Anterior Communicating Artery Aneurysm: Stent-Assisted Anterior Communicating Artery Aneurysm Coil Occlusion – A Duplicated AcomA as a Potentially Dangerous Cause of a Nonexpanding Stent
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The 55-year-old male patient was already suffering from severe three-vessel atherosclerotic heart disease. In December 2016 he had experienced an embolic stroke to the central territory of the right middle cerebral artery (MCA). The diagnostic work-up at that time revealed a 70% stenosis of the right internal carotid artery (ICA) and an incidental aneurysm of the anterior communicating artery (AcomA) measuring 7 mm in diameter and with a wide neck. The patient was scheduled for stent-assisted endovascular treatment. The endovascular strategy was to bridge the neck of the aneurysm from the right A2 segment to the left A1 segment. While deploying the stent, it became apparent that the distal end of the stent was opening well, but the proximal portion showed insufficient expansion. The stent was resheathed, and during this procedure, we acquired a DSA run in a slightly different projection. This run showed that we had attempted to deploy the stent in a very thin duplication of the AcomA, which had been invisible in the previous DSA runs. After maneuvering the microcatheter through the branch of the AcomA with the aneurysm, the stent could be regularly deployed, and the aneurysm was then completely occluded with detachable coils. Incomplete opening of self-expanding intracranial stents is not a rare observation, especially in the case of tortuous vessel anatomy or if the movement of the stent-bearing wire is restricted. Our example shows that anatomical variations of the AcomA complex also need to be taken into consideration should a self-expanding stent not fully expand. The increasing use of low-profile self-expanding stents and flow diverters that can be advanced through ever thinner microcatheters may facilitate the advancement of the microcatheter into anatomical variants that are so tiny that they may be invisible during standard DSA runs. In our patient, any attempt to open the stent with a balloon, which is often a strategy called upon for an incompletely expanded stent, would have been fatal. Potential complications due to inadvertent deployment of low-profile self-expanding stents into small-caliber intracranial arteries are the main topic of this chapter.
KeywordsAnterior communicating artery Saccular aneurysm Self-expanding stents Wall adaptation Endovascular treatment Stent-assisted coil embolization Anatomical variants of the anterior communicating artery complex
The patient was a 55-year-old male with a history of embolic stroke in the striatal territory of the right middle cerebral artery (MCA) and a residual hemiparesis of the left-hand side. During diagnostic work-up after the stroke in December 2016, the diagnosis of an incidental aneurysm of the anterior communicating artery (AcomA) was made. The patient was referred to our department in March 2017 for endovascular treatment of said aneurysm.
The main goal of the treatment was to prevent the further growth and rupture of the AcomA aneurysm. Based on this analysis and in consideration of the sharp bend of the right A1–A2 segment, we intended to deploy a self-expanding stent from the right A2 segment across the AcomA into the left A1 segment in order to bridge the neck of the aneurysm and subsequently occlude the aneurysm with detachable coils.
Procedure, 23.03.2017: angiography and transarterial implantation of a self-expanding stent and coil occlusion of a wide-necked AcomA aneurysm
Anesthesia: general anesthesia; 5000 IU unfractionated heparin (Heparin-Natrium, B. Braun) IV
Premedication: because of a low responder status to clopidogrel in the Multiplate test (Roche Diagnostics), the patient received 1× 100 mg ASA (Aspirin, Bayer Vital) PO daily and 2× 90 mg ticagrelor (Brilique, AstraZeneca) PO daily
Access #1: left common femoral artery, 4F sheath (Cordis), Tempo4 4F diagnostic catheter (Cordis)
Access #2: right common femoral artery, 8F sheath (Cordis); guide catheter: 8F Guider Softip (Boston Scientific); distal access catheter: Fargo DA (Balt Extrusion); microcatheter: Headway 17 (MicroVention); microguidewire: Traxess 0.014″ (MicroVention)
Self-expanding microstent: LVIS jr. 3.5/18 mm (MicroVention)
Detachable coils: 8 Axium (3D, bare platinum, nylon) (Medtronic): Axium 3D 7/15, Axium Helix 6/20, Axium Soft Helix 4/10, Axium Soft Helix 4/8, Axium Helix 3/8, Axium Helix 3/6, Axium Nylon Helix 2/6, Axium Nylon Helix 2/3
Duration: 1st–22th DSA run: 123 min; fluoroscopy time: 54 min
Post medication: 1× 100 mg ASA PO daily for life, 2× 90 mg ticagrelor PO daily for 1 year
Follow-up performed using 3 T MRI after 3 months, 1 year, and 2 years confirmed complete and stable occlusion of the AcomA aneurysm. Blood flow to both ACAs was normal, and there was no in-stent stenosis. The incidental 2 mm aneurysm of the left MCA did not change in size or configuration and will remain under observation.
