Abstract
A small fraction of intracranial aneurysms (IA) contains intrasaccular thrombosis (IST). This study explores the hemodynamic causes of IST formation in IAs. We performed computational hemodynamic analysis in 26 IAs: 13 thrombosed and 13 non-thrombosed. The IAs in the two cohorts were matching in size and anatomical location. The computational hemodynamic analysis used "patient-specific" IA geometries derived from 3D magnetic resonance imaging. A comprehensive hemodynamic analysis was conducted using commonly used hemodynamic metrics (e.g., wall shear stress [WSS] and its derivative), flow vortex analysis, and velocity informatics. We observed that more flow eddies and endothelial cell activation potential (ECAP) are present in thrombosed IAs. The flow eddies in thrombosed IAs change size and location over a cardiac cycle more significantly than those in non-thrombosed IAs. These two factors, coupled with more flow stagnation and positive WSS divergence in the thrombosed IAs, promoted thrombus formation in the thrombosed IA cohort.