Annular dilatation increased stress magnitudes more than two-fold in both the anterior and posterior leaflets and greatly delayed coaptation compared with normal in a finite element computer model.
Does simulated annular dilatation increase stress and delay coaptation in a finite element computer model of the mitral valve?
A finite element model demonstrates that mitral annular dilatation significantly increases leaflet and chordal stresses and impairs coaptation, potentially driving a degenerative cycle of tissue disruption and further dilatation.
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.
Karyn S. Kunzelman (Tue,) conducted a other in Mitral valve annular dilatation. Annular dilatation vs. Normal annular circumference was evaluated on Leaflet stress, chordal stress, and coaptation. Annular dilatation increased stress magnitudes more than two-fold in both the anterior and posterior leaflets and greatly delayed coaptation compared with normal in a finite element computer model.