Hemodynamically Induced Creation and Rupture of Secondary Intracranial Aneurysms: A Discriminant Study Using Anatomical and Phantom Models

Background and Purpose A daughter sac was described as an irregular protrusion of the aneurysm wall. Intracranial aneurysms (IAs) with daughter sacs elevate IA rupture risks. This research aimed to investigate hemodynamic factors associated with the inception of daughter sacs and IA rupture using anatomical and phantom IA models under various SIA scenarios through hemodynamic and statistical analysis.

Methods Using standardized reconstruction procedures, anatomical IA models of 45 cerebral aneurysms harboring 67 daughter sac scenarios were constructed from 3D rotational angiographies, and 67 phantom parental intracranial aneurysm (PIA) models representing the state before daughter sac formation were virtually created by prescriptively removing the blebs from the anatomic models. An in-vitro validated computational method with physiological pulsatile flow boundary condition was adopted to secure hemodynamic characteristics in both IA and PIA models. Statistical significance of hemodynamic parameters was analyzed to secure the critical hemodynamic indicators in correlation with rupture of IAs with SIA symptoms, and generation of SIA sacs.

Results Each identified daughter sac forms at least one vortex in the saccular flow, this fact in combination with 58% of recruited cases were seen in unruptured IAs suggests the number of flow vortices has no direct relationship with the rupture of IAs or with SIA sacs. Through univariate analysis, high wall shear stress (WSS) could lead to rupture of IAs on anterior communicating artery (ACA) bifurcation (AUC=0.778), while relatively low WSS lead to rupture of IAs on the internal carotid artery (ICA) (AUC=0.840). High surface-averaged time-averaged WSS (SATAWSS) (AUC=0.712) and surface-averaged time-averaged WSS gradient (SATAWSSG) (AUC=0.692) with lower maximum oscillatory shear index (OSI) (AUC=0.799) have a great potential to initiate the SIA sac.

Conclusion The hemodynamic parameters accounting for rupture of IAs with SIA sacs vary with specific aneurysm locations such as ACA and ICA. High SATAWSS and SATAWSSG with low maximum OSI could be a critical hemodynamic combination resulting in formation of a SIA and the initiation site is most likely located at the edge rather than the central point of the original hemodynamically impacted area.