Wall shear stress and endothelial cells dysfunction in the context of abdominal aortic aneurysms.

The formation of aneurysm of abdominal aorta (AAA), is a multi-factorial and predominantly degenerative process that results from a complex interplay between biological processes in the arterial wall and the hemodynamic stimuli on the wall, i.e. wall shear stresses (WSS) and elongations of the wall directly applied on vascular endothelial cells (EC) partly regulate the arterial wall remodelling (Golledge et al, 2006, Humphrey et al 2012). In the case of AAA, these mechanical stimuli strongly vary in space and time, leading to strong spatio-temporal gradients (Figure 1). The effect of these abnormal mechanical stimuli leads to EC dysfunction. This phenomenon plays a significant role in AAA pathology, where damage of EC, associated with changes of endothelial permeability and increased local inflammation, appears to be the initial step of AAA formation and expansion. In the last two decades, many in vitro studies have been performed in order to characterize the influence of WSS (Chiu and Chien 2011) on the EC biological response. Recently the coupling between elongation and WSS has been also investigated. However, these stimuli remain usually very far from the ones encountered in AAA during its expansion, and do not allow to clearly understand the links between blood WSS – AAA wall stress and elongations EC dysfunction. Within this context, new experiments need to be developed in order to reproduce such pathological loadings on EC. In the present study, we present results concerning the influence of WSS only on EC dysfunction in a parallel plate flow channel. A preliminary set of in vitro experiments have been performed applying three different values of WSS, which represent the WSS over a cardiac cycle at three different locations in a typical AAA geometry. These tests will be then used as reference in order to measure the influence of the pathological spatio-temporal gradients of WSS.