Patterns of systolic stress distribution on mitral valve anterior leaflet chordal apparatus. A structural mechanical theoretical analysis.

Increasing diffusion and complexity of mitral valve repair procedures may prompt an interest in the evaluation of the patterns of stress distribution on the chords, which are, from the structural mechanical point of view, the weakest element of valve apparatus. This theoretical analysis concentrates in particular on the mitral valve anterior leaflet. As is known, the vast majority of the chordae are attached to the anterior leaflet within the coaptation area; during systole they are then necessarily parallel, aligned along the same plane as that of the leaflets' coaptation surface, to which they are attached; moreover the thickness of the chordae increases significantly from the marginal chordae to the more central ones. In normal conditions during systole the progressively wider coaptation surface causes the increasing stress to be supported by an increasing number of progressively thicker chords, which are substantially parallel and aligned on the coaptation surface plane in such a way that they can share the stress between them, according to their thickness; in other words chords form a multifilament functional unit which enrolls elements of increasing thickness in response to the mounting stress. The geometrical modifications of the valve apparatus architecture (annulus dilatation, leaflet retraction, chordal elongation or retraction) often associated with valve insufficiency due to chordal rupture, have the common result of causing, during systole, a radial disarrangement of the direction of most of the secondary chordae which are no longer parallel, aligned on the coaptation surface plane. Due to the negligible elastic module of the valve leaflet, in this new arrangement the various chordae cannot share the stress between themselves as they do in a normal physiological situation; on the contrary the thinner chordae nearer to the free margin are also loaded with the peak systolic stress, thus generating conditions favoring their rupture. It can, therefore, be hypothesized that the anatomopathological picture of valve insufficiency due to chordal rupture may be the final event of a series of geometrical modifications of valve apparatus architecture, the common consequence of which is to load thinner marginal chords with peak systolic stress from which they are normally spared, thus favoring their rupture.