S. Nazari et al., Patterns of systolic stress distribution on mitral valve anterior leaflet chordal apparatus - A structural mechanical theoretical analysis, J CARD SURG, 41(2), 2000, pp. 193-202
Increasing diffusion and complexity of mitral valve repair procedures may p
rompt 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 coa
ptation area; during systole they are then necessarily parallel, aligned al
ong the same plane as that of the leaflets' coaptation surface, to which th
ey are attached; moreover the thickness of the chordae increases significan
tly from the marginal chordae to the more central ones. In normal condition
s during systole the progressively wider coaptation surface causes the incr
easing stress to be supported by an increasing number of progressively thic
ker chords, which are substantially parallel and aligned on the coaptation
surface plane in such a way that they can share the stress between them, ac
cording to their thickness; in other words chords form a multifilament func
tional unit which enrols elements of increasing thickness in response to th
e mounting stress. The geometrical modifications of the valve apparatus arc
hitecture (annulus dilatation, leaflet retraction, chordal elongation or re
traction) 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 para
llel, aligned on the coaptation surface plane, Due to the negligible elasti
c module of the valve leaflet, in this new arrangement the various chordae
cannot share the stress between themselves as they do in a normal physiolog
ical situation; on the contrary the thinner chordae nearer to the free marg
in are also Loaded with the peak systolic stress, thus generating condition
s favoring their rupture. It can, therefore, be hypothesized that the anato
mopathological picture of valve insufficiency due to chordal rupture may be
the final event of a series of geometrical modifications of valve apparatu
s 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.