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Cardiothoracic Surgery, Leiden University Medical Center, Postbus 9600, Leiden, Netherlands 2300 RC
(Email: j.braun{at}lumc.nl).
Finite element analysis provides a powerful tool to simulate an unlimited number of situations in a given model. The validity of the model is directly related to the amount and quality of the data entered. In addition, finite element models, by definition, hold a certain amount of assumptions, for instance, when it comes to defining material properties and responses to strain. Wenk and colleagues [1] have described the methods used to construct a finite element model that incorporates both the left ventricle (LV) and the mitral valve apparatus, which is a novelty.
In the past we have seen models concerning the LV, and models addressing the mitral valve, but these have never been combined into an integral concept. The unique approach by Wenk and colleagues clearly opens possibilities to study situations in which the interrelationship between the mitral valve and the LV is of paramount importance, which is obviously the case in functional mitral regurgitation of ischemic or nonischemic etiology.
The current model results from a combination of previous work from these authors and from other teams and incorporates data on LV wall characteristics, mitral valve leaflets, and chordae tendineae. The model is based on magnetic resonance imaging data obtained in a sheep model of moderate ischemic mitral regurgitation resulting from an induced posterobasal myocardial infarction. The model is then used to demonstrate that increased local dyskinesia in the infarcted region (simulated by decreasing the stiffness of the affected muscle area) further increases mitral regurgitation.
The validity of any model is determined by the value of its components. First, the anatomy of the mitral valve apparatus and LV of the sheep is different from that in humans; however, the mechanism through which ischemic mitral regurgitation occurs is similar, and this animal model has been validated widely in the past.
The complexity of the LV wall mechanics, also differing in the various regions of the infarct zones, has been well thought out in the past by these researchers, and they have rightfully adopted their previous findings in the current model, with well-described amendments having been made with regard to the papillary muscles.
When it comes to the mitral leaflets, findings from other research groups have been introduced. The properties of the mitral annulus might deserve more attention in a next model, in a way that it should take into account the fact that the annulus is stiffer in the anterior commissural region and less so in the A3-P3 region.
In my opinion, the way that the authors have dealt with the complex anatomy of the last component, the chordae, should be especially commended. Although the branching of the chords as seen in vivo cannot be exactly reproduced in the model as yet, the researchers have found a very nice way to incorporate both the complex anatomic and functional characteristics of the chordae tendineae.
In summary, Wenk and coworkers have set a new stage in finite element modeling with this sound and well-designed study. I am looking forward to further improved versions of this model, as announced by the authors. This will open new possibilities to further study the optimal surgical approach to functional mitral regurgitation, a disease that as we know, still has no single solution.
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