In a recent article, Messika-Zeitoun et al.1 set the record straight with definitive results on their algorithm simulating clip implantation in five patients with functional mitral regurgitation (FMR). This manuscript's publication is timely, given the 5-year follow-up after transcatheter repair of secondary mitral regurgitation (SMR) published by Stone et al. in the New England Journal of Medicine. The algorithm represents an effective preliminary approach for predicting residual MR. However, developing a predictive model that accurately identifies the factors that lead to transcatheter edge to edge repair (TEER) failure is a major challenge. The finite element analysis (FEA) simulations facilitate insight into this emerging therapeutic modality and assist in achieving optimal utilization. However, given the relatively brief historical record and the inherent technological complexity of TEER simulations, a number of pivotal questions remain unresolved.

First, in TEER, the mechanical properties of the mitral valve (MV) are clearly distinct at the level of both the leaflets and the connective scaffolding. The most effective approach for modelling MV leaflets is to use anisotropic hyperelastic materials comprising an isotropic matrix with a defined anisotropic direction, as determined by a single collagen family.2 For example, in the context of TEER, a scallop of the anterior mitral leaflet (AML) is attached to its counterpart. In vitro studies of mechanical testing have identified potential concerns regarding the active components present in the MV leaflets and the influence of prestrains on physiologic deformations during peak systole of the MV.3,4 This highlights the urgent need for further refinement in biomodelling techniques, particularly in numerical studies of the MV apparatus.

Second, it is crucial to fix the tips of the papillary muscles in place, with only minor variations in distance between the implantation base of the papillary muscles during end diastole and end systole. In SMR from traction tethering, the geometry is altered. In SMR, whether ischaemic (IMR) or FMR, tethering significantly transforms the geometric relationship. This leads to a distinct interval in interpapillary muscle distance (IPMD) with two principal vectors along which the papillary muscles (PMs) are displaced. There was no apical displacement of the papillary muscles during IMR or FMR, but displacement of the anterior papillary muscle occurred laterally during FMR. Posterolateral displacement of the PM was observed during both IMR and FMR. This geometric deformation must be specified correctly in the MV segmentation and finite element (FE) model5 (Figure 1).

Experimental studies on sheep show a clear link between apical AML tethering and posterolateral papillary muscle dislocation in cases of ischaemic or FMR. The schematic shows how leaflet tethering occurs during ischaemic and FMR. It shows that apical leaflet displacement is not caused by apical displacement of the posteromedial papillary muscle (PMPM). Instead, it is caused by a posterolateral displacement of the PMPM. AML, anterior mitral leaflet. Adapted with permission from the original work by Bothe et al.5
Figure 1

Experimental studies on sheep show a clear link between apical AML tethering and posterolateral papillary muscle dislocation in cases of ischaemic or FMR. The schematic shows how leaflet tethering occurs during ischaemic and FMR. It shows that apical leaflet displacement is not caused by apical displacement of the posteromedial papillary muscle (PMPM). Instead, it is caused by a posterolateral displacement of the PMPM. AML, anterior mitral leaflet. Adapted with permission from the original work by Bothe et al.5

In SMR, changes in annular diameter, tenting volume, and IPMD distort the spatial relationships of the MV apparatus, causing deformation. TEER without ring annuloplasty and papillary muscle approximation is insufficient to reduce the stress load on the anterior leaflet and prevent MR recurrence.6,7 The leaflets malcoaptate better due to the reduction in anteroposterior diameter. There is no agreement on how annular boundary conditions should be modelled in these simulations. Furthermore, the effect is not dependent on the position of the clip. A high-fidelity FEA model based on a human MV must be used to assess the sensitivity of these simulations to annular boundary conditions.

Finally, simulation is key to assessing perivalvular myocardial compliance. This approach allows us to investigate the impact of two crucial factors in valve functionality. In vitro studies on porcine AML yielded unquestionable measures of circumferential and radial strains, with values consistently ranging between 15% and 40% at peak systole.3,4 Krishnamurthy and colleagues used a linear inverse FEA technique to estimate material stiffness in bovine anterior leaflets, confirming that leaflet stiffness may have been underestimated.

Funding

None declared.

Data availability

The data will be made available on a case-by-case basis following discussion with the corresponding author.

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Author notes

Conflict of interest: None declared.

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