• Eleni Metaxa, Markus Tremmel, Sabareesh K Natarajan, Jianping Xiang, Rocco A Paluch, Max Mandelbaum, Adnan H Siddiqui, John Kolega, J Mocco, and Hui Meng.
• Toshiba Stroke Research Center, University at Buffalo, State University of New York, Buffalo, NY 14214, USA.
• Stroke. 2010 Aug 1; 41 (8): 1774-82.

Background And PurposeHemodynamic insult by bilateral common carotid artery ligation has been shown to induce aneurysmal remodeling at the basilar terminus in a rabbit model. To characterize critical hemodynamics that initiate this remodeling, we applied a novel hemodynamics-histology comapping technique.MethodsEight rabbits received bilateral common carotid artery ligation to increase basilar artery flow. Three underwent sham operations. Hemodynamic insult at the basilar terminus was assessed by computational fluid dynamics. Bifurcation tissue was harvested on day 5; histology was comapped with initial postligation hemodynamic fields of wall shear stress (WSS) and WSS gradient.ResultsAll bifurcations showed internal elastic lamina loss in periapical regions exposed to accelerating flow with high WSS and positive WSS gradient. Internal elastic lamina damage happened 100% of the time at locations where WSS was >122 Pa and WSS gradient was >530 Pa/mm. The degree of destructive remodeling accounting for internal elastic lamina loss, medial thinning, and luminal bulging correlated with the magnitude of the hemodynamic insult.ConclusionsAneurysmal remodeling initiates when local hemodynamic forces exceed specific limits at the rabbit basilar terminus. A combination of high WSS and positive WSS gradient represents dangerous hemodynamics likely to induce aneurysmal remodeling.

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