Typical Atherosclerotic Plaque Morphology

R. N. Poston; D. R.M. Poston

Mathematical Modelling of Natural Phenomena (2010)

  • Volume: 2, Issue: 2, page 142-149
  • ISSN: 0973-5348

Abstract

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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. 


How to cite

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Poston, R. N., and Poston, D. R.M.. "Typical Atherosclerotic Plaque Morphology." Mathematical Modelling of Natural Phenomena 2.2 (2010): 142-149. <http://eudml.org/doc/222304>.

@article{Poston2010,
abstract = { 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. 
},
author = {Poston, R. N., Poston, D. R.M.},
journal = {Mathematical Modelling of Natural Phenomena},
keywords = {atherosclerosis; atherosclerotic plaque; macrophage; smooth muscle cell; endothelium; lipid; fetus; computer simulation},
language = {eng},
month = {3},
number = {2},
pages = {142-149},
publisher = {EDP Sciences},
title = {Typical Atherosclerotic Plaque Morphology},
url = {http://eudml.org/doc/222304},
volume = {2},
year = {2010},
}

TY - JOUR
AU - Poston, R. N.
AU - Poston, D. R.M.
TI - Typical Atherosclerotic Plaque Morphology
JO - Mathematical Modelling of Natural Phenomena
DA - 2010/3//
PB - EDP Sciences
VL - 2
IS - 2
SP - 142
EP - 149
AB - 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. 

LA - eng
KW - atherosclerosis; atherosclerotic plaque; macrophage; smooth muscle cell; endothelium; lipid; fetus; computer simulation
UR - http://eudml.org/doc/222304
ER -

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