Math. Model. Nat. Phenom.
Volume 2, Number 2, 2007Reaction-diffusion waves
|Page(s)||142 - 149|
|Published online||15 July 2008|
Typical Atherosclerotic Plaque Morphology
School of Medicine, Guy's Campus, King's College London, United Kingdom
2 Ideaworks3D, London EC1, United Kingdom
Corresponding author: firstname.lastname@example.org
Atherosclerosis always develops in plaques, and the reasons are not clear. We test the hypothesis that plaque morphology results from a self-perpetuating propagating process driven by macrophages (Mphs). A computer model of atherogenesis was written in which the computer screen represents a surface view of a flattened area of an arterial wall on which greatly accelerated atherogenesis is depicted. Rate of Mph recruitment from blood monocytes is set as a steeply rising function of the number of Mphs locally present. Smooth muscle accumulation depends on Mph number, Mphs have a probability of death/loss, and lipid accumulation results directly from the death of Mphs. The program runs in reiterative cycles. From an initially normal wall, fatty streak-like foci of Mphs form at random sites, which may progress or regress. Some develop into progressive focal lesions resembling advanced plaques, which are Mph-rich and have a central fibrous cap-like central region of smooth muscle cells. Lipid accumulates centrally in them. To investigate a fetal origin of atherosclerosis, the simulation was initially loaded with Mphs: lesion development was greatly enhanced. These results strongly resemble atherosclerosis in vivo, and support the Mph-dependent hypothesis of spreading plaque growth.
Mathematics Subject Classification: 92C50 / 92-04
Key words: atherosclerosis / atherosclerotic plaque / macrophage / smooth muscle cell / endothelium / lipid / fetus / computer simulation
© EDP Sciences, 2007
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