Local pressure as a dominant hemodynamic driver of wall enhancement in anterior communicating artery aneurysms: a facet-level computational fluid dynamics and vessel wall imaging analysis.
Authors
Affiliations (7)
Affiliations (7)
- School of Medical Imaging, North Sichuan Medical College, Nanchong, China.
- Medical Imaging Key Laboratory of Sichuan Province, North Sichuan Medical College, Nanchong, China.
- Nuclear Medicine and Radiation Safety Key Laboratory of Sichuan Province, North Sichuan Medical College, Nanchong, China.
- Neurosurgery Center, Department of Cerebrovascular Surgery, The National Key Clinical Specialty, Engineering Research Center of Diagnostic and Therapeutic Technology and Devices for Cerebrovascular Diseases in Ministry of Education, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Zhujiang Hospital Institute for Brain Science and Intelligence, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
- School of Engineering and Technology, University of New South Wales, Canberra, Australia.
- Department of Neurosurgery, The First People's Hospital of Neijiang, Neijiang, China.
- Second Clinical Medical College, Southern Medical University, Guangzhou, China.
Abstract
Size-based risk stratification often overlooks small but unstable intracranial aneurysms (IAs). Aneurysm wall enhancement (AWE) on vessel wall imaging (VWI) is a validated marker of wall instability, yet the local hemodynamic drivers of this pathology, particularly in complex anterior communicating artery (ACoA) aneurysms, remain incompletely characterized. This study leverages a combined computational fluid dynamics (CFD)-VWI approach to characterize the mechanobiological coupling between local hemodynamics and quantitative wall remodeling in ACoA aneurysms. We retrospectively analyzed 24 patients harboring 25 ACoA aneurysms. A Vector-Integrated Surface Parametrization (VISP) pipeline achieved sub-voxel sampling density [through adaptive interpolation rather than imaging resolution beyond the native 0.6 mm magnetic resonance imaging (MRI) voxel] for co-registration of CFD and 3T-VWI, with wall enhancement defined at a contrast ratio (CR) ≥0.6. To identify hemodynamic drivers of enhanced wall thickness (EWT) while explicitly accounting for within-patient hierarchical clustering, four complementary analytical frameworks were applied in parallel: (I) intra-patient paired bootstrap tests (2,000 resamples) comparing enhanced and non-enhanced wall segments within each of the 13 AWE-positive patients; (II) a multivariate linear mixed model (LMM) with patient-level random intercepts for EWT severity (n=12,473 enhanced segments); (III) generalized estimating equations (GEEs) with cluster-robust variance for AWE presence (n=157,284 segments); and (IV) ensemble machine-learning models (Random Forest and XGBoost) interpreted via Shapley Additive exPlanations (SHAP) values across segment-level, patient-centered, and patient-level GroupKFold cross-validation (CV). Cross-patient generalization of EWT prediction was disclosed separately as an out-of-sample analysis. Focal AWE was identified in 14 of 25 aneurysms (13 patients), spatially coinciding with hemodynamic stagnation zones. Enhanced segments exhibited significantly lower local Pressure<sub>peak</sub> (∆ =-35.25 Pa, P<sub>FDR</sub> =0.02) and wall shear stress (WSS)<sub>peak</sub> (∆ =-3.97 Pa, P<sub>FDR</sub> <i><</i>0.001) compared to non-enhanced segments under intra-patient paired bootstrap testing. Three further frameworks converged on Pressure<sub>peak</sub> as the dominant independent driver of wall thickness among enhanced segments: multivariate LMM β=-0.181 (P=2.31×10<sup>-11</sup>); GEE β=-0.5452 (robust P=0.0499); and a Random Forest model, in which Pressure<sub>peak</sub> ranked first by SHAP feature importance at the segment level and remained among the top three across every CV regime. We present a facet-level CFD-VWI pipeline that achieves sub-voxel sampling density for spatially mapping local hemodynamics onto quantitative wall remodeling in ACoA aneurysms on a clinical 3T platform. Across four independent hierarchical analyses, local Pressure<sub>peak</sub> consistently emerged as the dominant independent hemodynamic driver of wall thickening among enhanced segments, complementing the established low-WSS association. This framework is intended as a mechanistic explanatory tool for local hemodynamic-AWE coupling; broader clinical translation will require larger, externally validated cohorts.