Anterior Cerebral Artery Aneurysm: Incidental, Giant, Partly Thrombosed Proximal Anterior Cerebral Artery Aneurysm with Stenosis of the A1 Segment, Treated with a p48 Flow Diverter with Angiographic Exclusion of the Aneurysm and Good Clinical Outcome

  • Rene Viso
  • Nicolas Perez
  • Ivan Lylyk
  • Jorge Chudyk
  • Pedro LylykEmail author
Living reference work entry


A 78-year-old male patient was referred for diagnostic work-up 31 months after an ischemic stroke affecting the left parietal lobe. An incidental giant, partly thrombosed aneurysm located on the left A1 segment of the anterior cerebral artery (ACA) causing compression of the third ventricle and a noncommunicating hydrocephalus was diagnosed. A stenosis of the left A1 segment proximal to the aneurysm neck was considered to be either an atherosclerotic lesion or due to a previous dissection. An external ventricular drain was placed prior to endovascular parent vessel reconstruction using a p48 (phenox) flow diverter (FD). MRI/MRA and DSA follow-up showed the complete occlusion of the aneurysm and a remodeling of the parent artery. The clinical condition of the patient was the same as before the intervention, and no new neurological deficit had occurred. The treatment of A1 aneurysms with FD stents is the main topic of this chapter.


Anterior cerebral artery aneurysm Giant aneurysm Flow diversion Hydrocephalus Dissecting aneurysm 


A 78-year-old male patient with a 55-pack year history of cigarette smoking and high arterial blood pressure. In September 2014, he suffered an ischemic stroke of his left parietal lobe, which had been left untreated. In 2017, he was referred to our institution. During the clinical examination, we found right lower limb paresis with no other neurological deficit.

Diagnostic Imaging

Noncontrast CT (NCCT), MRI/MRA showed a partially thrombosed giant left-hand ACA/A1 aneurysm, which was compressing the third ventricle and causing a noncommunicating hydrocephalus. A DSA examination was carried out confirming the presence of a giant left-hand ACA/A1 dissecting aneurysm. Both A2 segments of the ACAs were supplied through the left-hand A1 segment (Fig. 1).
Fig. 1

Diagnostic work-up of an incidental giant aneurysm originating from the left A1 segment. NCCT (a) shows the aneurysm with a calcified wall, bulging into the frontal horn of the right lateral ventricle. Axial T2WI (b) and T1WI (c) MRI as well as the sagittal T2WI MRI (d) show a giant ACA/A1 aneurysm oriented in an anterior and upward direction, thus causing a compression of the anterior horn of the right lateral and of the third ventricle. Partial thrombosis of the aneurysm sac is visible with heterogeneous signal intensity of said nonorganized thrombus. The thrombus is mainly hypointense on T2WI. On T1WI, it appears hyper- and isointense. On TOF MRA, this thrombus appears as a hyperintense ring inside the aneurysm sac (e, f). DSA with injection of the right ICA (g) shows that the right A1 segment is missing. DSA with injection of the left ICA (h, i, j) confirms that the left hand A1 segment gives origin to a giant, either dissecting or atherosclerotic aneurysm. There is a circular narrowing of the left A1 segment just proximal to the aneurysm neck (i, j). MIP VasoCT (k) shows the perfused part of the aneurysm. The space between this part of the aneurysm and the calcified aneurysm wall is filled with intra-aneurysmal thrombus. Rotational DSA with 3D reconstruction (j). The dimensions of the perfused part of the aneurysm are: fundus height 19.7 mm, fundus width 15 mm, neck width 5 mm

Treatment Strategy

The previous ischemic stroke was possibly related to the stenosis of the left A1 segment. Prior to the endovascular treatment, an external ventricular drain was placed in the posterior horn of the right lateral ventricle in order to prevent a potential increase of the hydrocephalus after the treatment of the aneurysm (Fig. 2). This was done at the beginning of the treatment due to an anticipated need for dual antiplatelet medication following the endovascular procedure and in order to avoid the risk of bleeding during EVD implantation. The goals of the treatment were to reduce the space occupying effect of the aneurysm, prevent its rupture, and reconstruct the diseased left A1 segment, which was stenotic and from which both A2 segments were supplied. It was planned to use a flow diverter to reconstruct the parent vessel and reduce flow into the aneurysm in order to induce a progressive thrombosis of the aneurysm sac. The majority of FD devices available require a 0.027″ inner diameter (ID) microcatheter. Due to the sharp angle between the left ICA and the left A1 segment, navigating a 0.027″ microcatheter was considered to be difficult at best. Therefore, a p48 (phenox) low-profile FD taking a 0.021″ ID microcatheter was chosen.
Fig. 2

