The management of intracranial aneurysms has evolved significantly over the past 2 decades. Anterior communicating artery aneurysms (AComAAs) represent a common and often challenging problem for physicians and patients. Experience and technological advances have broadened the indications for endovascular treatment of all aneurysms. Balloon-mounted catheters and intracranial stents are 2 technological advancements that have made the treatment of previously uncoilable aneurysms feasible. As with all intracranial aneurysms, complete angiographic occlusion remains the goal of care. Balancing the risks of thromboembolic complications with decreasing the risk of hemorrhage, especially in acutely ruptured aneurysms, represents an objective for vascular neurosurgeons.
Key points
- •
The anterior communicating artery (AComA) is a common location for ruptured and unruptured aneurysms and represents a vascular location with wide anatomic variability.
- •
Current data from both prospective and retrospective analyses have demonstrated endovascular treatment of ruptured and unruptured aneurysms as a safe and durable treatment compared with the previous standard of care, aneurysm clipping.
- •
Although not all AComAAs are suitable for endovascular treatment, technological advances, including balloon-assisted coil embolization (BACE) and stent-assisted coil embolization (SACE), have broadened indications.
- •
Experience and advancements in endovascular care of intracranial aneurysms have increased the ability for physicians to treat patients, but reduction of perioperative complications, including thromboembolic stroke and intraprocedural hemorrhage, remain an area for improvement.
Introduction
AComAAs represent a common location of intracranial aneurysms in the ruptured and unruptured patient population ( Fig. 1 ). Many large series find that AComAAs represent the most common location, up to 40%, of ruptured intracranial aneurysms in adults. Similar representation of AComAAs is found in trials of unruptured aneurysms. The anatomy of the AComA complex can be variable, with many permutations requiring physicians to tailor the treatment, surgically or endovascularly, depending on the anatomy.
With the results of the International Subarachnoid Aneurysm Trial (ISAT) published in 2002, the treatment of intracranial aneurysms has preferentially shifted toward endovascular treatment at most institutions. Although there remains a large role for open surgical clipping, the endovascular trend has further been facilitated by physician experience and novel technical developments, which have broadened indications of endovascular treatment. Given the increasing options in endovascular treatments, coupled with open vascular clipping, patient care can often be individualized to minimize risk to the patient.
This article discusses the anatomic variability associated with the AComA complex and anterior cerebral arteries (ACAs) and the presentation of AComAAs. Furthermore, the evidence for endovascular treatment of AComAAs is reviewed. Finally, how technological advancements that have broadened the scope of treatment is discussed and possible future advancements described.
Introduction
AComAAs represent a common location of intracranial aneurysms in the ruptured and unruptured patient population ( Fig. 1 ). Many large series find that AComAAs represent the most common location, up to 40%, of ruptured intracranial aneurysms in adults. Similar representation of AComAAs is found in trials of unruptured aneurysms. The anatomy of the AComA complex can be variable, with many permutations requiring physicians to tailor the treatment, surgically or endovascularly, depending on the anatomy.
With the results of the International Subarachnoid Aneurysm Trial (ISAT) published in 2002, the treatment of intracranial aneurysms has preferentially shifted toward endovascular treatment at most institutions. Although there remains a large role for open surgical clipping, the endovascular trend has further been facilitated by physician experience and novel technical developments, which have broadened indications of endovascular treatment. Given the increasing options in endovascular treatments, coupled with open vascular clipping, patient care can often be individualized to minimize risk to the patient.
This article discusses the anatomic variability associated with the AComA complex and anterior cerebral arteries (ACAs) and the presentation of AComAAs. Furthermore, the evidence for endovascular treatment of AComAAs is reviewed. Finally, how technological advancements that have broadened the scope of treatment is discussed and possible future advancements described.
Anatomy of the anterior cerebral and anterior communicating arteries
The normal ACA is often divided into 5 anatomic segments starting at carotid bifurcation. The A1 segment, or precommunicating segment, extends from the bifurcation of the internal carotid artery (ICA) to join the AComA. The precommunicating segment joins the AComA in a majority of cases (70%). The average length of the A1 segment is approximately 13 mm. Tortuosity in the precommunicating segment can make navigation of the microcatheter difficult en route to aneurysm treatment. The A2 (infracallosal) segment extends from the A1-AComA junction to the genu of the corpus callosum. The A3 (precallosal) segment extends around the callosal genu. The A4 (supracallosal) and A5 (postcallosal) segments course above the corpus callosum. There are several variations to the distal ACAs, including the unpaired azygous artery, bihemispheric ACA, and triplicated vessels ( Fig. 2 ).
Larger branches of the distal ACA include the orbitofrontal, frontopolar, and other cortical branches. In general these branches have little significance in planning for endovascular treatment of an AComAA. The pericallosal artery is the terminal branch of the ACA, extending from the A2 to A5. Its largest branch is the callosomarginal artery, which often arises near the genu of the corpus callosum and courses in the cingulate sulcus. The pericallosal or callosomarginal arteries can be catheterized distally to assist in tracking a guide catheter to the petrosal segment of the ICA for more proximal support.
