Mechanical & Materials Engineering, Department of

 

Document Type

Article

Date of this Version

9-2014

Citation

Journal of Biomechanical Engineering-Transactions of the ASME. 136(9), 091007 (8 pages). DOI: 10.1115/1.4027939
http://biomechanical.asmedigitalcollection.asme.org/article.aspx?articleid=1886124

Comments

Copyright (c) 2014 by ASME. Used by permission.

Abstract

A computational framework was implemented and validated to better understand the hypertensive artery remodeling in both geometric dimensions and material properties. Integrating the stress-modulated remodeling equations into commercial finite element codes allows a better control and visualization of local mechanical parameters. Both arterial thickening and stiffening effects were captured and visualized. An adaptive material remodeling strategy combined with the element birth and death techniques for the geometrical growth were implemented. The numerically predicted remodeling results in terms of the wall thickness, inner diameter, and the ratio of elastin to collagen content of the artery were compared with and fine-tuned by the experimental data from a documented rat model. The influence of time constant on the material remodeling was also evaluated and discussed. In addition, the geometrical growth and material remodeling were isolated to better understand the contributions of each element to the arterial remodeling and their coupling effect. Finally, this framework was applied to an image-based 3D artery generated from computer tomography to demonstrate its heterogeneous remodeling process. Results suggested that hypertension induced arterial remodeling are quite heterogeneous due to both nonlinear geometry and material adaptation process. The developed computational model provided more insights into the evolutions of morphology and material of the artery, which could complement the discrete experimental data for improving the clinical management of hypertension. The proposed framework could also be extended to study other types of stress-driven tissue remodeling including in-stent restenosis and grafting.

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