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Author Notes:

Muralidhar Padala PhD, Director, Structural Heart Research & Innovation Laboratory, 380B Northyards Blvd, Atlanta, GA 30313. Email: spadala@emory.edu. +1 404 (251) 0651

R.G is a scientific advisor for Edwards Lifesciences and receives a consulting fee. M.P. is an advisor for Edwards Lifesciences & Heart Repair Technologies and receives a consulting fee. None of these entities funded or were involved in any manner in this work.

Subject:

Research Funding:

This work was funded by the following grants to M.P: 14SDG20380081 from the American Heart Association; R01HL135145, R01HL133667, and R01HL140325 from the National Institutes of Health; and seed funding from the Carlyle Fraser Heart Center at Emory University Hospital Midtown

Keywords:

  • Science & Technology
  • Technology
  • Life Sciences & Biomedicine
  • Engineering, Biomedical
  • Transplantation
  • Engineering
  • functional mitral regurgitation
  • heart valve flow loop
  • circulatory system
  • heart failure
  • transcatheter heart valve interventions
  • PAPILLARY-MUSCLE APPROXIMATION
  • MYOCARDIAL-INFARCTION
  • VALVE GEOMETRY
  • REPAIR
  • LEAFLET
  • ANNULOPLASTY
  • RELOCATION
  • MECHANISM
  • IMPACT

Left Ventricular Thinning and Distension in Pig Hearts as a ReproducibleEx VivoModel of Functional Mitral Regurgitation

Tools:

Journal Title:

ASAIO JOURNAL

Volume:

Volume 66, Number 9

Publisher:

, Pages 1016-1024

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Functional mitral regurgitation in the setting of an enlarged heart is challenging to repair surgically with an annular approach, and the need to develop subannular and ventricular approaches is recognized yet unrealized because of the lack of models for investigations. In this study, we report a novel model of functional mitral regurgitation induced by left ventricular thinning and distension in pig hearts. Seven pig hearts were explanted at a local slaughterhouse, and left ventricular distension induced by thinning the ventricular myocardium by 60-65% of its original thickness. Distension of the thinned hearts with a 120 mmHg column confirmed significant left ventricular dilatation and mitral valve tethering. These hearts were then mounted into a pulsatile flow model and animated at 120 mmHg left ventricular pressure, 5 L/min cardiac output at 70 beats/min. Echocardiography was used to assess valvular kinematics and hemodynamics. Left ventricular wall thickness reduced by 60.5% ± 10.1% at the basal plane, 64.8% ± 11.3% at the equatorial plane, and 64.0% ± 11.4% at the apical plane after thinning. Upon distension, ventricular volumes increased by 852.4% ± 639.8% after left ventricular thinning, with an 89.5% ± 33.9% increase in sphericity index. Mitral valve systolic tenting height increased from 7.92 ± 2.06 to 15.02 ± 3.89 mm, systolic tethering area increased from 130.7 ± 38.2 to 409.9 ± 124.6 mm2and an average mitral regurgitation fraction of 24.4% ± 16.6% was measured. In a case study, use of multimodality imaging to test the efficacy of transcatheter mitral devices was confirmed. Ventricular wall thinning leading to passive left ventricular distension and dilatation is a reproducible ex vivo model of mitral valve tethering and functional mitral regurgitation, which in combination with multimodality imaging provides a good simulation model.

Copyright information:

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (https://creativecommons.org/licenses/by-nc/4.0/rdf).
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