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SUMMARY Quantification and characterization of the hemodynamic environment created after flow diversion treatment of cerebral aneurysms is important to understand the effects of flow diverters and their interactions with the biology of the aneurysm wall and the thrombosis process that takes place subsequently. This paper describes the construction of multi-modality image-based subject-specific CFD models of experimentally created aneurysms in rabbits and subsequently treated with flow diverters. Briefly, anatomical models were constructed from 3D rotational angiography images, flow conditions were derived from Doppler ultrasound measurements, stent models were created and virtually deployed, and the results were compared with in vivo digital subtraction angiography and Doppler ultrasound images. The models were capable of reproducing in vivoobservations, including velocity waveforms measured in the parent artery, peak velocity values measured in the aneurysm, and flow structures observed with digital subtraction angiography before and after deployment of flow diverters. The results indicate that regions of aneurysm occlusion after flow diversion coincide with slow and smooth flow patterns, whereas regions still permeable at the time of animal sacrifice were observed in parts of the aneurysm exposed to larger flow activity, that is, higher velocities, more swirling, and more complex flow structures. Copyright © 2014 John Wiley & Sons, Ltd.

In clinical practice, occlusion of embolized, intracerebral aneurysms is evaluated using angiography. Standard, two-dimensional digital subtract angiography (DSA) is unable to quantify irregular aneurysm remnants, and even three-dimensional rotational angiography cannot quantify the degree of occlusion. To better understand occlusion at the aneurysm neck, we compared angiographic results with MICROFIL perfusion, histology, and scanning electron microscopy (SEM) results in 20 elastase-induced saccular aneurysms in rabbits. Aneurysms were embolized with HydroCoil devices (n = 12) or platinum coils (n = 8). Aneurysm follow-up occurred at 2 (n = 10) and 6 (n = 10) weeks. Aneurysm occlusion was evaluated using DSA, MICROFIL perfusion, histological ground sections, and SEM. Groups were compared statistically using ANOVA and chi(2) tests. The MICROFIL perfusion results were not concordant with the angiographic results for the HydroCoil and platinum coil groups. Both increased and decreased occlusion was observed on the MICROFIL-perfused aneurysms when compared with angiography. The histologic occlusion results of the HydroCoil group were concordant with the angiographic results; however, unoccluded areas not visible on angiography were routinely observed on the ground sections in the platinum coil group. SEM imaging of the aneurysm neck consistently showed decreased occlusion than angiographic results for both the HydroCoil and platinum coil groups. Although histology and MICROFIL-perfusion analyses provided additional details of aneurysm occlusion when compared with angiography, complete visualization of the entire neck of the aneurysm and accurate assessment of aneurysm occlusion was possible only with SEM.

Background and Purpose— Even though endovascular coils have been widely used for the treatment of intracranial aneurysms, the cellular and molecular responses of aneurysms to the coils after embolization remain poorly understood. The aim of the present study was to understand the mechanism of apoptosis in aneurysms embolized with platinum coils in the rabbit model of elastase-induced aneurysms. Methods— Elastase-induced saccular aneurysms were created at the origin of the right common carotid artery in 30 rabbits. Aneurysms were allowed to mature for 8 weeks, after which 20 aneurysms were embolized with platinum coils by endovascular means. After 2 (n=10) and 4 (n=10) weeks of implantation, aneurysm samples harboring coils were harvested for apoptotic studies. The remaining 10 uncoiled aneurysms were used as controls; additional controls included the left common carotid artery, which had not undergone any surgical procedure. Control samples were harvested at 12 weeks after aneurysm creation. Results— Expression of procaspases-3, -8, and -9 was elevated in coiled aneurysms embolized with platinum coils at both time points when compared with uncoiled aneurysms and the left common carotid artery. Cleaved caspases-3, -8, and -9 were found to be expressed only at 4 weeks after embolization. Cells within the aneurysm cavity were terminal dUTP nick end-labeling–positive at 4 weeks only. These apoptotic cells were identified as smooth muscle actin–positive cells. Expression of tumor necrosis-α was high in coiled aneurysms when compared with controls. There was no significant difference in the expression of Fas ligand among groups. Decreased expression of antiapoptotic proteins Bcl-2 and phospho-Bad, as well as increased expression of proapoptotic proteins Bax and Bid, was observed in coiled aneurysms at both time points. Conclusions— Activation of apoptosis in aneurysms after embolization with platinum coils is induced by both tumor necrosis factor-α–mediated extrinsic and Bcl-2-mediated intrinsic pathways.