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- Gasser, T. Christian, et al.
(author)
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Biomechanical modeling the adaptation of soft biological tissue
- 2017
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In: Current Opinion in Biomedical Engineering. - : Elsevier B.V.. - 2468-4511. ; 1, s. 71-77
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Journal article (peer-reviewed)abstract
- External (mechanical) stimuli influence cell function at the level of gene expression and thereby contribute to the overall control of Soft Biological Tissues' (SBT) structure and function. SBT seem to adapt towards stable homeostatic mechanical conditions, and failure of reaching homeostasis may result in pathologies. SBT adaptation has to obey basic physical principles, and even within these constraints, a large number of SBT adaptation models have been proposed. Recent SBT models integrated the tissue's microstructure and directly addressed length scales of individual tissue constituents, which in turn allowed linking biomechanical and biochemical adaptation aspects. Despite adaptation models being based on very different hypotheses, many of them lead to physically reasonable results. Most interestingly, the recently developed homogenized Constrained Mixture Model reported very similar predictions than the original Constrained Mixture Model. This key observation indicates that the simpler kinematics-based approach is indeed able to capture the overall consequences of the continuous production and degradation of SBT constituents. However, mainly due to the scarcity of relevant experiment data, not a single model has been thoroughly validated against clearly specified modeling objectives. Consequently, much more interdisciplinary experimental work is required to guide SBT modeling activities. Nevertheless, predictive biomechanical SBT adaption models would not only be of considerable scientific interest, but would also have a large number of practical applications.
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- Grytsan, Andrii, et al.
(author)
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A Thick-Walled Fluid-Solid-Growth Model of Abdominal Aortic Aneurysm Evolution : Application to a Patient-Specific Geometry
- 2015
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In: Journal of Biomechanical Engineering. - : ASME International. - 0148-0731 .- 1528-8951. ; 137:3
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Journal article (peer-reviewed)abstract
- We propose a novel thick-walled fluid-solid-growth (FSG) computational framework for modeling vascular disease evolution. The arterial wall is modeled as a thick-walled nonlinearly elastic cylindrical tube consisting of two layers corresponding to the mediaintima and adventitia, where each layer is treated as a fiber-reinforced material with the fibers corresponding to the collagenous component. Blood is modeled as a Newtonian fluid with constant density and viscosity; no slip and no-flux conditions are applied at the arterial wall. Disease progression is simulated by growth and remodeling (G&R) of the load bearing constituents of the wall. Adaptions of the natural reference configurations and mass densities of constituents are driven by deviations of mechanical stimuli from homeostatic levels. We apply the novel framework to model abdominal aortic aneurysm (AAA) evolution. Elastin degradation is initially prescribed to create a perturbation to the geometry which results in a local decrease in wall shear stress (WSS). Subsequent degradation of elastin is driven by low WSS and an aneurysm evolves as the elastin degrades and the collagen adapts. The influence of transmural G&R of constituents on the aneurysm development is analyzed. We observe that elastin and collagen strains evolve to be transmurally heterogeneous and this may facilitate the development of tortuosity. This multiphysics framework provides the basis for exploring the influence of transmural metabolic activity on the progression of vascular disease.
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- Grytsan, Andrii, 1986-, et al.
(author)
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A thick-walled fluid–solid–growth model of abdominal aortic aneurysm evolution : Application to a patient-specific geometry
- 2014
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Reports (other academic/artistic)abstract
- We propose a model for abdominal aortic aneurysms that considers the wall (solid), the blood (fluid) and the wall growth within a three-dimensional finite element framework. The arterial wall is considered as a thick-walled nonlinearly elastic circular cylindrical tube consisting of two layers corresponding to the media-intima and adventitia, where each layer is treated as a fiber-reinforced material with the fibers corresponding to the collagenous component. The blood is modeled as a Newtonian fluid with constant density and viscosity; no slip and no-flux conditions are applied at the arterial wall. The metabolic activity in the arterial wall is reflected by elastin degradation which is coupled with the level of wall shear stress, while the collagen fiber network is continuously remodeled in the artery such that the collagen fiber strain tends towards a homeostatic strain. The computational framework consists of a structural FE-solver (CMISS), a fluid solver using a finite volume formulation and additional routines which pass the aneurysm geometry to the fluid solver and feeds CMISS with the information on the blood flow conditions. One illustrative patient-specific geometry of an abdominal aortic wall is discretized with hexahedral finite elements and the fluid domain is generated by an unstructured tetrahedral mesh with prism layers lining the boundary. The evolution of wall shear stress and elastin degradation is investigated over a time period of 10 years; the influence of transmurally non-uniform elastin degradation is analyzed. The results show that both the elastin and the collagen strains can become transmurally non-uniform during the aneurysm development. This effect cannot be captured by membrane formulations. The proposed methodology provides a realistic basis to further explore the development of patient-specific aneurysmal disease.
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