Evidence map›Paper›PMID 27696332›Full record

ArticleBiomechanics and modeling in mechanobiology2017

A novel constitutive model for passive right ventricular myocardium: evidence for myofiber-collagen fiber mechanical coupling.

Reza Avazmohammadi, Michael R Hill, Marc A Simon, Will Zhang, Michael S Sacks

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Article in Biomechanics and modeling in mechanobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

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41citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

41 citing papers in PubMed.

  1. A novel diffusion tensor based three-dimensional constitutive model for human breast tissue.Journal of the mechanical behavior of biomedical materials · 2025
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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Reza AvazmohammadiCenter for Cardiovascular Simulation, Institute for Computational Engineering and Sciences, University of Texas at Austin, Austin, TX, USA.
Michael R HillSchool of Mathematical Sciences, University of Nottingham, Nottingham, UK.
Marc A SimonDepartments of Cardiology and Bioengineering, Heart and Vascular Institute, University of Pittsburgh, Pittsburgh, PA, USA.
Will ZhangCenter for Cardiovascular Simulation, Institute for Computational Engineering and Sciences, University of Texas at Austin, Austin, TX, USA.
Michael S SacksCenter for Cardiovascular Simulation, Institute for Computational Engineering and Sciences, University of Texas at Austin, Austin, TX, USA. msacks@ices.utexas.edu.

Funding

Adaptive remodeling of the right ventricle in response to pulmonary hypertension: towards physical understanding and predictionF32HL132543 · NHLBI · UNIVERSITY OF TEXAS AT AUSTIN · PI AVAZMOHAMMADI, REZA · 2016 to 2018
$125k
"A new computational model of right ventricular hypertrophy"F32HL117535 · NHLBI · UNIVERSITY OF TEXAS AT AUSTIN · PI HILL, MICHAEL R · 2013 to 2014
$76k
American Heart Association-American Stroke Association 12PRE12050419NHLBI NIH HHS F32 HL117535NHLBI NIH HHS F32 HL132543
6 · The paper itself

Abstract

The function of right ventricle (RV) is recognized to play a key role in the development of many cardiopulmonary disorders, such as pulmonary arterial hypertension (PAH). Given the strong link between tissue structure and mechanical behavior, there remains a need for a myocardial constitutive model that accurately accounts for right ventricular myocardium architecture. Moreover, most available myocardial constitutive models approach myocardium at the length scale of mean fiber orientation and do not explicitly account for different fibrous constituents and possible interactions among them. In the present work, we developed a fiber-level constitutive model for the passive mechanical behavior of the right ventricular free wall (RVFW). The model explicitly separates the mechanical contributions of myofiber and collagen fiber ensembles, and accounts for the mechanical interactions between them. To obtain model parameters for the healthy passive RVFW, the model was informed by transmural orientation distribution measurements of myo- and collagen fibers and was fit to the mechanical testing data, where both sets of data were obtained from recent experimental studies on non-contractile, but viable, murine RVFW specimens. Results supported the hypothesis that in the low-strain regime, the behavior of the RVFW is governed by myofiber response alone, which does not demonstrate any coupling between different myofiber ensembles. At higher strains, the collagen fibers and their interactions with myofibers begin to gradually contribute and dominate the behavior as recruitment proceeds. Due to the use of viable myocardial tissue, the contribution of myofibers was significant at all strains with the predicted tensile modulus of [Formula: see text]32 kPa. This was in contrast to earlier reports (Horowitz et al. 1988) where the contribution of myofibers was found to be insignificant. Also, we found that the interaction between myo- and collagen fibers was greatest under equibiaxial strain, with its contribution to the total stress not exceeding 20 %. The present model can be applied to organ-level computational models of right ventricular dysfunction for efficient diagnosis and evaluation of pulmonary hypertension disorder.

Indexed as

Models, BiologicalAnimalsCollagenExtracellular MatrixHeartHeart VentriclesHypertension, PulmonaryMiceMyofibrilsStress, MechanicalCollagen

Identifiers

PMID27696332
PMCPMC5352519

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.