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ORIGINAL ARTICLE
Year : 2012  |  Volume : 60  |  Issue : 1  |  Page : 55-60

Endovascular treatment of complicated ruptured anterior communicating artery aneurysms based on the anatomical features of the anterior communicating artery complex


1 Department of Neurosurgery, Yiwu Central Hospital, Yiwu, Zhejiang Province, China
2 Department of Neurology, Yiwu Central Hospital, Yiwu, Zhejiang Province, China

Date of Submission15-Nov-2011
Date of Decision20-Nov-2011
Date of Acceptance01-Dec-2011
Date of Web Publication7-Mar-2012

Correspondence Address:
Chan-Hong Shi
No. 519, Nanmen Street, Yiwu, 322000, Zhejiang Province
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.93592

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 » Abstract 

Background: Endovascular therapy of complicated ruptured anterior communicating artery (ACoA) aneurysms is difficult due to their small size and unfavorable shape. Aim: Based on the anatomical features of the ACoA complex, we investigated the feasibility and efficacy of different coil embolism strategies for complicated ACoA aneurysms. Materials and Methods: Sixteen patients with complicated ruptured ACoA aneurysms received endovascular treatment. Aneurysm sac plus ACoA embolism or ACoA coil embolism were performed if the bilateral A1 segment was normally developed or unilateral A1 segment dysplasia (≥1/2 normal contralateral diameter) was present. Where unilateral A1 segment dysplasia (<1/2 normal contralateral diameter) or aplasia was present, sac embolism alone was performed. Follow-up angiography was performed, and clinical follow-up data were categorized as fully recovered, improved, unchanged or worsened. Results: Aneurysm sac plus ACoA (n=5) or ACoA alone (n=2) coil embolism was performed in seven patients with normal bilateral A1 segments (n=5) or dysplasia (n=2). Sac coil embolism was performed in nine patients with unilateral A1 segment dysplasia (n=1) or aplasia (n=8). Immediate angiography indicated total/near-total occlusion was achieved in 14 patients. Final angiographic (mean 11.9 ± 5.1 months) and clinical (mean 17.7 ± 5.9 months) follow-up confirmed total/near-total occlusion in 12 patients, one partial occlusion, two enlarged residual sacs and one reopened aneurysm. Clinical symptoms fully recovered in 10 patients, improved in four, were unchanged in one and worsened in one patient. Conclusion: This small middle-term follow-up study demonstrates coil embolism endovascular treatment of complicated ruptured ACoA aneurysms, based on the anatomical features of the ACoA complex, is feasible and effective.


Keywords: Aneurysm, anterior communicating artery, coil embolism, endovascular treatment


How to cite this article:
Li JW, Shi CH. Endovascular treatment of complicated ruptured anterior communicating artery aneurysms based on the anatomical features of the anterior communicating artery complex. Neurol India 2012;60:55-60

How to cite this URL:
Li JW, Shi CH. Endovascular treatment of complicated ruptured anterior communicating artery aneurysms based on the anatomical features of the anterior communicating artery complex. Neurol India [serial online] 2012 [cited 2019 Sep 16];60:55-60. Available from: http://www.neurologyindia.com/text.asp?2012/60/1/55/93592



 » Introduction Top


Anterior communicating artery (ACoA) aneurysms represent approximately 39% of treated aneurysms in the circle of Willis, and are often extremely small or have an unfavorable shape which makes microsurgical clipping or endovascular therapy difficult. [1],[2],[3],[4] The ACoA is an important communicating artery which links the anterior cerebral arteries and can become a functional artery, especially if unilateral dysplasia or aplasia of the A1 segment of the anterior cerebral artery (ACA) is present or when the distal internal carotid artery (ICA) is occluded. [5] In ACoA aneurysm patients with a well-developed Willis circle, ACoA does not normally participate in supplementing blood to the brain and it is often aneurismal to be part of ACoA aneurysms, which makes microsurgery or endovascular therapy difficult and thus may increase the aneurysm recurrence rate. This study was designed to assess the feasibility and efficacy of different coil embolism treatment strategies in a group of patients with complicated ACoA aneurysms, based on the anatomical features of the ACoA complex, with a mid-term angiographic and clinical follow-up.


