Superior function of a bicuspid over a monocuspid patch for reconstruction of a hypoplastic pulmonary root in pigs.

In an experimental study in pigs, the function of monocuspid and bicuspid patches was compared to improve surgical reconstruction of a hypoplastic pulmonary root. Segments from glutaraldehyde-treated porcine aortic roots served as monocuspid and bicuspid patches. Their leaflets and commissures were marked with radiopaque metal clips. Marker movements were recorded at 100 frames/sec. Quantification of pulmonary insufficiency, right ventricular stroke volume, as well as pressures in the right ventricle, pulmonary artery, and aorta was performed before and after patch plasty. The cyclic motion of the leaflets showed a three-phase pattern in monocuspid and bicuspid patches: (1) a rapid opening motion with a significantly longer distance to be covered in monocuspid patches (7.5 mm in monocuspid versus 4.9 mm in bicuspid patches); (2) a slow closing motion that was significantly greater in monocuspid patches (31.5% of maximal displacement in monocuspid versus 18.2% and 23.8% in bicuspid patches); (3) a similar rapid closure motion in both types of patches. The commissural expansion was less than 6% for monocuspid and bicuspid patches and began 10 to 20 msec before valve opening. Considerable irregularities in the movement of the different leaflet markers, especially in monocuspid patches, indicated leaflet buckling as a result of redundant leaflet tissue. There was a significant pulmonary regurgitant fraction only in monocuspid patches (19% in monocuspid versus 7% in bicuspid patches) that occurred during early diastole. No pressure gradients were observed across either type of patch. In monocuspid patches, a greater leaflet displacement during rapid closure was correlated with an increased pulmonary insufficiency (r = 0.8875). In conclusion, the function of a bicuspid patch is superior to that of a monocuspid patch for repair of a hypoplastic pulmonary root and allows the construction of a competent and stenosis-free valve mechanism.