ArticleBiomechanics and modeling in mechanobiology2023
Investigating the effects of microstructural changes induced by myocardial infarction on the elastic parameters of the heart.
Article in Biomechanics and modeling in mechanobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Real-Time Soft Tissue Deformation Framework for Haptic-Enabled Robotic Surgical Training in Virtual Reality.Annals of biomedical engineering · 2026Article
- Coaxially Electrospun Myocardial dECM- Based Nanofibrous Scaffolds Demonstrate Enhanced Cardiomyocyte Biocompatibility.Advanced healthcare materials · 2026Article
- Mechanical Modeling of Cardiac Fibrosis With Explicit Spatial Representation of Cellular Structure and Collagen Alignment.Journal of biomechanical engineering · 2026Article
- Body-Force Effects in Homogenised Models of Anisotropic Double Poroelastic Materials.La matematica · 2026Article
- The sobol sensitivity analysis of the pressure, stresses, and displacement arising from poroelastic modelling of hard mechanical systems.Scientific reports · 2025Article
- Multifunctional bioelectronics for brain-body circuits.Nature reviews bioengineering · 2025Article
- Homogenized multiscale modelling of an electrically active double poroelastic material representing the myocardium.Biomechanics and modeling in mechanobiology · 2025Article
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2 authors.
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Abstract
Within this work, we investigate how physiologically observed microstructural changes induced by myocardial infarction impact the elastic parameters of the heart. We use the LMRP model for poroelastic composites (Miller and Penta in Contin Mech Thermodyn 32:1533-1557, 2020) to describe the microstructure of the myocardium and investigate microstructural changes such as loss of myocyte volume and increased matrix fibrosis as well as increased myocyte volume fraction in the areas surrounding the infarct. We also consider a 3D framework to model the myocardium microstructure with the addition of the intercalated disks, which provide the connections between adjacent myocytes. The results of our simulations agree with the physiological observations that can be made post-infarction. That is, the infarcted heart is much stiffer than the healthy heart but with reperfusion of the tissue it begins to soften. We also observe that with the increase in myocyte volume of the non-damaged myocytes the myocardium also begins to soften. With a measurable stiffness parameter the results of our model simulations could predict the range of porosity (reperfusion) that could help return the heart to the healthy stiffness. It would also be possible to predict the volume of the myocytes in the area surrounding the infarct from the overall stiffness measurements.
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