This study investigates the contribution of infundibular versus pulmonary valve (PV) dysfunction on right ventricular (RV) function in a porcine model.
Clinical outcome after repair of tetralogy of Fallot is determined by the adaptation of the right ventricle to the physiological sequelae of the right ventricular outflow tract (RVOT) reconstruction. Recent surgical techniques are pursuing a PV-versus infundibulum-sparing approach.
In a porcine model, 3 types of RVOT dysfunction were created and compared with sham-operated controls: infundibular dysfunction (INF), PV insufficiency (PI), and combined infundibular–PV dysfunction (TAP). Both acute and chronic effects on RV function were studied by using conductance technology and magnetic resonance imaging.
In animals with PI, pulmonary regurgitant fraction progressed more in the presence of concomitant INF (54% in TAP versus 14% in PI; p = 0.03). Subsequently, RV end-systolic and end-diastolic volume increased more in both groups, resulting in decreased ejection fraction after 3 months. Preload-independent systolic indices showed acute impairment of RV contractility in all treatment groups but most in animals with infundibular scarring (INF and TAP). Further chronic deterioration was observed in animals of the TAP group. RV compliance improved proportionally most in the PI and TAP groups in relation to the extent of RV dilation.
Surgical RVOT dysfunction, whether it includes the infundibulum and/or the PV, has an immediate effect on RV performance. Although impaired RV contractility is due to intrinsic myocardial damage by infundibular distortion, it is chronically furthered by PI-related RV dilation. These findings support the adoption of a RVOT-sparing strategy to treat tetralogy of Fallot.