نبذة مختصرة : Endofibrosis is a multiscale and multiphysic vascular pathology induced by intensive practice of an endurance sport activity. The pathology produces an arterial wall thickening and a reduction of the arterial lumen calibre on a young and healthy population. Endofibrosis was addressed increasingly over the years in the vascular surgery literature but its physiopathology is poorly understood. Recently a link has been proposed between endofibrosis and another well-known vascular pathology : intimal hyperplasia. A clean understanding of the interactions of vascular cells, hemodynamics and vascular wall biochemistry is essential to completely understand the mechanisms that control vascular cell growth and the pathological onset. This manuscript is devoted to the development and the simulation of a multiscale and multiphysic model of endofibrosis/intimal hyperplasia. A novel computational multiscale framework of a bio-chemo-mechanical model for intimal hyper- plasia is proposed. Within the arterial wall, our model is made of kinetic differential equations for key vascular cell types, collagen and growth factors. The hemodynamics is modeled with the Navier-Stokes equations. Coupling hypothesis among time and space scales are proposed to build a tractable modelling of such a complex pathology. We investigate the interactions between hemodynamics, cellular dynamics and biochemistry on the development of intimal hyperpalsia/endofibrosis by applying our model to various in silico experiments. Firstly, we present a monodimensional test-case for validation by comparing the results with animal models experiments on intimal hyperplasia. Our model permits to capture many cellular phenomena which have a central role in the physiopathology of intimal hyperplasia. Results are quantitatively and qualitatively consistent with experimental findings at both short and long timescales. Then, using a compartimental approach, we simulate our remodeling and tissue growth model in an idealized 2D-axisymmetric artery on which steady ...
No Comments.