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. 2021 May;161(5):1776-1783.
doi: 10.1016/j.jtcvs.2020.01.086. Epub 2020 Feb 19.

A novel cross-species model of Barlow's disease to biomechanically analyze repair techniques in an ex vivo left heart simulator

Affiliations

A novel cross-species model of Barlow's disease to biomechanically analyze repair techniques in an ex vivo left heart simulator

Annabel M Imbrie-Moore et al. J Thorac Cardiovasc Surg. 2021 May.

Abstract

Objective: Barlow's disease remains challenging to repair, given the complex valvular morphology and lack of quantitative data to compare techniques. Although there have been recent strides in ex vivo evaluation of cardiac mechanics, to our knowledge, there is no disease model that accurately simulates the morphology and pathophysiology of Barlow's disease. The purpose of this study was to design such a model.

Methods: To simulate Barlow's disease, a cross-species ex vivo model was developed. Bovine mitral valves (n = 4) were sewn into a porcine annulus mount to create excess leaflet tissue and elongated chordae. A heart simulator generated physiologic conditions while hemodynamic data, high-speed videography, and chordal force measurements were collected. The regurgitant valves were repaired using nonresectional repair techniques such as neochord placement.

Results: The model successfully imitated the complexities of Barlow's disease, including redundant, billowing bileaflet tissues with notable regurgitation. After repair, hemodynamic data confirmed reduction of mitral leakage volume (25.9 ± 2.9 vs 2.1 ± 1.8 mL, P < .001) and strain gauge analysis revealed lower primary chordae forces (0.51 ± 0.17 vs 0.10 ± 0.05 N, P < .001). In addition, the maximum rate of change of force was significantly lower postrepair for both primary (30.80 ± 11.38 vs 8.59 ± 4.83 N/s, P < .001) and secondary chordae (33.52 ± 10.59 vs 19.07 ± 7.00 N/s, P = .006).

Conclusions: This study provides insight into the biomechanics of Barlow's disease, including sharply fluctuating force profiles experienced by elongated chordae prerepair, as well as restoration of primary chordae forces postrepair. Our disease model facilitates further in-depth analyses to optimize the repair of Barlow's disease.

Keywords: Barlow's disease; biomechanics; disease model; mitral regurgitation; valve repair.

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Figures

Figure 1.
Figure 1.
(A) Intraoperative example of human Barlow’s disease. (B) A bovine valve in its native pressurized state, for reference to compare to the ex vivo Barlow’s disease model. (C) Explanted bovine valve sewn into a porcine-sized mounting ring to simulate Barlow’s disease; valve pictured during systole in a left heart simulator with a leakage volume of 28.3ml. (D) A Barlow’s disease model valve after neochordal repair with a leakage volume of 3.4ml.
Figure 2.
Figure 2.
(A) Mean flow confirmed successful repair of the Barlow’s disease model with significantly lower leakage volumes after neochordal repair (25.9±2.9 vs 2.1±1.8ml, p<0.001). Shaded region represents standard deviation. (B) Mean pressure tracings also showed successful repair of the Barlow’s disease model with aortic and left ventricular pressures significantly raised to baseline levels—see Table 1 for hemodynamic values.
Figure 3.
Figure 3.
Force tracings over the course of one cardiac cycle for composites of each class of chordae at baseline with the Barlow’s model (A) and after neochordal repair (B). Forces were measured using Fiber Bragg Grating strain sensors sewn to native chordae. Primary chordae forces were lower post-repair (0.51±0.17 vs 0.10±0.05N p<0.001), while no significant difference was found for secondary chordae forces (0.41±0.21 vs 0.35±0.12N, p=0.374).
Figure 4.
Figure 4.
The development and biomechanical analysis of a novel cross-species model of Barlow’s mitral valve disease. Bovine mitral valves (n=4) were evaluated in a left heart simulator using porcine mounts resulting in an ex vivo simulation of the excess, prolapsing leaflet tissue characteristic of Barlow’s disease. All models were successfully repaired, supporting the use of this model not only as a means of analyzing the biomechanics of the disease state, but also as a tool to optimize surgical repair techniques.
Central Picture.
Central Picture.
Novel cross-species model simulates Barlow’s disease for ex vivo biomechanical analysis.

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References

    1. Barlow JB, Bosman CK. Aneurysmal protrusion of the posterior leaflet of the mitral valve. Am. Heart J 1966;71(2):166–178. doi:10.1016/0002-8703(66)90179-7. - DOI - PubMed
    1. Anyanwu AC, Adams DH. Etiologic classification of degenerative mitral valve disease: Barlow’s disease and fibroelastic deficiency. Semin Thorac Cardiovasc Surg 2007;19(2):90–96. doi:10.1053/j.semtcvs.2007.04.002. - DOI - PubMed
    1. Lawrie GM. Barlow disease: Simple and complex. J. Thorac. Cardiovasc. Surg 2015;150(5):1078–1081. doi:10.1016/j.jtcvs.2015.09.030. - DOI - PubMed
    1. Lancellotti P, Moura L, Pierard LA, et al. European Association of Echocardiography recommendations for the assessment of valvular regurgitation. Part 2: mitral and tricuspid regurgitation (native valve disease). Eur J Echocardiogr 2010;11(4):307–332. doi:10.1093/ejechocard/jeq031. - DOI - PubMed
    1. Lawrie GM, Earle EA, Earle NR. Nonresectional repair of the barlow mitral valve: importance of dynamic annular evaluation. Ann. Thorac. Surg 2009;88(4): 1191–1196. doi:10.1016/j.athoracsur.2009.05.086. - DOI - PubMed

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