Key result
A biochemical and mechanical model of intimal thickening suggests that to achieve experimental growth rates, growth must be mainly cytokine-induced rather than stress-induced.
A biomechanical model of intimal thickening indicates that cytokine release, rather than mechanical stress, is the primary driver of arterial growth in atherosclerosis.
Cytokine-driven growth may predominate in intimal thickening; hypothesis-generating for atherosclerosis mechanisms, no clinical implications yet.
In this paper, we investigate an axisymmetric model of intimal thickening using hyperelasticity theory. Our model describes the growth of the arterial intima due to cell proliferation which, in turn, is driven by the release of a cytokine such as platelet-derived growth factor (PDGF). With the growth rate tied to both local stress and the local concentration of PDGF, we derive a quadruple free boundary problem with different regions of the vessel wall characterized by different homeostatic stress. We compare our model predictions to rabbit and rodent models of atherosclerosis and find that in order to achieve the growth rates reported in the experiments, growth must be mainly cytokine induced rather than stress induced. Our model is also able to reproduce Glagov remodelling where, as a vessel becomes more diseased, the lumen expands before rapidly contracting.
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Fok et al. (2015) studied Injury-induced intimal thickening / Atherosclerosis. Biochemical and mechanical model of intimal thickening was evaluated on Growth rate of arterial intima. A biochemical and mechanical model of intimal thickening suggests that to achieve experimental growth rates, growth must be mainly cytokine-induced rather than stress-induced.
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