 » Materials and Methods Top


Patients and aneurysms

From January 2007 to April 2010, 16 complicated ruptured ACoA aneurysms in 16 patients were treated by coil embolism in our department. The age ranged from 32 to 77 years (mean 55.1 ± 13.3 years) and included seven males and nine females. Complicated ACoA aneurysms were defined if it meets one of the following features: 1) aneurysms with a maximum body diameter less than 3 mm; 2) with a wide aneurysm neck (≥4 mm or dome/neck ratio <2); 3) an unfavorable aneurysm shape such as an upward/posterior aneurysm fundus or multiple bubbles projecting from the aneurysm body. All 16 aneurysms were complicated degenerative saccular aneurysms. Detailed information of the patients and the aneurysm characteristics are provided in [Table 1]. The ACoA complex and the A1 and A2 segments of the bilateral anterior cerebral arteries were classified as one of three types: 1) normal bilateral A1 segment development; 2) unilateral A1 segment dysplasia or 3) unilateral A1 segment aplasia.
Table 1: Summary of 22 complicated ruptured ACoA aneurysms treated by endovascular treatment

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Procedures

Cerebral vascular angiography was performed under local anesthesia via a right femoral approach. A 6F sheath was placed into the right femoral artery and selective catheterization was performed using a 5F vertebral catheter (Terumo, Tokyo, Japan). Information regarding the aneurysm morphology and the relationship with the ACoA was obtained from 2D and 3D rotational/reconstruction angiograms prior to endovascular treatment. Patients received general anesthesia, selective catheterization of the ICA was performed using a 6F guiding catheter (Envoy; Cordis, Miami Lakes, FL, USA) and superselective catheterization of the aneurysm was carried out using a 260-cm-long 0.014-inch-diameter micro-guidewire (Platinum; Boston Scientific, Natick, MA, USA) and a microcatheter (Encholen 10; eV3, Irvine, CA, USA or SL 10; Boston Scientific, Natick, Mass). Endovascular coil embolism strategies were selected on the basis of the following criteria: (1) if the bilateral A1 segment was normally developed then the AcoA and/or aneurysm sac could be safely embolized; (2) if dysplasia was present in the unilateral A1 segment, an ipsilateral ICA angiogram with contralateral ICA compression under a conscious state was performed and ACoA embolism was only considered if the dysplasia in the A1 segment diameter reached up to 1/2 of the contralateral corresponding site, otherwise sac coil embolism alone was performed; (3) if the unilateral A1 segment had aplasia, aneurysm sac coil embolism alone was performed to maintain ACoA patency. The detached platinum coils used for embolization included Guglielmi detachable coils (Boston Scientific), MicroPlexTM coils (Microventions Co, Aliso Viejo, CA, USA) and Trufill Orbit detachable coils (Cordis, Johnson and Johnson Medical Miami Lakes, FL, USA). Stent (Neuroform, Boston Scientific) or balloon (Hyperform; eV3) assistance techniques were used to preserve either the ACoA or A1/A2 segments of the anterior cerebral artery.

After guidance catheter targeting, a bolus of 4000-5000 U heparin was intravenously injected, and an additional 1000 U were administered every hour during the procedure. Nimodipine (10 mg in 250 ml saline) was intravenously transfused during the procedure to prevent intracranial vasospasm. Non-enhanced brain computed tomography (CT) scans were performed to detect intracranial hemorrhage or ischemic events, and detailed neurologic examinations were conducted pre- and post-procedure. If a stent was used, patients received double-antiplatelet therapy (75 mg/d clopidogrel and 100 mg/d aspirin orally) for at least three days before the procedure, and 5000 U low-molecular-weight heparin was subcutaneously injected every 12 h for three days postoperatively, followed by an anti-platelet therapy plan for at least six months.

Evaluation

Aneurysm coil embolism was classified as total/near-total (95-100% occlusion), subtotal (80-95% occlusion) or partial occlusion (less than 80% occlusion) by immediate angiography after the procedure. During angiographic follow-up, the recurrence of aneurysms after coiling was assessed and categorized as a reopened aneurysm or an enlarged residual sac. Clinical outcomes were assessed in the outpatient clinics or by telephone interview. Follow-up data were collected, retrospectively analyzed and graded as full recovery, improvement, unchanged or worsened compared to the neurological symptoms which existed before treatment. Procedure-related morbidity was defined as a neurological deficit occurring within 24 h of the technique, which could be attributed to the procedure. Neurological deficits, including cerebral hemorrhage or infarction, were considered procedure-related if they were due to aneurysm rupture, coil herniation, vessel perforation, acute thrombosis or vasospasm. In the case of death, the neuroradiologists determined whether death was related to the procedure or not.


