Publication:
Interstitial flow, pressure and residual stress in the aging carotid artery model in FEBio

dc.contributor.coauthorAltundemir, Sercan
dc.contributor.coauthorUguz, A. Kerem
dc.contributor.departmentDepartment of Mechanical Engineering
dc.contributor.kuauthorPekkan, Kerem
dc.contributor.kuauthorLashkarinia, Seyedeh Samaneh
dc.contributor.schoolcollegeinstituteCollege of Engineering
dc.date.accessioned2025-01-19T10:32:54Z
dc.date.issued2023
dc.description.abstractVascular smooth muscle cells (VSMCs) are subject to interstitial flow-induced shear stress, which is a critical parameter in cardiovascular disease progression. Transmural pressure loading and residual stresses alter the hydraulic conductivity of the arterial layers and modulate the interstitial fluid flux through the arterial wall. In this paper, a biphasic multilayer model of a common carotid artery (CCA) with anisotropic fiber-reinforced soft tissue and strain-dependent permeability is developed in FEBio software. After the verification of the numerical predictions, age-related arterial thickening and stiffening effects on arterial deformation and interstitial flow are computed under physiological geometry and physical parameters. We found that circumferential residual stress shifts outward in each layer and its gradient increases up to 6 times with aging. Internally pressurized CCA displays nonlinear deformation. In the aged artery, the circumferential stress becomes greater on the media layer (82-158 kPa) and lower on the intima and adventitia (19-23 kPa and 25-28 kPa, respectively). The radial compression of the intima reduces the total hydraulic conductivity by 48% in the young and 16% in the aged arterial walls. Consequently, the average radial interstitial flux increases with pressure by 14% in the young and 91% in the aged arteries. Accordingly, the flow shear stress experienced by the VSMCs becomes more significant for aged arteries, which may accelerate cardiovascular disease progression compared to young arteries.
dc.description.indexedbyWOS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.issue1
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuN/A
dc.description.sponsorshipWe acknowledge TUBITAK awards 120C139 and 118S108 providing partial funding (KP).
dc.description.volume23
dc.identifier.doi10.1007/s10237-023-01766-7
dc.identifier.eissn1617-7940
dc.identifier.issn1617-7959
dc.identifier.quartileQ2
dc.identifier.scopus2-s2.0-85169838288
dc.identifier.urihttps://doi.org/10.1007/s10237-023-01766-7
dc.identifier.urihttps://hdl.handle.net/20.500.14288/26496
dc.identifier.wos1058945200001
dc.keywordsFEBio
dc.keywordsArterial wall mechanics
dc.keywordsVascular smooth muscle cell
dc.keywordsPermeability
dc.keywordsInterstitial flow
dc.keywordsVascular aging
dc.language.isoeng
dc.publisherSpringer Heidelberg
dc.relation.grantnoTUBITAK [118S108]; [120C139]
dc.relation.ispartofBiomechanics and Modeling in Mechanobiology
dc.subjectBiophysics
dc.subjectEngineering, Biomedical
dc.titleInterstitial flow, pressure and residual stress in the aging carotid artery model in FEBio
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.kuauthorPekkan, Kerem
local.contributor.kuauthorLashkarinia, Seyedeh Samaneh
local.publication.orgunit1College of Engineering
local.publication.orgunit2Department of Mechanical Engineering
relation.isOrgUnitOfPublicationba2836f3-206d-4724-918c-f598f0086a36
relation.isOrgUnitOfPublication.latestForDiscoveryba2836f3-206d-4724-918c-f598f0086a36
relation.isParentOrgUnitOfPublication8e756b23-2d4a-4ce8-b1b3-62c794a8c164
relation.isParentOrgUnitOfPublication.latestForDiscovery8e756b23-2d4a-4ce8-b1b3-62c794a8c164

Files