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Stress Analysis of Carotid Arterial Stenosis With 3-D Fluid-Structure Interaction Simulations

[+] Author Affiliations
Giulia Fabbri, Quan Long, Hao Gao, Carola Koenig, Michael W. Collins

Brunel University, Uxbridge, Middlesex, UK

Michele Pinelli

University of Ferrara, Ferrara, Italy

Paper No. SBC2007-176451, pp. 513-514; 2 pages
doi:10.1115/SBC2007-176451
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

Atherosclerotic plaques may rupture without warning and cause subsequential acute syndromes such as myocardial infarction and cerebral stroke. Plaque disruption tends to occur at points where the plaque surface is weakest i.e. at points where biomechanical stresses caused by the pulsatile blood flow are concentrated. Therefore, both plaque vulnerability (intrinsic disease) and rupture triggers (extrinsic forces) are important for plaque disruption [1]. The former predisposes the plaque to rupture while the latter may precipitate it.

Copyright © 2007 by ASME

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