The treatment was well tolerated. The clinical condition of the patient was rated mRS 3 due to his previous ischemic stroke.
During the first attempt to deploy the stent, we had been confronted with a tapering of the stent from distal to proximal. This is a none too rare observation with self-expanding intracranial stents and may occur for various reasons such as insufficient distal migration of the stent delivery wire or tortuous vessel anatomy. Closed cell stents (e.g., Enterprise, Cerenovus) are more prone to incomplete vessel wall adaption than stents with an open cell design (Heller et al. 2013). Incomplete expansion has also been observed with braided stents such as the LVIS jr. we had used for this patient. Cho et al. (2014) reported 5 incomplete segmental expansions in 55 patients treated with LVIS.
In case of incomplete expansion or insufficient wall adaption of braided stents, several bailout strategies have been suggested (Al-Mufti et al. 2019). These include complete deployment and manipulation with a microwire and microcatheter (“wagging” and “bumping”) or careful dilatation with a balloon or additional placement of a self-expanding stent (Kühn et al. 2017). In our patient any of these measures would have caused potentially life-threatening injury to the small-caliber duplication of the AcomA.
In our case, incomplete stent opening was the result of the unintended catheterization of a duplication of the AcomA. This duplicated AcomA was very thin and was neither seen on the preceding DSA runs nor was it visible in 3D rotational DSA. In the road map projection, this small additional AcomA was overlaid by the aneurysm bearing AcomA. When we first deployed the stent, we did this under the assumption that we were bridging the aneurysm neck. That this was not the case only became clear when we switched to a slightly different projection. In addition, the manipulation within the duplicated AcomA might have facilitated the contrast agent to enter this small branch. After we recognized the individual anatomy, we maneuvered the microcatheter into the correct AcomA, and the rest of the treatment was uneventful.
This experience underlines that beyond technical considerations and material properties, familiarity with anatomical variations is of utmost importance. Recent publications considering anatomical variations of the AcomA complex are based on MR angiography, CT angiography, and DSA. Those reports primarily focus on anatomical variations that are within the spatial resolution of cross-sectional imaging methods such as arteria cerebri anterior azygos and duplications, triplications, and fenestrations of A1 segments and AcomA as anatomical variations or in association with aneurysms (de Gast et al. 2008; Krzyżewski et al. 2015; Makowicz et al. 2013; Weil et al. 2011). From neurosurgical observations and cadaver studies, it is known that anatomical variations of the AcomA complex may include very tiny vessels that are beyond visibility in cross-sectional imaging techniques (Gurdal et al. 2004; Kardile et al. 2013; Janardhan Rao et al. 2017). Vasović et al. (2014) presented a comprehensive anatomical compilation of the wide spectrum of variations in the AcomA complex in an adult autopsy series. They found anatomical variations including aplasia, hypoplasia, fenestration, duplication, and multiplications in 87 of 266 examined brains (33%). Among these, duplication of the AcomA was most frequent with an incidence of 18%. In this series of 87 brain specimens, there were only 4 aneurysms. In a selection of patients with aneurysms, the incidence of AcomA variations might even be higher.
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