NCCT (a) and T2WI MRI (b) after the placement of an external ventricular drain in the posterior horn of the right lateral ventricle in preparation for the endovascular FD treatment


Procedure, 16.05.2017: treatment of a giant aneurysm originating from the left A1 segment by endovascular reconstruction of the parent artery with a p48 FD

Anesthesia: general anesthesia, 10,000 IU unfractionated heparin (Riveparin, Ribero) IV

Premedication: 1× 100 mg ASA (Aspirin, Bayer Vital) PO daily and 1× 10 mg of prasugrel (Procardia, Rommers) PO daily, both started 5 days before the intervention

Access: right femoral artery, 8F sheath (Terumo); guide catheter: Shuttle 8F guide catheter (Cook); intermediate catheter: Navien A+ 072 (Medtronic); microcatheter: Trevo pro 18 MC (Stryker); microguidewire: Transend 0.014″ (Stryker)

Implant: p48 3/12 mm (phenox)

Course of treatment: The left ICA was catheterized with an 8F Shuttle guide catheter and a Navien A+ 072. The intermediate catheter was placed in the petrous segment of the left ICA. A Trevo pro 18 microcatheter was navigated with a Transend 0.014″ microguidewire to the left A2 segment and a 3/12 mm p48 FD device was implanted without difficulty. The subsequent DSA run showed a significant intra-aneurysmal flow reduction with contrast medium stagnation. The opacification of both A2 segments and their dependent cortical vessels was within normal limits. The EVD was removed on the next day (Fig. 3)
Fig. 3

A giant aneurysm of the left A1 segment, treated with a p48 FD. Deployment of the p48 flow diverter (a). A subsequent DSA run showing a significantly reduced intra-aneurysmal flow immediately after the implantation of the device with contrast medium stagnation (b, c, d). The MIP of a VasoCT confirms the correct wall apposition of the p48 FD (e, f). The fact that the stenosis of the left A1 segment disappeared right after the FD deployment without balloon angioplasty suggests an underlying dissection. Atherosclerotic plaque would rather have prevented the p48 from completely expanding


Duration: 1st–7th DSA run: 40 min; fluoroscopy time: 23 min

Complications: none

Postmedication: 1× 100 mg ASA PO daily for life and 1× 10 mg prasugrel PO daily for 6 months.

Clinical Outcome

The procedure was well tolerated and the patient was discharged home without further neurological deficit 2 days later.

Follow-Up Examinations

MRI/MRA and DSA were performed 2, 4 and 6 months after the procedure showing progressive organization of the intra-aneurysmal thrombus with improvement of the hydrocephalus, and no new neurological deficit at the clinical examination (Fig. 4).
Fig. 4

MRI/MRA after 2, 4, and 6 months and 6 months DSA follow-up in a patient with a giant symptomatic left ACA/A1 dissecting aneurysm after a p48 device had been implanted. Axial FLAIR (a, d, g), T2WI TSE (b, e, h), and MRA images (c, f, i). The size of the thrombosed aneurysm is slightly diminished with improvement in the hydrocephalus and a significant modification of the intra aneurysmal thrombus signal intensity. There is no edema around the aneurysm and the midline shift has partially resolved. The 6-month follow-up DSA shows complete occlusion of the aneurysm with patency of the p48. There is no in-stent stenosis (j, k). Remodeling of the parent artery with improvement of the left A1 segment stenosis (l)


The incidence of intracranial aneurysm arising from the A1 segment of the ACA is low, at about 1–2% (Tekkök and Açikgöz 2001) with an increasing number of reports in recent years, possibly due to the advance in technology of non-invasive diagnostic imaging (Ding et al. 2017). Usually, these aneurysms are small, between 3.5 and 7 mm in 67% of cases (Wakabayashi et al. 1985). The presence of a giant aneurysm (greater than 25 mm) in the A1 segment is very unusual with only a few cases having been reported in the literature (Tekkök and Açikgöz 2001). A1 aneurysms are frequently associated with multiple brain aneurysms in 25–70% of cases (Park et al. 2013). The most frequent clinical presentation of large and giant A1 aneurysms is decreased vision due to the compression of the optic pathway or dementia due to the compression of the basal forebrain or hydrocephalus (Castro et al. 2013). Some authors mention that for an aneurysm to induce dementia it needs to measure at least 3.5 cm (Lownie et al. 2000). In cases of hydrocephalus after an aneurysm rupture, treatment using an EVD is controversial (Hellingman et al. 2007), as some authors report a risk of aneurysm rupture after the EVD has been placed due to decompression and intracranial pressure changes (Gigante et al. 2010). In a recent meta-analysis, a conclusive association between aneurysm rupture and the EVD placement was found, however, the authors also report other factors in the clinical condition of the patients that may be associated with rehemorrhage, such as being high on the Fisher scale or being in poor neurological condition (Cagnazzo et al. 2017).

