In Vitro Measurement of the Coaptation Force Distribution in Normal and Functional Regurgitant Porcine Mitral Valves

Abstract

Closure of the left atrioventricular orifice is achieved when the anterior and posterior leaflets of the mitral valve press together to form a coaptation zone along the free edge of the leaflets. This coaptation zone is critical to valve competency and is maintained by the support of the mitral annulus, chordae tendinae, and papillary muscles. Myocardial ischemia can lead to an altered performance of this mitral complex generating suboptimal mitral leaflet coaptation and a resultant regurgitant orifice. This paper reports on a two-part experiment undertaken to measure the dependence of coaptation force distribution on papillary muscle position in normal and functional regurgitant porcine mitral heart valves. Using a novel load sensor, the local coaptation force was measured in vitro at three locations (A1–P1, A2–P2, and A3–P3) along the coaptation zone. In part 1, the coaptation force was measured under static conditions in ten whole hearts. In part 2, the coaptation force was measured in four explanted mitral valves operating in a flow loop under physiological flow conditions. Here, two series of tests were undertaken corresponding to the normal and functional regurgitant state as determined by the position of the papillary muscles relative to the mitral valve annulus. The functional regurgitant state corresponded to grade 1. The static tests in part 1 revealed that the local force was directly proportional to the transmitral pressure and was nonuniformly distributed across the coaptation zone, been strongest at A1–P1. In part 2, tests of the valve in a normal state showed that the local force was again directly proportional to the transmitral pressure and was again nonuniform across the coaptation zone, been strongest at A1–P1 and weakest at A2–P2. Further tests performed on the same valves in a functional regurgitant state showed that the local force measured in the coaptation zone was directly proportional to the transmitral pressure. However, the force was now observed to be weakest at A1–P1 and strongest at A2–P2. Movement of the anterolateral papillary muscle (APM) away from both the annular and anterior–posterior (AP) planes was seen to contribute significantly to the altered force distribution in the coaptation zone. It was concluded that papillary muscle displacement typical of myocardial ischemia changes the coaptation force locally within the coaptation zone.