27%, moderate 39%, severe 34%).

CONCLUSIONS

Pulmonary homograft monocusp reconstruction is an alternative strategy for RVOT reconstruction and provides early but gradually diminishing protection against pulmonary insufficiency without a risk of stenosis. As expected, PHM function decreases over time as the RVOT grows and the homograft tissue undergoes structural deterioration.