The Heart Valve Society

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Effects of Annuloplasty on In Vivo MV Tissue Stress And Cellular Phenotype
Chung-Hao Lee1, Michael S. Sacks2.
1University of Oklahoma, Norman, OK, USA, 2University of Texas at Austin, Austin, TX, USA.

BACKGROUND Recent studies indicated high recurrence of severe mitral regurgitation after repair, and found that excessive tissue stress and the resulting tissue damage are important etiological factors for repair failures. These repair-induced altered stresses lead to changes in mitral valve interstitial cell (MVIC) biosynthesis, which are essential to MV organ-level biomechanical responses. Thus, the objective of this study was to make an important connection of MV tissue and cellular responses to the in vivo functional state that sheds insight into MV function in response to mitral annuloplasty.
METHODS Extant sonoscrytal data were used to obtain tissue-level kinematic deformations of ovine MV anterior leaflet (MVAL) over cardiac cycles for normal (n=6) and repaired (n=3) groups. An inverse finite element (FE) modeling framework was adopted to quantify functional mechanical properties of the MVAL and to estimate the in vivo tissue stresses. Downscale FE simulations were performed to examine layer-specific mechanical responses of the MVICs under in vivo conditions for both study groups.
RESULTS At the tissue level, estimated in vivo stresses at peak pressure loading were ~510 kPa and ~740 kPa in the circumferential and radial directions, respectively, with relatively smaller inherent pre-stresses of 20-30 kPa (Fig. 1a). As for the predicted cellular responses, surgical ring-induced geometry changes resulted in notable reduction of the fibrosa nuclear aspect ratios (NARs) from 4.91 to 3.49 (Fig. 1b) and relatively smaller decrease in atrialis NARs from 3.76 to 3.58. These findings suggested that layer-specific fiber compositions, extracellular matrix mechanical properties, and microstructural orientations are the primary drivers for re-distributions of external pressure over the four MVAL tissue layers due to surgical repair.
CONCLUSIONS We simulated in vivo MVIC deformations of the normal and repaired MVALs. This important piece of information will provide valuable insight into the remodeling of cellular mechanobiology in response to surgery-induced changes in tissue-level mechanical loading/deformation. Integration of such information with a multiscale modeling framework will ultimately facilitate individual-optimized MV therapeutic strategy with improved long-term surgical outcomes.


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