Numerical simulation of arterial remodeling in pulmonary autografts

Famaey, Nele; Vastmans, Julie; Fehervary, Heleen; Maes, Lauranne; Vanderveken, Emma; Rega, Filip; Mousavi, S. Jamaleddin; Avril, Stéphane

doi:10.1002/zamm.201700351

Cited by 28 publications

(51 citation statements)

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“…Kinematic growth theories commonly split multiplicatively the total deformation gradient into elastic and inelastic parts, where the inelastic one is related to growth . This theory has been widely used for single‐constituent solid continuum as well as for homogenized and nonhomogenized constrained mixture models (CMMs). For example, Valentín et al modelled arterial wall adaptation and maladaptation to different cases, such as loss of smooth muscle cells (SMCs), elastin degradation, and changes in fiber orientations and quantities.…”

Section: Introductionmentioning

confidence: 99%

A new finite‐element shell model for arterial growth and remodeling after stent implantation

Laubrie

Mousavi

Avril

2019

Numer Methods Biomed Eng

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The goal of this paper is to study computationally how blood vessels adapt when they are exposed to a mechanobiological insult, namely, a sudden change of their biomechanical conditions such as proteolytic injuries or implantation.Adaptation occurs through growth and remodeling (G&R), consisting of mass production or removal of structural proteins, such as collagen, until restoring the initial homeostatic biomechanical conditions. In some circumstances, the initial conditions can never be recovered, and arteries evolve towards unstable pathological conditions, such as aneurysms, which are responsible for significant morbidity and mortality. Therefore, computational predictions of G&R under different circumstances can be helpful in understanding fundamentally how arterial pathologies progress. For that, we have developed a low-cost open-source finite-element 2D axisymmetric shell model (FEM) of the arterial wall. The constitutive equations for static equilibrium used to model the stress-strain behavior and the G&R response are expressed within the homogenized constrained mixture theory. The originality is to integrate the layer-specific behavior of both arterial layers (media and adventitia) into the model. Considering different mechanobiological insults, our results show that the resulting arterial dilatation is strongly correlated with the media thickness. The adaptation to stent implantation is particularly interesting. For large stent oversizing ratios, the artery cannot recover from the mechanobiological insult and dilates forever, whereas dilatation stabilizes after a transient period for more moderate oversizing ratios. We also show that stent implantation induces a different response in an aneurysm or in a healthy artery, the latter yielding more unstable G&R. Finally, our G&R model can efficiently predict, with very low computational cost, fundamental aspects of arterial adaptation induced by clinical procedures. KEYWORDSarterial growth and remodeling, axisymmetric shell model, homogenized constrained mixture theory, layer-specific behavior, stent implantation Int J Numer Meth Biomed Engng. 2020;36:e3282.wileyonlinelibrary.com/journal/cnm

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Section: Introductionmentioning

confidence: 99%

A new finite‐element shell model for arterial growth and remodeling after stent implantation

Laubrie

Mousavi

Avril

2019

Numer Methods Biomed Eng

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“…Many efforts are undertaken to model the adaptation processes that take place after exposing pulmonary artery to a new mechanical environment 14 . Studies examining the remodeling of failed pulmonary autografts, as well as studies investigating arterial remodeling following hypertension, mention an increased extracellular matrix deposition and, consequently, a change in mechanical properties 2,8,[15][16][17][18][19][20][21] .…”

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Mechano-biological adaptation of the pulmonary artery exposed to systemic conditions

Vanderveken

Vastmans

Claus

et al. 2020

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Cardiac surgeries may expose pulmonary arterial tissue to systemic conditions, potentially resulting in failure of that tissue. our goal was to quantitatively assess pulmonary artery adaptation due to changes in mechanical environment. In 17 sheep, we placed a pulmonary autograft in aortic position, with or without macroporous mesh reinforcement. It was exposed to systemic conditions for 6 months. All sheep underwent 3 ECG-gated MRI's. Explanted tissue was subjected to mechanical and histological analysis. Results showed progressive dilatation of the unreinforced autograft, while reinforced autografts stabilized after two months. Some unreinforced pulmonary autograft samples displayed more aorta-like mechanical behavior with increased collagen deposition. the mechanical behavior of reinforced autografts was dominated by the mesh. the decrease in media thickness and loss of vascular smooth muscle cells was more pronounced in reinforced than in unreinforced autografts. In conclusion, altering the mechanical environment of a pulmonary artery causes changes in its mechano-biological properties.

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“…In the same year, Virag et al [73] extended the model of aneurysm development by Karšaj et al [66] by incorporating the evolution of multiple layers of an intraluminal thrombus. More recently, Famaey et al [74] studied the influence of the Ross procedure on arterial wall mechanics, where the pulmonary artery is exposed to a seven fold increase in blood pressure. They studied four virtual tests using one single element with boundary conditions assigned using Laplace's law.…”

Section: Constrained Mixture Theorymentioning

confidence: 99%

Computational modeling of cardiac growth and remodeling in pressure overloaded hearts—Linking microstructure to organ phenotype

2020

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Cardiac growth and remodeling (G&R) refers to structural changes in myocardial tissue in response to chronic alterations in loading conditions. One such condition is pressure overload where elevated wall stresses stimulate the growth in cardiomyocyte thickness, associated with a phenotype of concentric hypertrophy at the organ scale, and promote fibrosis. The initial hypertrophic response can be considered adaptive and beneficial by favoring myocyte survival, but over time if pressure overload conditions persist, maladaptive mechanisms favoring cell death and fibrosis start to dominate, ultimately mediating the transition towards an overt heart failure phenotype. The underlying mechanisms linking biological factors at the myocyte level to biomechanical factors at the systemic and organ level remain poorly understood. Computational models of G&R show high promise as a unique framework for providing a quantitative link between myocardial stresses and strains at the organ scale to biological regulatory processes at the cellular level which govern the hypertrophic response. However, microstructurally motivated, rigorously validated computational models of G&R are still in their infancy.This article provides an overview of the current state-of-the-art of computational models to study cardiac G&R. The microstructure and mechanosensing/mechanotransduction within cells of the myocardium is discussed and quantitative data from previous experimental and clinical studies is summarized. We conclude with a discussion of major challenges and possible directions of future research that can advance the current state of cardiac G&R computational modeling. Statement of SignificanceThe mechanistic links between organ-scale biomechanics and biological factors at the cellular size scale remain poorly understood as these are largely elusive to investigations using experimental methodology alone. Computational G&R models show high promise to establish quantitative links which allow more mechanistic insight into adaptation mechanisms and may be used as a tool for stratifying the state and predict the progression of disease in the clinic. This review provides a comprehensive overview of research in this domain including a summary of experimental data. Thus, this study may serve as a basis for the further development of more advanced G&R models which are suitable for making clinical predictions on disease progression or for testing hypotheses on pathogenic mechanisms using in-silico models.

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Numerical simulation of arterial remodeling in pulmonary autografts

Abstract: Stress-stretch curves of planar biaxial tests of healthy aortic tissue ( ) Average stress in a fiber family at time , see Equation 23 Undeformed collagen fiber orientation vector Deviatoric part of a constituent-specific right Cauchy-Green tensor, see Equation 3

Cited by 28 publications

References 32 publications

A new finite‐element shell model for arterial growth and remodeling after stent implantation

A new finite‐element shell model for arterial growth and remodeling after stent implantation

Mechano-biological adaptation of the pulmonary artery exposed to systemic conditions

Computational modeling of cardiac growth and remodeling in pressure overloaded hearts—Linking microstructure to organ phenotype

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