Analysis of hemodynamics and wall mechanics at sites of cerebral aneurysm rupture. (14th May 2014)

• Record Type: Journal Article
• Authors: Cebral, Juan R; Vazquez, Mariano; Sforza, Daniel M; Houzeaux, Guillaume; Tateshima, Satoshi; Scrivano, Esteban; Bleise, Carlos; Lylyk, Pedro; Putman, Christopher M
• Is Part Of: Journal of neurointerventional surgery. Volume 7:Number 7(2015)
• Page Start: 530
• Page End: 536
• Publication Date: 2014-05-14
• Subjects: Nervous system -- Surgery -- Periodicals; Cerebrovascular disease -- Surgery -- Periodicals; 617.48
• DOI: 10.1136/neurintsurg-2014-011247
• Languages: English
• ISSNs: 1759-8478

Abstract

Abstract : Background: It is thought that aneurysms evolve as the result of progressive degradation of the wall in response to abnormal hemodynamics characterized by either high or low wall shear stress (WSS). Objective: To investigate the effects of these two different hemodynamic pathways in a series of cerebral aneurysms with known rupture sites. Methods: Nine aneurysms in which the rupture site could be identified in three-dimensional images were analyzed. The WSS distribution was obtained from computational fluid dynamics (CFD) simulations. Internal wall stresses were computed using structural wall models under hemodynamic loads determined by the CFD models. Wall properties (thickness and stiffness) were modulated with the WSS distribution (increased or decreased in regions of high or low WSS) to test possible wall degradation pathways. Rupture probability indices (RPI) were calculated to compare different wall models. Results: Most rupture sites aligned with the intrasaccular flow stream and downstream of the primary impaction zone. The model that best explained the rupture site (produced higher RPI) in eight of the nine aneurysms (89%) had thinner and stiffer walls in regions of abnormally high WSS. The remaining case (11%) was best explained by a model with thinner and stiffer walls in regions of abnormally low WSS. Conclusions: Aneurysm rupture seems to be caused by localized degradation and weakening of the wall in response to abnormal hemodynamics. Image-based computational models assuming wall thinning and stiffening in regions of abnormally high WSS were able to explain most of the observed rupture sites.