Abstract
BACKGROUND: Despite technical and diagnostic progress there are still open questions in the understanding of the pathophysiology of intracranial aneurysms. OBJECTIVE: Within 44 days we observed the de novo genesis and rupture of an aneurysm of the basilar artery in a patient. We performed computational fluid dynamics on 3-dimensional (3D) models of the inconspicuous vessel and the same vessel ...
Abstract
BACKGROUND: Despite technical and diagnostic progress there are still open questions in the understanding of the pathophysiology of intracranial aneurysms. OBJECTIVE: Within 44 days we observed the de novo genesis and rupture of an aneurysm of the basilar artery in a patient. We performed computational fluid dynamics on 3-dimensional (3D) models of the inconspicuous vessel and the same vessel with aneurysm. Based on the simulations we propose a mechanism of genesis of fast-growing aneurysms. METHODS: Three-dimensional mesh models were built using computed tomography-angiography slices. Flow was modeled as a non-Newtonian blood model with shear-dependent dynamic viscosity. We investigated flow velocity, wall pressure, impingement point, wall shear stress (WSS), and asymmetric flows in 3D models of the vessel tree of the basilar artery. RESULTS: Impingement point and wall pressure had no clear relation to the origin of the aneurysm. The impingement point faded away during aneurysm growth. Instead we found an area of permanently low WSS in the original basilar artery. This location corresponded to the origin of the later developing aneurysm. Aneurysm growth was facilitated by an increasing overall expansion of the basilar tip and a constant decrease of WSS. CONCLUSION: Assuming a preexisting reduced resistibility of the vessel wall to pressure changes and an area of permanently low WSS, an increase in pressure induces geometrical changes. These cause changes of intravascular flow distribution, lowering the already low WSS in specific locations. This leads to endothelial damage in this area and to a decreasing stability of the vessel wall, causing aneurysm development, growth, and rupture.
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