Abstract
Hemodynamic insults--high wall shear stress (WSS) combined with high positive WSS gradient (WSSG)--have been proposed to link to cerebral aneurysm initiation. We report 4 cases of aneurysms with proximal stenosis, including 1 de novo aneurysm, that might be associated with hemodynamic insults caused by the proximal stenosis. In 4 clinical cases, the diameter stenosis was 37% to 49% (mean, 42%) located 2.7 to 4.7 mm (mean, 3.7 mm) from the apex. We performed computational fluid dynamics simulations for 2 cases: a ruptured basilar terminus aneurysm with proximal stenosis (which had an angiogram taken 15 years previously that showed no aneurysm and no stenosis) and a cavernous carotid artery aneurysm with proximal stenosis. In both cases, the stenosis caused unphysiologically high WSS (> 7 Pa) at the apex, nearly doubling the WSS and WSSG values. To investigate the relationship between stenosis and distal hemodynamic elevation, we created a series of T-shaped vascular models by varying the degree and location of stenosis. We found that stenosis > 40% by diameter located within 10 mm from the apex caused unphysiologically high WSS and WSSG. All 4 clinical cases satisfied these conditions. Proximal stenosis could produce high WSS and high positive WSSG at the apex, thus potentially inducing de novo aneurysm formation. BT, basilar terminusCFD, computational fluid dynamicsICA, internal carotid arteryWSS, wall shear stressWSS, wall shear stress gradient.
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