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Original research
Analysis of hemodynamics and wall mechanics at sites of cerebral aneurysm rupture
  1. Juan R Cebral1,
  2. Mariano Vazquez2,
  3. Daniel M Sforza1,
  4. Guillaume Houzeaux2,
  5. Satoshi Tateshima3,
  6. Esteban Scrivano4,
  7. Carlos Bleise4,
  8. Pedro Lylyk4,
  9. Christopher M Putman5
  1. 1Center for Computational Fluid Dynamics, George Mason University, Fairfax, Virginia, USA
  2. 2CASE—High Performance Computational Mechanics, Barcelona Supercomputing Center, Barcelona, Spain
  3. 3Department of Interventional Neuroradiology, UCLA Medical Center, Los Angeles, California, USA
  4. 4Department of Interventional Neuroradiology, Instituto Clínico ENERI, Buenos Aires, Argentina
  5. 5Department of Interventional Neuroradiology, Inova Fairfax Hospital, Falls Church, Virginia, USA
  1. Correspondence to Dr Juan R Cebral, Center for Computational Fluid Dynamics, George Mason University, 4400 University Drive, MSN 3F3, Fairfax, VA 22030, USA; jcebral{at}


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.

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