A biochemical and mechanical model of injury-induced intimal thickening.

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.