Circulation Research, Vol 36, 277-285, Copyright © 1975 by American Heart Association
ARTICLES |
MH Friedman, V O'Brien and LW Ehrlich
Numerical simulations of pulsatile blood flow through a symmetrical branch modeling the aortic bifurcation were carried out to assess several hemodynamic theories of atherogenesis by comparing the distribution of hemodynamic variables with that of early lesions in arterial branches. Considerable spatial and temporal variations in wall shear were found when the flow was pulsatile; the highest values occurred at the convex corner on the outer wall of the branch and in the neighborhood of the flow divider tip, and the lowest shears were experienced by the outer wall of the daughter vessel a short distance distal to the corner. Transient flow reversal occurred almost everywhere in the branch, and a transient separated region was found corresponding to the low-shear region in the daughter vessel. The shear profiles and the calculated separated region were influenced to some degree by the extent of flow development at the branch inlet and markedly by the branch area ratio. All of the proposed hemodynamic promoters of atherosclerosis that were examined--high shear, low shear, and separation--were found at sites in the branch where lesions commonly develop. Comparisons with a steady-flow calculation at the same mean flow rate showed that the severity of all of these proposed hemodynamic determinants was increased by pulsatility.
This article has been cited by other articles:
![]() |
H. Y. Stevens, B. Melchior, K. S. Bell, S. Yun, J.-C. Yeh, and J. A. Frangos PECAM-1 is a critical mediator of atherosclerosis Dis. Model. Mech., September 1, 2008; 1(2-3): 175 - 181. [Abstract] [Full Text] [PDF] |
||||
![]() |
S.-W. Lee, L. Antiga, J. D. Spence, and D. A. Steinman Geometry of the Carotid Bifurcation Predicts Its Exposure to Disturbed Flow Stroke, August 1, 2008; 39(8): 2341 - 2347. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. L. Smith and C. F. Pacchia Sleep Apnoea & Hypertension: Physiological bases for a causal relation: Sleep apnoea and hypertension: role of chemoreflexes in humans Exp Physiol, January 1, 2007; 92(1): 45 - 50. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. V. van Thienen, J. O. Fledderus, R. J. Dekker, J. Rohlena, G. A. van IJzendoorn, N. A. Kootstra, H. Pannekoek, and A. J.G. Horrevoets Shear stress sustains atheroprotective endothelial KLF2 expression more potently than statins through mRNA stabilization Cardiovasc Res, November 1, 2006; 72(2): 231 - 240. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. J. Dekker, J. V. van Thienen, J. Rohlena, S. C. de Jager, Y. W. Elderkamp, J. Seppen, C. J.M. de Vries, E. A.L. Biessen, T. J.C. van Berkel, H. Pannekoek, et al. Endothelial KLF2 Links Local Arterial Shear Stress Levels to the Expression of Vascular Tone-Regulating Genes Am. J. Pathol., August 1, 2005; 167(2): 609 - 618. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. J. Dekker, S. van Soest, R. D. Fontijn, S. Salamanca, P. G. de Groot, E. VanBavel, H. Pannekoek, and A. J. G. Horrevoets Prolonged fluid shear stress induces a distinct set of endothelial cell genes, most specifically lung Kruppel-like factor (KLF2) Blood, August 13, 2002; 100(5): 1689 - 1698. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Miyao, K. Kugiyama, H. Kawano, T. Motoyama, H. Ogawa, M. Yoshimura, T. Sakamoto, and H. Yasue Diffuse intimal thickening of coronary arteries in patients with coronary spastic angina J. Am. Coll. Cardiol., August 1, 2000; 36(2): 432 - 437. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Nagel, N. Resnick, C. F. Dewey Jr, and M. A. Gimbrone Jr Vascular Endothelial Cells Respond to Spatial Gradients in Fluid Shear Stress by Enhanced Activation of Transcription Factors Arterioscler Thromb Vasc Biol, August 1, 1999; 19(8): 1825 - 1834. [Abstract] [Full Text] [PDF] |
||||
|
Circulation Research Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1975 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |