Growth and residual stresses of arterial walls

Ren, Jiusheng

doi:10.1016/j.jtbi.2013.08.008

Cited by 10 publications

(8 citation statements)

References 44 publications

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“…Axial growth is similarly neglected, based on a lack of experimental data on axial growth of airways. The growth models of Ren ( 2013 ) and Grytsan et al. ( 2017 ) do account for both isotropic and varying degrees of anisotropic growth but do not consider heterogeneous spatial distributions.…”

Section: Discussionmentioning

confidence: 99%

A theoretical model of inflammation- and mechanotransduction-driven asthmatic airway remodelling

Hill

Philp

Billington

et al. 2018

Biomech Model Mechanobiol

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Inflammation, airway hyper-responsiveness and airway remodelling are well-established hallmarks of asthma, but their inter-relationships remain elusive. In order to obtain a better understanding of their inter-dependence, we develop a mechanochemical morphoelastic model of the airway wall accounting for local volume changes in airway smooth muscle (ASM) and extracellular matrix in response to transient inflammatory or contractile agonist challenges. We use constrained mixture theory, together with a multiplicative decomposition of growth from the elastic deformation, to model the airway wall as a nonlinear fibre-reinforced elastic cylinder. Local contractile agonist drives ASM cell contraction, generating mechanical stresses in the tissue that drive further release of mitogenic mediators and contractile agonists via underlying mechanotransductive signalling pathways. Our model predictions are consistent with previously described inflammation-induced remodelling within an axisymmetric airway geometry. Additionally, our simulations reveal novel mechanotransductive feedback by which hyper-responsive airways exhibit increased remodelling, for example, via stress-induced release of pro-mitogenic and pro-contractile cytokines. Simulation results also reveal emergence of a persistent contractile tone observed in asthmatics, via either a pathological mechanotransductive feedback loop, a failure to clear agonists from the tissue, or a combination of both. Furthermore, we identify various parameter combinations that may contribute to the existence of different asthma phenotypes, and we illustrate a combination of factors which may predispose severe asthmatics to fatal bronchospasms.Electronic supplementary materialThe online version of this article (10.1007/s10237-018-1037-4) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

A theoretical model of inflammation- and mechanotransduction-driven asthmatic airway remodelling

Hill

Philp

Billington

et al. 2018

Biomech Model Mechanobiol

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“…There have been many theoretical studies investigating the causes and effects of residual stresses in arteries, cf., e.g., Bustamante and Holzapfel [21], Holzapfel and Ogden [22], Ren [23], Schröder and Brinkhues [24], Waffenschmidt and Menzel [25], but such works are outside our current focus on patient-specific FE-based simulations. Alastrué et al [26] introduced a computational method to account for residual stresses in patient-specific simulations of arteries based on a single so-called 'opening angle' determined from a classical residual stress experiment (cf., e.g., Fung [1]).…”

Section: Introductionmentioning

confidence: 99%

A method for incorporating three-dimensional residual stretches/stresses into patient-specific finite element simulations of arteries

Pierce

Fastl

Rodríguez-Vila

et al. 2015

Journal of the Mechanical Behavior of Biomedical Materials

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The existence of residual stresses in human arteries has long been shown experimentally. Researchers have also demonstrated that residual stresses have a significant effect on the distribution of physiological stresses within arterial tissues, and hence on their development, e.g., stress-modulated remodeling. Through progress in medical imaging, image analysis and finite element (FE) meshing tools it is now possible to construct in vivo patient-specific geometries and thus to study specific, clinically relevant problems in arterial mechanics via FE simulations. Classical continuum mechanics and FE methods assume that constitutive models and the corresponding simulations start from unloaded, stress-free reference configurations while the boundary-value problem of interest represents a loaded geometry and includes residual stresses. We present a pragmatic methodology to simultaneously account for both (i) the three-dimensional (3-D) residual stress distributions in the arterial tissue layers, and (ii) the equilibrium of the in vivo patient-specific geometry with the known boundary conditions. We base our methodology on analytically determined residual stress distributions (Holzapfel and Ogden, 2010, J. R. Soc. Interface 7, 787-799) and calibrate it using data on residual deformations (Holzapfel et al., 2007, Ann. Biomed. Eng. 35, 530-545). We demonstrate our methodology on three patient-specific FE simulations calibrated using experimental data. All data employed here are generated from human tissues - both the aorta and thrombus, and their respective layers - including the geometries determined from magnetic resonance images, and material properties and 3-D residual stretches determined from mechanical experiments. We study the effect of 3-D residual stresses on the distribution of physiological stresses in the aortic layers (intima, media, adventitia) and the layers of the intraluminal thrombus (luminal, medial, abluminal) by comparing three types of FE simulations: (i) conventional calculations; (ii) calculations accounting only for prestresses; (iii) calculations including both 3-D residual stresses and prestresses. Our results show that including residual stresses in patient-specific simulations of arterial tissues significantly impacts both the global (organ-level) deformations and the stress distributions within the arterial tissue (and its layers). Our method produces circumferential Cauchy stress distributions that are more uniform through the tissue thickness (i.e., smaller stress gradients in the local radial directions) compared to both the conventional and prestressing calculations. Such methods, combined with appropriate experimental data, aim at increasing the accuracy of classical FE analyses for patient-specific studies in computational biomechanics and may lead to increased clinical application of simulation tools.

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“…where H 1 (Ω m ) denotes the Hilbert space of functions, with square-integrable gradient, defined in Ω m . Since in the characterization problem Ω m is unknown, it is worthwhile to express equation (10) in terms of x a , allowing to perform the integration in the known configuration Ω a . A change of variables leads to…”

Section: Materials Configuration ω Mmentioning

confidence: 99%

“…However, it has also been recognized [2,6,7] that the in-vivo unloaded configuration of any vascular district is neither stress-free nor strain-free [8]. This led to an increasing number of investigations [9,10] studying the effects of residual stresses (RSs) in arterial wall mechanics. In the last decades a shifting in the role researchers assign to RSs has taken place, from conceiving RSs as a mere side effect of growth to a conception in which RSs are viewed as an adaptive and protective mechanism.…”

Section: Introductionmentioning

confidence: 99%

Identification of residual stresses in multi-layered arterial wall tissues using a variational framework

Ares

Blanco

Urquiza

et al. 2017

Computer Methods in Applied Mechanics and Engineering

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Growth and residual stresses of arterial walls

Cited by 10 publications

References 44 publications

A theoretical model of inflammation- and mechanotransduction-driven asthmatic airway remodelling

A theoretical model of inflammation- and mechanotransduction-driven asthmatic airway remodelling

A method for incorporating three-dimensional residual stretches/stresses into patient-specific finite element simulations of arteries

Identification of residual stresses in multi-layered arterial wall tissues using a variational framework

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