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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.

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Development of a diagnostic tool for predicting the behavior of cerebral aneurysms was the inspiration of many research groups in recent years. In the present study a fluid–solid-growth (FSG) model for the early development of a cerebral aneurysm was presented in a 3D model of the internal carotid artery (ICA). This model is the result of two parallel mechanisms: first, defining arterial wall as a living tissue with the ability of degradation, growth and remodeling and second, full coupling of the wall and the blood flow. Taking into account the shear dependent nature of elastin degradation and mural-cell-mediated destructive activities, here, the degradation process has been linked to high effective stress of the vascular wall. The evolving properties of the elastinous and collagenous constituents have been predicted during the early development of the aneurysm and the code is applicable to more complicated aneurismal growth models.

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