Key result
In a finite element computer model, annular dilatation increased stress magnitudes more than two-fold in both leaflets and greatly delayed coaptation compared with normal geometry.
Annular dilatation increases mitral valve leaflet and chordal stress by over two-fold and prevents full coaptation in a computational model, suggesting a biomechanical mechanism for progressive degenerative valve disease.
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May implicate annular dilatation in degenerative mitral regurgitation progression; computational model leaves open need for in vivo validation.
The purpose of this study was to examine the effects of annular dilatation on coaptation, and leaflet and chordal stresses, using a three dimensional finite element computer model. To do this, the whole mitral valve was simulated using ANSYS 4.4A software. Normal model geometry, collagen fiber orientation, tissue thickness, and material properties were determined from fresh porcine valves. For annular dilatation, the annular circumference was increased by 18% versus normal, Isovolumic contraction and rapid ventricular ejection were simulated. Data showed that, in the annular dilatation model, the stress magnitudes increased more than two-fold compared with normal in both the anterior leaflet and posterior leaflet. Coaptation was greatly delayed in the dilatation model, and the leaflets never fully coapted. Chordal stresses were also greatly increased in the dilatation model. In conclusion, increased stress due to annular dilatation may lead to tissue disruption, further dilatation, delayed coaptation, and increased regurgitation, in a ‘closed-loop’ degenerative process.
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Kunzelman et al. (1997) studied Mitral valve annular dilatation. Annular dilatation (18% increase in annular circumference) vs. Normal model geometry was evaluated on Coaptation, and leaflet and chordal stresses. In a finite element computer model, annular dilatation increased stress magnitudes more than two-fold in both leaflets and greatly delayed coaptation compared with normal geometry.
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