Residual strain effects on the stress field in a thick wall finite element model of the human carotid bifurcation

Delfino, A.; Stergiopulos, Nikolaos; Moore, James E.; Meister, Jean-Jacques

doi:10.1016/s0021-9290(97)00025-0

Cited by 343 publications

(297 citation statements)

References 26 publications

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“…Finite element meshes for the solid (vascular wall) and fluid (blood) domain were generated with an average size of 0.4 mm. To implement the simulation, we adopted two well established hemodynamic parameters: the arterial wall was modeled as nonlinear, isotropic hyperelastic material (18), and the blood was treated as incompressible Newtonian fluid (19). We then performed fully coupled, 3D nonlinear fluid-structure interaction analysis to simulate the blood flow, vessel wall mechanics, and their interactions in two complete cardiac cycles.…”

Section: Analysis Of Flow and Shear Stress Patterns In The Carotid Armentioning

confidence: 99%

Distinct endothelial phenotypes evoked by arterial waveforms derived from atherosclerosis-susceptible and -resistant regions of human vasculature

Dai

Kaazempur-Mofrad

Natarajan

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

602

509

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Atherosclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in humans and experimental animals, suggests an important role for local hemodynamic forces in atherogenesis. To explore how endothelial cells (EC) acquire functional͞dysfunctional phenotypes in response to vascular region-specific flow patterns, we have used an in vitro dynamic flow system to accurately reproduce arterial shear stress waveforms on cultured human EC and have examined the effects on EC gene expression by using a high-throughput transcriptional profiling approach. The flow patterns in the carotid artery bifurcations of several normal human subjects were characterized by using 3D flow analysis based on actual vascular geometries and blood flow profiles. Two prototypic arterial waveforms, ''athero-prone'' and ''athero-protective,'' were defined as representative of the wall shear stresses in two distinct regions of the carotid artery (carotid sinus and distal internal carotid artery) that are typically ''susceptible'' or ''resistant,'' respectively, to atherosclerotic lesion development. These two waveforms were applied to cultured EC, and cDNA microarrays were used to analyze the differential patterns of EC gene expression. In addition, the differential effects of atheroprone vs. athero-protective waveforms were further characterized on several parameters of EC structure and function, including actin cytoskeletal organization, expression and localization of junctional proteins, activation of the NF-B transcriptional pathway, and expression of proinflammatory cytokines and adhesion molecules. These global gene expression patterns and functional data reveal a distinct phenotypic modulation in response to the wall shear stresses present in atherosclerosis-susceptible vs. atherosclerosisresistant human arterial geometries.

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Section: Analysis Of Flow and Shear Stress Patterns In The Carotid Armentioning

confidence: 99%

Distinct endothelial phenotypes evoked by arterial waveforms derived from atherosclerosis-susceptible and -resistant regions of human vasculature

Dai

Kaazempur-Mofrad

Natarajan

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

602

509

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“…tissues as isotropic (Delfino et al, 1997;Maher et al, 2011). The anisotropic components are exponential functions of the invariants and :…”

Section: Anisotropic Hyperelastic Constitutive Modelmentioning

confidence: 99%

“…The mechanical behaviour of arterial tissue and plaque is commonly described using hyperelastic material models (Delfino et al, 1997;Holzapfel et al, 2000;Lally et al, 2004;Maher et al, 2009); however these models typically do not incorporate damage effects and as a result are limited when modelling the effects of non-physiological loading during surgical interventions. The Mullins effect theory does not implicitly account for inelastic strains and many damage models omit permanent set from the formulation (Alastrué et al, 2007;Balzani et al, 2006;Calvo et al, 2007;Hokanson and Yazdani, 1997).…”

Section: Introductionmentioning

confidence: 99%

An anisotropic inelastic constitutive model to describe stress softening and permanent deformation in arterial tissue

Maher

Creane

Lally

et al. 2012

Journal of the Mechanical Behavior of Biomedical Materials

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.A n anisotropic inelastic constitutive model to describe stress softening and permanent deformation in arterial tissue A bstractInelastic phenomena such as softening and unrecoverable inelastic strains induced by loading have been observed experimentally in soft tissues such as arteries. These phenomena need to be accounted for in constitutive models of arterial tissue so that computational models can accurately predict the outcomes of interventional procedures such as balloon angioplasty and stenting that involve non-physiological loading of the tissue. In this study, a novel constitutive model is described that accounts for inelastic effects such as Mullins-type softening and permanent set in a fibre reinforced tissue. The evolution of inelasticity is governed by a set of internal variables. Softening is introduced through a typical continuum damage mechanics approach, while the inelastic residual strains are introduced through an additive split in the stress tensor. Numerical simulations of aorta and carotid arterial tissue subjected to uniaxial testing in the longitudinal, circumferential and axial directions reproduce the anisotropic inelastic behaviour of the tissue. Material parameters derived from best-fits to experimental data are provided to describe these inelastic effects for both aortic and carotid tissue.

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“…The finally employed mesh consisted of 71,352 elements (eight elements in radial direction) and further reduction in element size resulted in less than five percent change in calculated stress values. Delfino et al (1997) developed an isotropic incompressible Fung type (Fung et al, 1979) exponential strain energy function (W) from experimental studies of human carotid arteries, …”

Section: Finite Element Analysismentioning

confidence: 99%

The role of the carotid sinus in the reduction of arterial wall stresses due to head movements—potential implications for cervical artery dissection

Callaghan

Soellinger

Baumgartner

et al. 2009

Journal of Biomechanics

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The role of the carotid sinus in the reduction of arterial wall stresses due to head movements--potential implications for cervical artery dissection Abstract Spontaneous dissection of the cervical internal carotid artery (sICAD) is a major cause of stroke in young adults. A tear in the inner part of the vessel wall triggers sICAD as it allows the blood to enter the wall and develop a transmural hematoma. The etiology of the tear is unknown but many patients with sICAD report an initiating trivial trauma. We thus hypothesised that the site of the tear might correspond with the location of maximal stress in the carotid wall. Carotid artery geometries segmented from magnetic resonance images of a healthy subject at different static head positions were used to define a path of motion and deformation of the right cervical internal carotid artery (ICA). Maximum head rotation to the left and rotation to the left combined with hyperextension of the neck were investigated using a structural finite element model. A role of the carotid sinus as a geometrically compliant feature accommodating extension of the artery is shown. At the extreme range of the movements, the geometrical compliance of the carotid sinus is limited and significant stress concentrations appear just distal to the sinus with peak stresses at the internal wall on the posterior side of the vessel following maximum head rotation and on the anteromedial portion of the vessel wall following rotation and hyperextension. Clinically, the location of sICAD initiation is 10-30 mm distal to the origin of the cervical ICA, which corresponds with the peak stress locations observed in the model, thus supporting trivial trauma from natural head movements as a possible initiating factor in sICAD. BM-D-08-00610ROriginalThe role of the carotid sinus in the reduction of arterial wall stresses due to head movements -potential implications for cervical artery dissection

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Residual strain effects on the stress field in a thick wall finite element model of the human carotid bifurcation

Cited by 343 publications

References 26 publications

Distinct endothelial phenotypes evoked by arterial waveforms derived from atherosclerosis-susceptible and -resistant regions of human vasculature

Distinct endothelial phenotypes evoked by arterial waveforms derived from atherosclerosis-susceptible and -resistant regions of human vasculature

An anisotropic inelastic constitutive model to describe stress softening and permanent deformation in arterial tissue

The role of the carotid sinus in the reduction of arterial wall stresses due to head movements—potential implications for cervical artery dissection

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