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Pressure Induced Strain at Femoral Artery Bypass Graft Junctions

[+] Author Affiliations
Triona Campbell, Reena Cole, Michael O’Donnell

University of Limerick, Limerick, Ireland

Paper No. SBC2007-176342, pp. 1057-1058; 2 pages
doi:10.1115/SBC2007-176342
From:
  • ASME 2007 Summer Bioengineering Conference
  • ASME 2007 Summer Bioengineering Conference
  • Keystone, Colorado, USA, June 20–24, 2007
  • Conference Sponsors: Bioengineering Division
  • ISBN: 0-7918-4798-5
  • Copyright © 2007 by ASME

abstract

Femoral or femoropopliteal artery bypass graft junctions have a predilection for failure due to restenosis. It has been clinically proven that vascular reconstructions tend to restenose within a short period of time [1]. Extensive studies have cited wall shear stresses as being primarily responsible and definite correlations between hydrodynamic stresses in the arterial wall and arterial disease have been shown [2,3]. However intensive investigations into wall shear stresses have lead to conflicting arguments on the proliferation and propagation of stenoses. It was concluded by Freidman [4] that the intima at sites exposed to relatively high or unidirectional shears thickened initially, but as time progressed the greatest thicknesses were ultimately achieved at sites exposed to lower or more oscillatory shear environments. A contradicting view was expressed by Nazemi [5] that low wall shear stress contributed to the onset of atherosclerotic plaque formation, whilst high wall shear stress encouraging plaque growth. A number of studies have however established a statistically significant correlation between pressure and intimal hyperplasia and concluded that blood pressure and not blood flow is the primary factor responsible for the localization of atherosclerosis [6–8].

Copyright © 2007 by ASME
Topics: Pressure , Junctions

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