Estimating passive mechanical properties in a myocardial infarction using MRI and finite element simulations

Dimitri Mojsejenko, Jeremy R. McGarvey, Shauna M. Dorsey, Joseph H. Gorman, Jason A. Burdick, James J. Pilla, Robert C. Gorman, Jonathan F. Wenk

Producción científica: Articlerevisión exhaustiva

53 Citas (Scopus)

Resumen

Myocardial infarction (MI) triggers a series of maladaptive events that lead to structural and functional changes in the left ventricle. It is crucial to better understand the progression of adverse remodeling, in order to develop effective treatment. In addition, being able to assess changes in vivo would be a powerful tool in the clinic. The goal of the current study is to quantify the in vivo material properties of infarcted and remote myocardium 1 week after MI, as well as the orientation of collagen fibers in the infarct. This will be accomplished by using a combination of magnetic resonance imaging (MRI), catheterization, finite element modeling, and numerical optimization to analyze a porcine model ($$N = 4$$N=4) of posterolateral myocardial infarction. Specifically, properties will be determined by minimizing the difference between in vivo strains and volume calculated from MRI and finite element model predicted strains and volume. The results indicate that the infarct region is stiffer than the remote region and that the infarct collagen fibers become more circumferentially oriented 1 week post-MI. These findings are consistent with previous studies, which employed ex vivo techniques. The proposed methodology will ultimately provide a means of predicting remote and infarct mechanical properties in vivo at any time point post-MI.

Idioma originalEnglish
Páginas (desde-hasta)633-647
Número de páginas15
PublicaciónBiomechanics and Modeling in Mechanobiology
Volumen14
N.º3
DOI
EstadoPublished - jun 15 2015

Nota bibliográfica

Publisher Copyright:
© 2014, Springer-Verlag Berlin Heidelberg.

Financiación

This study was supported by National Institutes of Health grants R01 HL063954 (Gorman), R01 HL111090 (Burdick), and T32 HL007954 (Burdick) and by a grant from the American Heart Association 14BGIA18850020 (Wenk). The user-defined material subroutine was originally developed under grant R01 HL077921.

FinanciadoresNúmero del financiador
National Institutes of Health (NIH)
National Institutes of Health (NIH)R01 HL063954, T32 HL007954, R01 HL111090
National Institutes of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)R01HL077921
National Heart, Lung, and Blood Institute (NHLBI)
American the American Heart Association14BGIA18850020, R01 HL077921
American the American Heart Association

    ASJC Scopus subject areas

    • Biotechnology
    • Modeling and Simulation
    • Mechanical Engineering

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