Abstract Body: Background and Purpose—Intracranial aneurysms (IAs) with daughter sacs (DSs) have an increased risk for rupture yet the hemodynamic factors contributing to DS pathophysiology are still under-investigated. This study aimed to investigate hemodynamic factors in DS generation and rupture using anatomic and ablated IA models under various DS scenarios.
Methods—113 computational models of 43 patients with at least one IA containing a DS were built based on 3D rotational angiographical images using benchmarked model reconstruction procedures. Of these 43 patients, there were 19 ruptured (RIAs) and 26 unruptured IAs (UIAs). Ablated models representing the aneurysm before the DS formation were rebuilt by virtually ablating the blebs from the anatomic models. In-vitro validated computational fluid dynamics simulations were conducted for both anatomic IA and ablated IA models under physiologically pulsatile flow conditions. Wall shear stress (WSS) associated parameters were used to analyze the hemodynamic factor on the DS pathophysiology statistically.
Results and Discussion—There was a statistically significant difference seen between RIAs and UIAs in hemodynamic performances at the entire aneurysmal sac region (P<0.01). Specifically, there was a significant difference in maximum instantaneous WSS (MIWSS), maximum instantaneous WSS gradient (MIWSSG), maximum time-averaged WSS (MTAWSS), and maximum time-averaged WSS (MTAWSSG) observed between RIAs and UIAs arising from the internal carotid artery, anterior cerebral artery, and middle cerebral artery. The difference in maximum oscillatory shear index (OSI) between RIAs and UIAs was not consistent at these aneurysmal locations. In addition, on the local DS bleb region, the hemodynamic comparisons between UIAs and RIAs were not consistent with the comparisons on the entire aneurysmal sac region. Future studies include the introduction of new parameters (i.e., instantaneous/time-averaged surface-averaged WSS, WSSG, and OSI) to investigate specific hemodynamic factors associated with DS and IA rupture. Hemodynamics between anatomic and ablated IA models will also be compared to determine its contributions on DS bleb inception. In conclusion, these findings are significant as they do suggest possible factors contributing to IA rupture. Continued research in this area will help develop a diagnostic tool to analyze IA rupture risk better than current available methods.