Intracranial Aneurysm Wall Phenotypes: Clinical, Morphological, and Hemodynamic Influences.

backgroundIntracranial aneurysm (IA) wall remodeling remains a critical yet poorly understood process despite extensive research into clinical, morphological, and hemodynamic determinants of IA formation, growth, and rupture. This study aimed to systematically characterize IA wall phenotypes-thin walled, thick walled, and heterogeneous-and to identify clinical, morphological, and hemodynamic determinants associated with these categories using intraoperative imaging and advanced computational analyses.

methodsIntraoperative video recordings allowed for detailed annotation of wall regions, classifying distinct areas as red-translucent-acellular (thin) or white-hyperplastic/fibrotic and yellow-atherosclerotic (thick), along with associated blebs. Based on these observations, 12 subcategories were initially defined and then consolidated into 3 groups: Group A (thin-walled), Group B (thick-walled), and Group C (heterogeneous-walled). Statistical analyses, including chi-square tests, Mann-Whitney

resultsAnalysis of 135 IAs from 122 patients revealed that older age and smoking were strongly associated with thick-walled (Group B) and heterogeneous (Group C) aneurysms, whereas younger patients predominantly exhibited thin-walled aneurysms (Group A). Group A aneurysms were generally smaller, more elongated, and subjected to higher wall shear stress (WSS) and greater local curvature, suggesting shear-induced thinning. In contrast, Group B aneurysms were larger, with wider necks, exhibited lower WSS and higher relative residence time, and were likely influenced by chronic inflammatory processes, leading to a more fibrotic or atherosclerotic remodeling. Group C aneurysms demonstrated the most complex remodeling patterns; they displayed both thin and thick regions, irregular shapes, and strong intra-aneurysmal flow characterized by high inflow rates and turbulent flow complexity, which may contribute to simultaneous thinning and thickening within the same lesion.

conclusionThese results suggest that IA wall remodeling follows a continuum influenced by an interplay of clinical, morphological, and hemodynamic factors. Recognizing these distinct phenotypes may improve risk stratification and inform personalized treatment strategies. Although the direct prediction of rupture risk remains to be established, this multidimensional approach provides novel insights into the pathophysiological evolution of IA wall characteristics and highlights potential avenues for further investigation.