AJP - Heart AJP: Cell Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 297: H802-H810, 2009. First published June 19, 2009; doi:10.1152/ajpheart.00318.2009
0363-6135/09 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
297/2/H802    most recent
00318.2009v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Hoshino, T.
Right arrow Articles by Demer, L. L.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hoshino, T.
Right arrow Articles by Demer, L. L.

Mechanical stress analysis of a rigid inclusion in distensible material: a model of atherosclerotic calcification and plaque vulnerability

Tetsuya Hoshino,1 Lori A. Chow,2 Jeffrey J. Hsu,3 Alice A. Perlowski,3 Moeen Abedin,3 Jonathan Tobis,3 Yin Tintut,3 Ajit K. Mal,1,2 William S. Klug,1,2 and Linda L. Demer2,3,4

Departments of 1Mechanical and Aerospace Engineering, 2Biomedical Engineering, 3Medicine (Cardiology), and 4Physiology, University of California, Los Angeles, California

Submitted 2 April 2009 ; accepted in final form 15 June 2009

The role of atherosclerotic calcification in plaque rupture remains controversial. In previous analyses using finite element model analysis, circumferential stress was reduced by the inclusion of a calcium deposit in a representative human anatomical configuration. However, a recent report, also using finite element analysis, suggests that microscopic calcium deposits increase plaque stress. We used mathematical models to predict the effects of rigid and liquid inclusions (modeling a calcium deposit and a lipid necrotic core, respectively) in a distensible material (artery wall) on mechanical failure under uniaxial and biaxial loading in a range of configurations. Without inclusions, stress levels were low and uniform. In the analytical model, peak stresses were elevated at the edges of a rigid inclusion. In the finite element model, peak stresses were elevated at the edges of both inclusions, with minimal sensitivity to the wall distensibility and the size and shape of the inclusion. Presence of both a rigid and a soft inclusion enlarged the region of increased wall stress compared with either alone. In some configurations, the rigid inclusion reduced peak stress at the edge of the soft inclusion but simultaneously increased peak stress at the edge of the rigid inclusion and increased the size of the region affected. These findings suggest that the presence of a calcium deposit creates local increases in failure stress, and, depending on relative position to any neighboring lipid pools, it may increase peak stress and the plaque area at risk of mechanical failure.

plaque rupture; vulnerable plaque; atherosclerosis; vascular calcification



Address for reprint requests and other correspondence: L. L. Demer, Division of Cardiology, The David Geffen School of Medicine at UCLA, 10833 LeConte Ave., Box 951679, Los Angeles, CA 90095-1679 (e-mail: ldemer{at}mednet.ucla.edu)







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2009 by the American Physiological Society.