Changes in the hemodynamic stresses occurring during the enlargement of abdominal aortic aneurysms.

摘要

This research seeks to improve the understanding of the mechanisms accounting for the growth of abdominal aortic aneurysms (AAA), by quantifying the role that mechanical stimuli play in the disease processes. In recent years, the development of vascular diseases has been associated with the formation of disturbed patterns of wall shear stresses (WSS) and gradients of wall shear stresses (GWSS). They have been shown to affect the wall structural integrity, primarily via the changes induced on the morphology and functions of the endothelial cells (EC) and circulating blood cells.; Particle Image Velocimetry measurements of the pulsatile blood flow have been performed in aneurysm models, while changing systematically their geometric parameters. The parametric study shows that the flow separates from the wall even at early stages of the disease (dilatation ≤50%). A large vortex ring forms in symmetric aneurysms, followed by internal shear layers. Two regions with distinct patterns of WSS have been identified: a region of flow detachment, with low oscillatory WSS, and a downstream region of flow reattachment, where large negative WSS and sustained GWSS are produced as a result of the impact of the vortex ring.; The loss of symmetry in the models engenders a helical flow pattern due to the non-symmetric vortex shedding. The dominant vortex, whose strength increases with the asymmetry parameter, is shed from the most bulged wall (anterior). It results in the formation of a large recirculating region, where ECs are subjected to quasi-steady reversed WSS of low magnitude, while the posterior wall is exposed to quasi-healthy WSS. GWSS are generated at the necks and around the point of impact of the vortex.; Lagrangian tracking of blood cells inside the different models of aneurysms shows a dramatic increase in the cell residence time as the aneurysm grows. While recirculating, cells experience high shear stresses close to the walls and inside the shear layers, which may lead to cell activation. The vortical structure of the flow also convects the cells towards the wall, increasing the probability for cell deposition and ipso facto for the formation of an intraluminal thrombus.