 » Results Top


Patients

Of the 16 patients treated in this study, five patients had normal bilateral A1 segment development of the ACoA complex, three patients had unilateral A1 segment dysplasia and eight patients had unilateral A1 segment aplasia. In our study, only five of 16 (31.2%) patients have normal developed bilateral A1 segments of the ACA. In the five patients with normal bilateral A1 segment development, aneurysm sac plus ACoA coil embolism was performed in three patients [Figure 1] and the other two patients were treated with only ACoA coil embolism. In the three patients with unilateral A1 segment dysplasia, two patients underwent sac plus ACoA coil embolism (≥1/2 diameter of normal contralateral A1 segment) [Figure 2] and the other received sac embolism alone (<1/2 diameter of normal contralateral A1 segment) [Figure 3]. Sac coil embolism alone was performed in the eight patients with unilateral A1 segment aplasia.
Figure 1: Anteroposterior (a) and working position (b) control angiography showing a tiny ACoA aneurysm (narrow arrow) in a patient with a normal contralateral A1 indicated by a wide arrow (c). Using the balloon remodeling technique, the aneurysm and ACoA were both embolized with coils (d) and angiography of the contralateral ICA was performed to detect filling of the aneurysm sac during the procedure (e). A neuroform stent was used to prevent coil herniation into the A1-A2 segments of the right ACA (f). Anteroposterior (g) and working position (h) control angiography after the procedure revealed total occlusion of the aneurysm

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Figure 2: Anteroposterior (a) and working position (b) control angiography showing a tiny ACoA aneurysm (narrow arrow) in a patient with contralateral A1 dysplasia (wide arrow) which provided sufficient blood flow during the contralateral ICA compression test (c). The aneurysm and ACoA were both embolized with coils (d) and anteroposterior (e) and working position (f) control angiography after the procedure revealed total occlusion of the aneurysm

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Figure 3: Anteroposterior (a) and working position (b) control angiography showing a lobulated aneurysm (narrow arrow) based directly on the ACoA, in a patient with contralateral A1 dysplasia, indicated by a wide arrow (c). The lobulated aneurysm was embolized with coils (d), and anteroposterior (e) and working position (f) control angiography after the procedure revealed total occlusion of the aneurysm and good patency of the ACoA

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Immediate angiographic results

All the study patients were successfully treated with coil embolization. The balloon remodeling technique was used in four patients, a stent assistance technique was used in three patients and a balloon plus stent assistance technique was used in one patient. Immediate angiography revealed that total or near-total occlusion was achieved in 14 of the 16 patients, including all of the seven patients who received either aneurysm sac embolism or sac plus ACoA embolism. The two patients who received sac embolism alone achieved only partial occlusion.

Angiographic and clinical follow-up

At the end of the angiographic follow-up (mean 11.9 ± 5.1, range 3 to 21 months), control angiography confirmed total or near-total occlusion of the aneurysms in 12 patients, partial occlusion in one patient, an enlarged residual sac in two patients and a reopened aneurysm in one patient. All the patients with recurring aneurysms, including the enlarged residual sacs in two patients and the patient with a reopened aneurysm had received sac embolism alone. At the end of the clinical follow-up (mean 17.7 ± 5.9, range 9 to 32 months), the symptoms had fully recovered in 10 patients, improved in four patients, were unchanged in one patient and had worsened in one patient.

Complications

No aneurysm rupture or coil migration occurred during any procedure. Acute thrombosis occurred in one patient when stent assistance technology was used, which led to ipsilateral anterior cerebral artery occlusion and left permanent neurological deficiency.


 » Discussion Top


The deep location, complex arterial relationships and unfavorable morphology of complicated ACoA aneurysms often render microsurgical clipping difficult. [6],[7] Endovascular treatment has been reported to be an effective and feasible treatment for complicated ACoA aneurysms, particularly with extremely tiny (<3 mm) aneurysms, where the fundus projects upwards/posteriorly or when there are multiple aneurysm bubbles. [2],[8],[9] However, endovascular treatment of ACoA aneurysms is still a high-risk procedure due to the frequent association of these anomalies with the ACoA complex. Previous classification systems for the ACoA complex included four types based on the number and course of the ACoA: I single ramus type; II, two rami type; III, three rami type and IV, specific type. [5] However, this classification does not consider A1 segment variations; therefore, is of less clinical relevance in endovascular treatment. In this study, we classified the ACoA complex into three types which have more applicability for the endovascular treatment of complicated ACoA aneurysms. Based on these classifications, we treated a small group of patients with complicated ACoA aneurysms using either aneurysm sac embolism and/or ACoA embolism and evaluated the feasibility of the procedures with a mid-term angiographic and clinical follow-up.

