Mitral valve compensation for annular dilatation: In vitro study into the mechanisms of functional mitral regurgitation with an adjustable annulus model

Background and aim of the study: Mitral annulus dilatation has been identif ied as an important factor in functional mitral regurgitation (FMR). Howeve r, the pathophysiologic interaction of annular dilatation and papillary mus cle (PM) displacement in FMR, which occurs clinically in left ventricular ( LV) dilatation, is still not well understood. It is difficult to separate t hese competing factors in vivo, leading to confusion in identifying the rea l role of the annular dilatation in FMR and its interaction with PM displac ement. Methods: To better understand the competing factors, an in vitro model was developed with a D-shaped adjustable mitral annulus that could be changed f rom 5.5 cm(2) to 13.0 cm2 during experiments, independent of varying PM pos itions. Six excised normal porcine mitral valves were mounted in a left ven tricular model with the adjustable annulus device and tested in a physiolog ic pulsatile flow system under normal cardiac output and left ventricular p ressure (5.0 l/min, 120 mmHg). Papillary muscles were placed in normal and then displaced to an apical posterolateral position, to simulate pathologic al conditions seen clinically. Regurgitation was measured directly by a flo w probe and the mitral valve geometry and leaflet coaptation were recorded by video camera through the model's atrium window. In addition, 2D echocard iography was used to evaluate leaflet coaptation and color Doppler flow map ping to detect the regurgitant flow field. Results: The results showed that in normal PM position, the mitral regurgit ant was consistently at low level until the annulus was enlarged to 1.75 ti mes the normal size, at which time it increased sharply. Papillary muscle a pical posterolateral displacement, which simulates a dilated LV, caused reg urgitation to occur earlier (1.5 times the normal annulus size), and had an increased regurgitant volume (p <0.05). The leaflet gaps were first observ ed at the commissural areas of the valves, consistent with the location of regurgitant jets detected by color Doppler flow mapping. Asymmetric PM disp lacement created more regurgitation than both the symmetric PM tethering (p = 0.063) and normal PM position (p <0.01). The regurgitant jets were obser ved at the same commissural side as the PM displacement, even without signi ficant enlargement of the annulus. Conclusions: This in vitro study provides insight into the interaction betw een annular dilatation and PM displacement on FMR. The resulting effects an d their overall similarity to clinical observation could help further under stand the mechanism of FMR and provide additional information to improve fu ture therapeutic strategies.