Relevant for the treatment of A1 aneurysms is a classification based on the location of the aneurysm origin at the A1 artery, which differentiates proximal, middle, and distal locations (Yasargil 1984). Of importance are the perforating vessels at the proximal A1 segment, supplying the optic chiasm, hypothalamus, basal ganglia, and superior thalamus (Bhaisora et al. 2014). It is crucial to study both A1 segments prior to the endovascular treatment, especially the hemodynamics at the A1–A2 transition and of the AcomA, if endovascular jailing or parent vessel occlusion (PVO) is being contemplated (Lv et al. 2009). Attention should be paid to vascular anomalies and variants of the AcomA complex commonly associated with A1 aneurysms (e.g., hypoplasia or aplasia of the contralateral A1 segment, AcomA fenestration, duplication, or azygos ACA) (Park et al. 2013). In the patient presented in this chapter, the right A1 was absent and therefore deconstructive treatment with PVO of the left A1 segment was not an option.

Endovascular treatment using coils is challenging in these types of case due to the difficulty in accessing the aneurysm dome. The complex vessel anatomy and aneurysm orientation would require complex microcatheter curves to maintain stability (Alurkar et al. 2012). In a report of 48 patients with a combined total 50 aneurysms of the ACA, (7 ruptured and 43 nonruptured), complete occlusion of the aneurysm was achieved in only 11 of these aneurysms, while 27 still had a neck remnant, and 12 a residual perfusion of the aneurysmal sac. Only three aneurysms were treated using a stent-assisted coil occlusion technique. The notorious recanalization of the proximal aneurysms of the A1 segment was observed at a rate of about 28%, compared to middle and distal A1 aneurysms that showed recanalization in 0% and in 10%, respectively (Cho et al. 2014). In nonruptured aneurysms and in order to avoid the risk of recanalization at the proximal segment of the A1 and the risk of aneurysm perforation due to intrasaccular catheterization, especially in small aneurysms, different options are available. A deconstructive technique (i.e., PVO) is a straightforward procedure if the AcomA and the contralateral A1 segment are suitable. Endovascular reconstruction of an A1 segment using an FD has become an endovascular option to redirect the arterial flow away from the aneurysm towards the parent artery, inducing a progressive thrombosis of the aneurysm with reconstruction of the parent vessel by endothelial growth over the struts of the device (Ionita et al. 2011). Endovascular FD reconstruction of the ACA in general has been described as both a feasible and safe technique. In a series of eight patients with aneurysms of the ACA (with three of them located on the A1 segment), after FD 71% of the patients had total aneurysm occlusion with an angiographic neck remnant being found in 29% of the patients. There was no technical failure or complications in these eight cases (Clarençon et al. 2017). In a report of 20 patients with a total of 20 aneurysms of the ACA treated by FD, a complete or almost complete occlusion was achieved in 12/16 patients with follow-up DSA with two complications reported: a caudate infarct 48 h after the procedure with full recovery of the patient and a delayed intraparenchymal hematoma with final mRS 6 (Dabus et al. 2017). In a retrospective series of 26 patients with 27 ACA aneurysms (including 9 A1 aneurysms) treated with FD, 16 out of 20 DSA controls showed complete aneurysm occlusion, 1 patient with just a small neck remnant. There had also been one procedure-related death (Bhogal et al. 2017). In general, flow diversion might become a viable treatment option for most A1 aneurysms, irrespective of the aneurysm’s location and orientation.



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© Springer Nature Switzerland AG 2019

Authors and Affiliations

  • Rene Viso
    • 1
  • Nicolas Perez
    • 1
  • Ivan Lylyk
    • 1
  • Jorge Chudyk
    • 1
  • Pedro Lylyk
    • 1
    Email author
  1. 1.Clinica La Sagrada Familia, ENERIBuenos AiresArgentina

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