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Multicenter Study
. 2011 Jan;32(1):20-5.
doi: 10.3174/ajnr.A2370. Epub 2010 Nov 11.

Intra-aneurysmal thrombosis as a possible cause of delayed aneurysm rupture after flow-diversion treatment

Affiliations
Multicenter Study

Intra-aneurysmal thrombosis as a possible cause of delayed aneurysm rupture after flow-diversion treatment

Z Kulcsár et al. AJNR Am J Neuroradiol. 2011 Jan.

Abstract

Background and purpose: FD technology enables reconstructive repair of otherwise difficult-to-treat intracranial aneurysms. These stentlike devices may induce progressive aneurysm thrombosis without additional implants and may initiate complete reverse vessel remodeling. The associated vascular biologic processes are as yet only partially understood.

Materials and methods: From 12 different centers, 13 cases of delayed postprocedural aneurysm rupture were recorded and analyzed. Symptom, aneurysm location and morphology, and the time elapsed from treatment until rupture were analyzed.

Results: There were 10 internal carotid and 3 basilar artery aneurysms. Mean aneurysm diameter was 22 ± 6 mm. Eleven patients were symptomatic before treatment. A single FD was used for all saccular aneurysms, while fusiform lesions were treated by using multiple devices. A supplementary loose coiling of the aneurysm was performed in 1 patient only. Ten patients developed early aneurysm rupture after FD treatment (mean, 16 days; range, 2-48 days); in 3 patients, rupture occurred 3-5 months after treatment. In all cases, most of the aneurysm cavity was thrombosed before rupture. The biologic mechanisms predisposing to rupture under these conditions are reviewed and discussed

Conclusions: FDs alone may modify hemodynamics in ways that induce extensive aneurysm thrombosis. Under specific conditions, however, instead of reverse remodeling and cicatrization, aggressive thrombus-associated autolysis of the aneurysm wall may result in delayed rupture.

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Figures

Fig 1.
Fig 1.
Patient No. 3. A, Posteroanterior view DSA image of an incidentally discovered left ICA parophthalmic aneurysm. B, Persistence of the inertia-driven inflow jet (arrow) is shown after device deployment. C and D, Nonenhanced CT scan 2 days after intervention shows already partial thrombosis of the aneurysm (C), and a CT angiogram at day 5 shows massive subarachnoid hemorrhage and only a minor portion of the aneurysm that is still perfused, corresponding to the inflow jet area (open arrow) (D).
Fig 2.
Fig 2.
Patient No. 6. A and B, Posteroanterior view DSA image of a symptomatic fusiform aneurysm of the basilar trunk (A) and lateral view after FD treatment (B) demonstrate contrast stasis in the aneurysm. C, 3D CT angiogram obtained 3 days after treatment shows patency of the basilar trunk and lack of aneurysm filling. D, Macroscopic view of the basilar artery and aneurysm after postmortem examination shows a massive thrombus volume bulging through the aneurysm wall defect. E, HE-stained microscopic view of the edge of the aneurysm wall rupture shows a partially maintained but vanishing adventitia (black arrow) and disappearance of the vascular tunica media (white arrow).
Fig 3.
Fig 3.
Patient No. 5. A and B, Giant fusiform aneurysm of the right distal ICA, right oblique view before (A) and after FD implantation, with a persisting inflow jet (thick arrow) (B). C, Cross-section of the aneurysm after postmortem examination shows organized thrombus filling most the aneurysm lumen. Note a dissecting cavity with liquefied clot between the organized thrombus and the thick part of the aneurysm wall (arrow). D, Microscopic view of the aneurysm after HE-staining at the rupture site shows necrosis and almost complete disappearance of the aneurysm wall.

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