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Research Papers

A Structure-Based Model of Arterial Remodeling in Response to Sustained Hypertension

[+] Author and Article Information
Alkiviadis Tsamis

Laboratory of Hemodynamics and Cardiovascular Technology, École Polytechnique Fédérale de Lausanne, AI 1140, Station 15, CH-1015 Lausanne, Switzerlandalkiviadis.tsamis@epfl.ch

Nikos Stergiopulos

Laboratory of Hemodynamics and Cardiovascular Technology, École Polytechnique Fédérale de Lausanne, AI 1140, Station 15, CH-1015 Lausanne, Switzerland

Alexander Rachev

 Georgia Institute of Technology, 315 Ferst Drive, IBB Building, Atlanta, GA 30332alexander.rachev@me.gatech.edu

J Biomech Eng 131(10), 101004 (Sep 01, 2009) (8 pages) doi:10.1115/1.3192142 History: Received November 28, 2008; Revised May 11, 2009; Published September 01, 2009

A novel structure-based mathematical model of arterial remodeling in response to a sustained increase in pressure is proposed. The model includes two major aspects of remodeling in a healthy matured vessel. First, the deviation of the wall stress and flow-induced shear stress from their normal physiological values drives the changes in the arterial geometry. Second, the new mass that is produced during remodeling results from an increase in the mass of smooth muscle cells and collagen fibers. The model additionally accounts for the effect of the average pulsatile strain on the recruitment of collagen fibers in load bearing. The model was used to simulate remodeling of a human thoracic aorta, and the results are in good agreement with previously published model predictions and experimental data. The model predicts that the total arterial volume rapidly increases during the early stages of remodeling and remains virtually constant thereafter, despite the continuing stress-driven geometrical remodeling. Moreover, the effects of a perfect or incomplete restoration of the arterial compliance on the remodeling outputs were analyzed. For instance, the model predicts that the pattern of the time course of the opening angle depends on the extent to which the average pulsatile strain is restored at the end of the remodeling process. Future experimental studies on the time course of compliance, opening angle, and mass fractions of collagen, elastin, and smooth muscle cells can validate and improve the introduced hypotheses of the model.

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Copyright © 2009 by American Society of Mechanical Engineers
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Figures

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Figure 1

The zero-stress Bo and deformed B configuration of an artery cross section

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Figure 2

Time course of normalized thickness at the stress-free configuration (a), axial stretch ratio (b), deformed inner radius (c), and opening angle (d). Dashed line shows values for m=0.6, solid line for m=1, and dotted line for m=1.4.

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Figure 3

Time course of normalized mass increase (a) and mass fractions of the wall constituents (b). Dashed line shows values for m=0.6, solid line for m=1, and dotted line for m=1.4.

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Figure 4

Time course of normalized wall stresses (a) and distribution of circumferential stress across the wall thickness (b). Dashed line shows values for m=0.6, solid line for m=1, and dotted line for m=1.4.

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Figure 5

Time course of normalized collagen parameter b (a), arterial compliance (b), mean fiber engagement strain (c), and fiber engagement variance (d). Dashed line shows values for m=0.6, solid line for m=1, and dotted line for m=1.4.

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Figure 6

Theoretical prediction for the relation between pressure-inner radius (a), compliance-pressure (b), and average circumferential stress-stretch ratio (c). Thick-solid line shows values under normotensive conditions, dashed line shows values at the final adapted state for m=0.6, solid line for m=1, and dotted line for m=1.4.

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