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Estrada AC, Yoshida K, Clarke SA, et al. Longitudinal Reinforcement of Acute Myocardial Infarcts Improves Function by Transmurally Redistributing Stretch and Stress. J Biomech Eng. 2020;142(2)doi: 10.1115/1.4044030.
Estrada, A. C., Yoshida, K., Clarke, S. A., & Holmes, J. W. (2020). Longitudinal Reinforcement of Acute Myocardial Infarcts Improves Function by Transmurally Redistributing Stretch and Stress. Journal of biomechanical engineering, 142(2), . https://doi.org/10.1115/1.4044030
Estrada, Ana Cristina, et al. "Longitudinal Reinforcement of Acute Myocardial Infarcts Improves Function by Transmurally Redistributing Stretch and Stress." Journal of biomechanical engineering vol. 142,2 (2020). doi: https://doi.org/10.1115/1.4044030
Estrada AC, Yoshida K, Clarke SA, Holmes JW. Longitudinal Reinforcement of Acute Myocardial Infarcts Improves Function by Transmurally Redistributing Stretch and Stress. J Biomech Eng. 2020 Feb 01;142(2). doi: 10.1115/1.4044030. PMID: 31201738; PMCID: PMC7104755.
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J Biomech Eng. 2020 Feb 01;142(2). doi: 10.1115/1.4044030.

Longitudinal Reinforcement of Acute Myocardial Infarcts Improves Function by Transmurally Redistributing Stretch and Stress.

Journal of biomechanical engineering

Ana Cristina Estrada, Kyoko Yoshida, Samantha A Clarke, Jeffrey W Holmes

Affiliations

  1. Department of Biomedical Engineering, University of Virginia, P.O. Box 800759, Health System, Charlottesville, VA 22908.
  2. Department of Biomedical Engineering, University of Virginia, P.O. Box 800759, Health System, Charlottesville, VA 22908; Department of Medicine, School of Medicine, University of Virginia, P.O. Box 800759, Health System, Charlottesville, VA 22908; Robert M. Berne Cardiovascular Research Center, University of Virginia, P.O. Box 800759, Health System, Charlottesville, VA 22908; The Center for Engineering in Medicine, University of Virginia, P.O. Box 800759, Health System, Charlottesville, VA 22908.

PMID: 31201738 PMCID: PMC7104755 DOI: 10.1115/1.4044030

Abstract

A wide range of emerging therapies, from surgical restraint to biomaterial injection to tissue engineering, aim to improve heart function and limit adverse remodeling following myocardial infarction (MI). We previously showed that longitudinal surgical reinforcement of large anterior infarcts in dogs could significantly enhance systolic function without restricting diastolic function, but the underlying mechanisms for this improvement are poorly understood. The goal of this study was to construct a finite element model that could match our previously published data on changes in regional strains and left ventricular function following longitudinal surgical reinforcement, then use the model to explore potential mechanisms for the improvement in systolic function we observed. The model presented here, implemented in febio, matches all the key features of our experiments, including diastolic remodeling strains in the ischemic region, small shifts in the end-diastolic pressure-volume relationship (EDPVR), and large changes in the end-systolic pressure-volume relationship (ESPVR) in response to ischemia and to patch application. Detailed examination of model strains and stresses suggests that longitudinal reinforcement reduces peak diastolic fiber stretch and systolic fiber stress in the remote myocardium and shifts those peaks away from the endocardial surface by reshaping the left ventricle (LV). These findings could help to guide the development of novel therapies to improve post-MI function by providing specific design objectives.

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