Atherosclerosis is an inflammatory disease which starts when low density lipoproteins (LDL) enter the intima of blood vessel where they are oxidized (ox-LDL). The ox-LDL is considered as a dangerous agent by the immune system provoking an anti-inflammatory response. This immune response triggers the recruitment of monocytes into the intima where they differentiate into macrophages and foam cells. The latter amplifies the production of inflammatory cytokines and further recruitment of monocytes. This auto-amplified process is compensated by the secretion of anti-inflammatory cytokines (biochemical anti-inflammation) and triggers the migration of smooth muscle cells to form a fibrous cap that covers the lipid core. These fibrous caps with the lipid core are called atherosclerosis plaque. It changes the geometry of the blood vessel by narrowing it and interacts with the blood flow. This interaction may have dangerous consequences related to the plaque rupture or to the formation of blood clot. The PhD thesis is devoted to mathematical modelling of these phenomena. It consists of two major parts : We develop mathematical models based on reaction-diffusion equations in order to describe the inflammatory process. The first model is one-dimensional. It allows us to explain how the development of atherosclerosis depends on the cholesterol (ox-LDL) concentration. If its concentration in the intima is low, then the disease will not develop. Intermediate ox-LDL concentrations can lead to the disease development under certain conditions. We show that the inflammation propagates as a reaction-diffusion wave. High ox-LDL concentrations will necessary result in the disease development. Even a small perturbation of the non inflammatory case leads to a travelling wave propagation which corresponds to a chronic inflammatory response. We then study a two-dimensional model which represents a reaction-diffusion system in a strip. The second dimension corresponds to the cross-section of the intima, nonlinear boundary conditions describe the recruitment of monocytes as a function of the cytokines concentration. We prove the existence of travelling waves and confirm our previous results which show that atherosclerosis develops as a reaction-diffusion wave. The theoretical results of the two models are confirmed by numerical simulations that show that the two-dimensional model converge to the one-dimensional one if the thickness of the intima tends to zero. When the plaque is formed, it interacts with blood flow resulting in various mechanical and bio-chemical effects. We develop a fluid-structure interaction model. The atheroma plaque is composed of a lipid pool and a fibrous cap and both are modeled as hyper elastic materials. The blood is supposed to be a non-Newtonian fluid with a variable viscosity modeled by the Carreau law. The parameters used in our simulations are taken from experimental data found in literature. We investigate the non-Newtonian effects on the re circulations downstream of the atheroma plaque and on the stress over the plaque. The simulations show that the Newtonian model significantly overestimates the re circulations in comparison with the non-Newtonian model. They also show that the Newtonian model slightly underestimates the stress over the plaque for usual shear rates, but this underestimation can become significant for low shear rates.
