COMPUTATIONAL MODELING OF FORMATION OF A CEREBRAL ANEURYSM UNDER THE INFLUENCE OF SMOOTH MUSCLE CELL RELAXATION

Abstract

The mechanics of cerebral aneurysm pathogenesis, evolution and rupture are not yet well understood. This paper presents a numerical analysis of the formation of a saccular cerebral aneurysm in for the first time in a 3D model of the basilar artery bifurcation under normal and hypertensive blood pressure. Due to the excessive endothelium derived nitric oxide produced in high wall shear stress, we assumed that smooth muscle cell relaxation is the origin of the aneurysm formation. Arterial wall remodeling under constant tension was considered to be the other mechanism of disease evolution. The wall was constructed from two elastic and hyperelastic isotropic regions. The flow was considered steady, laminar, Newtonian, and incompressible. The fully coupled fluid and structure models were solved with the finite elements package ADINA 8.5. The wall shear stress, effective stress and deformation distributions under normal and hypertensive blood pressure were compared to a healthy bifurcation. The model shows that although the malfunction of the endothelial cell layer and the corresponding smooth muscle cell-related loss of vascular tone is important to the inception of the disease; A saccular aneurysm may not be formed by this mechanism alone, and also requires the fiber-related arterial wall remodeling for further development.