Anterior Communicating Artery Aneurysm: Stent-Assisted Anterior Communicating Artery Aneurysm Coil Occlusion – A Duplicated AcomA as a Potentially Dangerous Cause of a Nonexpanding Stent

  • Stephan FelberEmail author
Living reference work entry


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.


Anterior 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.

Diagnostic Imaging

MRI showed sequelae of a previous ischemia in the supply territory of the right lenticulostriate arteries. DSA with contrast medium injection of the right internal carotid artery (ICA) revealed a saccular aneurysm originating from the AcomA, mainly filled via the right anterior cerebral artery (ACA) A1 segment. The more detailed angiography with simultaneous injections of both ICAs showed the A1 segments of the ACAs of almost equal diameter. The aneurysm had a broad neck that extended from the right A2 segment across the AcomA. The left A2 segment of the ACA was not included in the aneurysm neck (Fig. 1).
Fig. 1

Diagnostic imaging in a 55-year-old male patient after he had suffered an embolic stroke to the supply territory of the right middle cerebral artery 3 months previously. The T2-weighted MRI showed an ischemic defect in the territory of the striatal branches of the right MCA (a). DSA of the right ICA revealed a saccular aneurysm of the AcomA (fundus diameter 7 mm) (b). The aneurysm filled primarily from the right A1 segment. Magnified DSA runs in preparation for endovascular treatment from the right (c) and left (d) ICA and including runs with simultaneous injection of both ICAs (e) and 3D rotational angiography (f) showed that the aneurysm originated from a short AcomA. The right A1-AcomA-A2 junction and the proximal 2 mm of the right A2 segment were included in the aneurysm neck

Treatment Strategy

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

Course of treatment: the A2 segment of the right ACA was approached via the A1 segment of the left ACA with a Headway 17 microcatheter and a Traxcess 0.014″ microguidewire. Then a 3.5/18 mm self-expanding LVIS jr. microstent was advanced. During stent deployment, the stent opened as expected in the right ACA A2 segment, however, there appeared to be some tapering of the stent at the AcomA level. The stent was resheathed, and DSA runs in slightly different projections revealed that the microcatheter was not in the aneurysm bearing AcomA, rather in a tiny duplicated AcomA. The stent was withdrawn, and the microcatheter was brought back and then maneuvered through the aneurysm bearing AcomA. Said stent was again deployed, and the aneurysm was occluded with detachable coils as intended (Fig. 2).
Fig. 2

Stent-assisted coil occlusion of a wide-necked AcomA aneurysm. Contrast medium was injected from the right ICA, and the microcatheter was steered from the left ICA via the left A1 segment and the AcomA into the right A2 segment as shown on the road map image (a). The self-expanding intracranial stent was deployed from the right A2 segment via the AcomA (b). At the level of the AcomA and the aneurysm neck, it became obvious that the stent had not opened to the full extent of the vessel diameter (c). DSA runs after resheathing the stent into the microcatheter with a more cranial projection (d, e) revealed that the microcatheter was not in the AcomA from where the aneurysm originated but in a small-caliber duplication of the AcomA (magnified view (f)). After identifying the correct anatomy, the microcatheter was easily directed via the aneurysm bearing AcomA into the A2 segment of the right ACA (g), and then the stent was fully deployed (h, i). The aneurysm was catheterized through the LVIS jr. stent using the same microcatheter, and detachable coils were implanted until the aneurysm had been completely excluded (j, k, l, m)

Duration: 1st–22th DSA run: 123 min; fluoroscopy time: 54 min

Complications: none

Post medication: 1× 100 mg ASA PO daily for life, 2× 90 mg ticagrelor PO daily for 1 year

Follow-Up Examination

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.

Clinical Outcome

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.

Looking at the specimens of Vasović et al. (2014), it is obvious that data from imaging series reveals lower incidences because tiny duplications may be beyond the resolution of MRA and CTA and may be masked on DSA runs. Our case is similar to case 46 in this series (Fig. 3) and can be classified as a complete duplication of the AcomA. Deploying the stent in such a small-caliber duplication and then making an attempt to widen the nonexpanded part of the stent would have led to a potentially life-threatening vessel rupture. Entry into such small vessels is facilitated by the use of low-profile stents and corresponding microcatheters. Therefore, as our technology continues to become ever more sophisticated, it is increasingly important to be aware of anatomical variations.
Fig. 3

Anatomical specimen showing a duplication of the AcomA with the proximal branch being hypoplastic. (Photograph taken from Vasović et al. (2014) (published Open Access, reproduction with permission of the corresponding author))



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© Springer Nature Switzerland AG 2020

Authors and Affiliations

  1. 1.Department of Diagnostic and Interventional Radiology and NeuroradiologyGemeinschaftsklinikum MittelrheinKoblenzGermany

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