Long time evolution of atherosclerotic plaques

被引:55
作者
Bulelzai, M. A. K. [1 ]
Dubbeldam, Johan L. A. [1 ]
机构
[1] Delft Univ Technol, NL-2628 CD Delft, Netherlands
关键词
Atherosclerosis; Remodeling; Shear stress; Plaque growth; Hemodynamics; ENDOTHELIAL SHEAR-STRESS; INTRAVASCULAR ULTRASOUND; OXIDATION; MONOCYTES; MODEL; ATHEROGENESIS; MACROPHAGES; LESIONS; CELLS; SIZE;
D O I
10.1016/j.jtbi.2011.11.023
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The evolution of atherosclerosis in general, and the influence of wall shear stress on the growth of atherosclerotic plaques in particular, is an intricate phenomenon which is still only partly understood. We therefore propose a qualitative mathematical model which consists of a number of ordinary differential equations for the concentrations of the most relevant constituents of the atherosclerotic plaque. These equations were studied both for the case that the wall shear stress is a parameter (model A), and for the case in which the plaque evolution is coupled to the blood flow (model B) which results in a time dependent wall shear stress. We find that both models exhibit a class of marginally stable equilibria, all reflecting states in which the plaque only grows for a short period of time after a perturbation. The uncoupled model A, however, shows bi-stability between this class of equilibria and another equilibrium state in which the plaque experiences unlimited growth in time, if the LDL cholesterol intake exceeds a threshold value. In model B the bi-stability vanishes, but we find that there is still a critical value of the LDL cholesterol intake beyond which the lumen radius drastically decreases. We show that this decrease is quite sensitive to the value of the wall shear stress. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1 / 10
页数:10
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