Colocalization of thin-walled dome regions with low hemodynamic wall shear stress in unruptured cerebral aneurysms

Abstract

Object Wall shear stress (WSS) plays a role in regulating endothelial function and has been suspected in cerebral aneurysm rupture. The aim of this study was to evaluate the spatial relationship between localized thinning of the aneurysm dome and estimated hemodynamic factors, hypothesizing that a low WSS would correlate with aneurysm wall degeneration. Methods Steady-state computational fluid dynamics analysis was performed on 16 aneurysms in 14 patients based on rotational angiographic volumes to derive maps of WSS, its spatial gradient (WSSG), and pressure. Local dome thickness was estimated categorically based on tissue translucency from high-resolution intraoperative microscopy findings. Each computational model was oriented to match the corresponding intraoperative view and numerically sampled in thin and normal adjacent dome regions, with controls at the neck and parent vessel. The pressure differential was computed as the difference between aneurysm dome points and the mean neck pressure. Pulsatile time-dependent confirmatory analysis was carried out in 7 patients. Results Matched-pair analysis revealed significantly lower levels of WSS (0.381 Pa vs 0.816 Pa; p < 0.0001) in thin-walled dome areas than in adjacent baseline thickness regions. Similarly, log WSSG and log WSS × WSSG were both lower in thin regions (both p < 0.0001); multivariate logistic regression analysis identified lower WSS and higher pressure differential as independent correlates of lower wall thickness with an area under the curve of 0.80. This relationship was observed in both steady-state and time-dependent pulsatile analyses. Conclusions Thin-walled regions of unruptured cerebral aneurysms colocalize with low WSS, suggesting a cellular mechanotransduction link between areas of flow stasis and aneurysm wall thinning.