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dc.contributorWichita State University. Department of Aerospace Engineering
dc.contributor.authorShaik, Eleyas
dc.contributor.authorHoffmann, Klaus A.
dc.contributor.authorDietiker, JF.
dc.date.accessioned2012-02-10T21:49:35Z
dc.date.available2012-02-10T21:49:35Z
dc.date.issued2007-03
dc.identifier.citationShaik E, KA Hoffmann, and JF Dietiker. 2007. "Numerical simulations of pulsatile flow in an end-to-side anastomosis model". Molecular & Cellular Biomechanics : MCB. 4 (1): 41-53.en_US
dc.identifier.issn1556-5297
dc.identifier.issn1556-5300
dc.identifier.urihttp://hdl.handle.net/10057/4453
dc.identifier.urihttp://dx.doi.org/10.3970/mcb.2007.004.041
dc.descriptionClick on the DOI link below to access the article(may not be free)en_US
dc.description.abstractA potential interaction between the local hemodynamics and the artery wall response has been suggested for vascular graft failure by intimal hyperplasia (IH). Among the various hemodynamic factors, wall shear stress has been implicated as the primary factor responsible for the development of IH. In order to explore the role of hemodynamics in the formation of IH in end-to-side anastomosis, computational fluid dynamics is employed. To validate the numerical simulations, comparisons with existing experimental data are performed for both steady and pulsatile flows. Generally, good agreement is observed with the velocity profiles whereas some discrepancies are found in wall shear stress (WSS) distributions. Using the same end-to-side anastomosis geometry, numerical simulations are extended using a femoral artery waveform to identify the possible role of unsteady hemodynamics. In the current simulations, Carreau-Yasuda model is used to account for the non-Newtonian nature of blood. Computations indicated a disturbed flow field at the artery-graft junction leading to locally elevated shear stresses on the vascular wall. Furthermore, the shear stress distribution followed the same behavior with oscillating magnitude over the entire flow cycle. Thus, distal IH observed in end-to-side artery-graft models may be caused by the fluctuations in WSS's along the wall.en_US
dc.language.isoen_USen_US
dc.publisherTech Science Pressen_US
dc.relation.ispartofseriesMolecular & Cellular Biomechanics;2007:, v.4, no.1
dc.subjectArtery bypassen_US
dc.subjectComputational fluid dynamicsen_US
dc.subjectEnd-to-side anastomosisen_US
dc.subjectHemodynamicsen_US
dc.subjectIntimal hyperplasiaen_US
dc.titleNumerical simulations of pulsatile flow in an end-to-side anastomosis modelen_US
dc.typeArticleen_US
dc.description.versionPeer reviewed
dc.rights.holderCopyright © 2007, Tech Science Press


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