Effects of annular size, transmitral pressure, and mitral flow rate on the edge-to-edge repair: An in vitro study

Background. Although edge-to-edge repair is an established adjunctive procedure, there is still debate on its long-term durability and efficacy. Methods. Fifteen porcine mitral valves were studied in a physiologic left heart simulator with a variable size annulus ( dilated = 8.22 cm(2), normal = 6.86 cm(2), contracted = 5.5 cm(2)). Mitral valves were tested under steady and physiologic pulsatile flow conditions ( cardiac outputs: 4 to 6 L/min), at peak transmitral pressures between 100 mm Hg and 140 mm Hg. A miniature force transducer was used to measure the Alfieri stitch force ( FA). Mitral flow rate ( MFR), transmitral pressure, effective orifice area, mitral regurgitation, and FA were monitored. Results. The edge-to-edge repair led to a decrease in effective orifice area of 16.55% +/- 8.22%; further reduction in effective orifice area was attained with annular contraction. Mitral regurgitation after the edge-to-edge repair was significantly higher ( p < 0.05) with annular dilation. In the pulsatile experiments, two peaks in FA were observed: one during systole ( F-A = 0.059 +/- 0.024 N) and a second during diastole ( F-A = 0.072 +/- 0.021 N). Multivariate analysis of variance analysis showed that during systole, transmitral pressure and mitral annular area ( MAA) had significant effects on F-A [ F-A = ( 4.40 x 10(-4)) transmitral pressure ( mm Hg) + ( 5.0 x 10(-3)) MAA ( cm(2)) - 0.05 ( R-2 = 0.80)], whereas during diastole MFR and MAA had significant effects on F-A [ F-A = ( 1.03 x 10(-4)) MFR2 ( L/min) - ( 1.60 x 10(-3)) MAA ( cm(2)) + 0.02 ( R-2 = 0.90)]. Conclusions. With annular dilation, mitral regurgitation persisted even after the edge-to-edge repair. The edge-to-edge repair does not cause clinically relevant mitral valve stenosis in a normal size mitral valve. Mitral flow rate and transmitral pressure are the main determinants of F-A during the cardiac cycle. Increasing annular area increases F-A during systole but decreases F-A during diastole. Systolic F-A may become dominant with increases in MAA or peak transmitral pressure, or both.