During endovascular treatment of complicated ACoA aneurysms, fundus which project upwards or posteriorly or are wide-necked are likely to cause catheterization failure, coil escape or herniation. In this situation, the ACoA complex can supply enough blood flow to the feeding area if the A1 segment is normally developed or displays unilateral dysplasia, and we believe that coil embolism of both the aneurysm sac and ACoA is the best option, and may effectively reduce the aneurysm recurrence rate. Tiny ACoA aneurysms (<3 mm) have a high risk of microcatheter catheterization or coiling; therefore, simple ACoA embolism avoids manipulation of the aneurysm sac and effectively reduces the risk of aneurysm rupture and the manipulation time. However, bilateral ICA angiography should be performed to confirm the patency of both distal anterior cerebral arteries and confirm that the aneurysm sac was not visualized from the contralateral anterior cerebral artery. [10] In our study, five cases received sac with ACoA coil embolism, including three patients with a normal A1 development and two with unilateral A1 dysplasia. The follow-up angiograms demonstrated complete occlusion in all these five patients. ACoA embolism alone was performed in two patients with normal A1 development who had tiny aneurysm sacs, and the subsequent follow-up angiograms confirmed complete occlusion in these patients. For patients with unilateral A1 dysplasia or aplasia which cannot provide sufficient blood flow to the feeding area, the patency of the ACoA must be maintained as a functional artery. This increases the difficulty of manipulation and may reduce the coil embolism and neck occlusion rate, thus the safety and effectiveness of sac embolism may be poorer than sac with ACoA embolism or ACoA embolism alone. In this study, eight cases with unilateral A1 dysplasia or aplasia received traditional sac embolism. The immediate angiograms revealed partial occlusion in two patients, and follow-up angiograms confirmed an enlarged residual sac in two patients and a reopened aneurysm in one patient. These complications occurred at a much lower rate in patients receiving sac with ACoA embolism or ACoA embolism alone.

An in-stent thrombosis complication occurred in one patient during this study, however, as the aneurysm sac was only partially embolized and the patient was at an acute subarachnoid hemorrhage stage, no further thrombosis treatment was performed during the procedure. This patient received only anticoagulation therapy and antiplatelet aggregation treatment after the procedure, and when discharged, only mild speech function impairment remained.

This small-cohort clinical study indicates that endovascular treatment of complicated ruptured ACoA aneurysms using coil embolism, based on the anatomic features of the ACoA complex, is feasible and effective. Sac and ACoA embolism or ACoA embolism alone in patients with normal bilateral A1 segment development may be safer and more effective than traditional aneurysm sac embolism, and further comparative studies of larger patient populations are required to fully determine the safety and efficacy of this technique.

 
 » References Top

1.Gonzalez N, Sedrak M, Martin N, Vinuela F. Impact of anatomic features in the endovascular embolization of 181 anterior communicating artery aneurysms. Stroke 2008;39:2776-82.  Back to cited text no. 1
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2.Tsutsumi M, Aikawa H, Onizuka M, Kodama T, Nii K, Matsubara S, et al. Endovascular treatment of tiny ruptured anterior communicating artery aneurysms. Neuroradiology 2008;50:509-15.  Back to cited text no. 2
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3.Kassell NF, Torner JC, Haley EC Jr, Jane JA, Adams HP, Kongable GL. The International Cooperative Study on the Timing of Aneurysm Surgery. Part 1: Overall management results. J Neurosurg 1990;73:18-36.  Back to cited text no. 3
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4.Yasargil MG. Microneurosurgery. Vol. 2. New York: Thieme; 1984. p. 169-84.  Back to cited text no. 4
    
5.Zhao B, Zhong M, Yang H, Liu J, Tan XX, Zheng K, et al. The developmental variations of the anterior communicating artery complex and its clinical significance of the aneurysms. Chin J Neurosurg 2009;25:982-5.  Back to cited text no. 5
    
6.Hernesniemi J, Dashti R, Lehecka M, Niemelä M, Rinne J, Lehto H, et al. Microneurosurgical management of anterior communicating artery aneurysms. Surg Neurol 2008;70:8-29.  Back to cited text no. 6
    
7.Hino A, Fujimoto M, Iwamoto Y, Oka H, Echigo T. Surgery of Proximal Anterior Cerebral Artery Aneurysms. Acta Neurochir (Wien) 2002;144:1291-6.  Back to cited text no. 7
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8.Huang Q, Xu Y, Hong B, Zhao R, Zhao W, Liu J. Stent-Assisted Embolization of Wide-Neck Anterior Communicating Artery Aneurysms: Review of 21 Consecutive Cases. AJNR Am J Neuroradiol 2009;30:1502-6.  Back to cited text no. 8
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9.Birknes JK, Hwang SK, Pandey AS, Cockroft K, Dyer AM, Benitez RP, et al. Feasibility and limitations of endovascular coil embolization of anterior communicating artery aneurysms: Morphological considerations. Neurosurgery 2006;59:43-52.  Back to cited text no. 9
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10.Kwon SC, Park JB, Shin SH, Sim HB, Lyo IU, Kim Y. The efficacy of simultaneous bilateral internal carotid angiography during coil embolization for anterior communicating artery aneurysms. J Korean Neurosurg Soc 2011;49:257-61.  Back to cited text no. 10
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    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1]

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