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The Relationship Between Intimal Thickening and the Hemodynamic Environment of the Arterial Wall

  • M. H. Friedman
Conference paper

Abstract

The time-varying shear rates at the walls of human arteries are estimated from laser Doppler anemometer measurements in flow-through casts of human aortic and coronary bifurcations, through which physiologically realistic, fluid dynamically scaled, pulsatile flows are passed. These shear rates are then correlated against morphological measurements at corresponding sites in the vessels from which the casts had been made. These correlations suggest that the dependence of intimai thickening rate on mural shear is complex and changes over time; in particular, the intimai thickness at sites exposed to high or more unidirectional shear stresses increases quickly to a modest value, growing slowly thereafter, while the thickness at sites exposed to low or more oscillatory shears rises more slowly but, after time, reaches higher values. This behavior can be the result of competing shear-dependent processes. This explanation of the experimental results is supported by a mathematical model of intimai thickening that incorporates a selection of the biological processes that take place in the arterial wall as it responds to its hemodynamic environment. A best parsimonious fit to the data is obtained when, at sites exposed to relatively high shear, smooth muscle cells accumulate more rapidly in the intima but express extracellular matrix at a slower rate.

Keywords

Shear Rate Pulsatile Flow Oscillatory Shear Intimal Thickness Aortic Bifurcation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. [1]
    Friedman MH, Hutchins GM, Bargeron CB, Deters OJ, Mark FF (1981) Atherosclerosis 39: 425–436PubMedCrossRefGoogle Scholar
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    Friedman MH, Bargeron CB, Deters OJ, Hutchins GM, Mark FF (1987) Atherosclerosis, in pressGoogle Scholar
  3. [3]
    Friedman MH, Deters OJ (1987) J. Biornechanical Engineering 109: 25–26CrossRefGoogle Scholar
  4. [4]
    Friedman MH, Hutchins GM, Bargeron CB, Deters OJ, Mark FF (1981) J. Biomechanical Engineering 103: 204–207CrossRefGoogle Scholar
  5. [5]
    Friedman MH, Deters OJ, Bargeron CB, Hutchins GM, Mark FF (1986) Atherosclerosis 60: 161–171PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Tokyo 1988

Authors and Affiliations

  • M. H. Friedman
    • 1
  1. 1.Applied Physics LaboratoryThe Johns Hopkins UniversityLaurelUSA

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