Critical arteries, especially susceptible to injury during endovascular or surgical treatment of AComAAs, are the perforating arteries of the ACA. On average, there are 8 basal perforating arteries, or medial lenticulostriate arteries, that arise from the A1, A2, and AComA. They supply the anterior hypothalamus, optic chiasm, lamina terminalis, medial portion of the anterior commissure, pillars of the fornix, anterior perforated substance, and anterior third ventricle. One large perforating artery, and most consistent, is the recurrent artery of Heubner. Arising from the proximal A2 in a majority of cases, it doubles back over the parent ACA above the carotid bifurcation and into the medial sylvian fissure where it enters the anterior perforated substance. The recurrent artery supplies the anterior caudate, adjacent internal capsule, anterior putamen and globus pallidus, and the uncinate fasciculus. Although a malpositioned clip during open aneurysm surgery can injure or occlude the recurrent artery causing significant neurologic deficits, a similar catastrophe can occur from microcatheter or microwire injury during endovascular treatment.
In normal anatomy, the bilateral A1 segments are connected by the AComA with equal contribution. Although it can be difficult to identify angiographically by standard views, the average AComA diameter averages approximately 1 mm and usually measures between 2 and 3 mm long. There is significant variability in the ACA-AComA complex with greater than one-half of specimens having an imbalance of A1 contribution in one cadaveric study. A true hypoplastic A1, or A1 segment measuring less than 1.5 mm in diameter, however, is present in only 10% of cases. The larger the degree asymmetry between A1 segments, the higher the diameter and vascular compensation necessitated of the AComA ( Fig. 3 ). This asymmetry can lead to alterations in hemodynamics and delayed aneurysm formation, because AComAAs have a high rate (up to 85%) of A1 hypoplasia. This pathophysiology has also been suggested in the de novo development of AComA in the setting of carotid occlusion ( Fig. 4 ).
Other common variations of the AComA include fenestrations, complete duplications, or triplications. In general, anatomic studies identify more of such anatomic variations (up to 40%) than are found on diagnostic cerebral arteriography (DCA). Three-dimensional rotational angiography (3DRA) can increase angiographers’ ability to visualize fenestrations. Although some investigations have found an increased incidence of AComAAs associated with fenestrations, these findings have not been consistent. Such anatomic variations have little impact during surgical or endovascular treatment. They do, however, underline the necessity to have an adequate working view during endovascular treatment.
Clinical presentation, diagnosis, and decision to treat
As with all intracranial aneurysms, ruptured AComAAs can have variable features at presentations, with some patients only complaining of mild headache and other unfortunate patients presenting with severe neurologic injury or death ( Fig. 5 ). Many unruptured AComAAs present as an incidental finding from unrelated symptoms. Unlike posterior communicating artery or posterior circulation aneurysms, AComAAs are not typically associated with symptomatology from local mass effect. There are, however, a few exceptions in the literature. In a large series of giant AComAAs, lesions greater than 3.5 cm were associated with dementia from local mass effect. Visual symptoms or loss from mass effect on the optic apparatus is a well-described phenomenon of large, inferiorly projecting aneurysms. More peculiar symptoms of Korsakoff psychosis and pulsatile tinnitus have been reported.
The detection of intracranial aneurysms with the use of noninvasive imaging has improved significantly over the past 2 decades. CT angiography (CTA) has been described as having a sensitivity of 99% for aneurysms 3 mm or larger and having a high sensitivity (97%) and specificity (100%) for AComAAs. Magnetic resonance angiography (MRA) has similarly been shown to have a high sensitivity and specificity in detecting intracranial aneurysms. Although not statistically significant ( P = .054), one study found a strong trend toward improved diagnosis with higher-resolution (3T) MRA.
Noninvasive angiographic imaging has improved in detecting intracranial aneurysms, but DCA remains the gold standard. There is some evidence that suggests advanced 3-D CTA reconstructions can be useful in determining an endovascular or surgical treatment of intracranial aneurysms, and some institutions have prescribed to this method of triage. Many institutions, including the authors’, however, continue to use DCA with 3DRA as the standard in decision making.
The poor natural history after a ruptured intracranial aneurysm necessitates treatment of the overwhelming majority of patients. With a rehemorrhage rate of 50% at 6 months, the decision is often not whether to treat but how to treat. Medical and surgical advancements have improved mortality after aneurysmal subarachnoid hemorrhage (SAH). In their 1968 article, Hunt and Hess found an overall mortality of 35% after admission to the hospital. In contrast, modern studies consistently demonstrated disability and mortality rates with significant improvement, such as the ISAT, which found a 5-year mortality rate of 11.9% regardless of treatment.
In the subset of anterior circulation aneurysms, patients with AComAAs often fair better overall compared with their posterior circulation counterparts. In ISAT and the recent Barrow Ruptured Aneurysm Trial (BRAT), endovascular management of ruptured aneurysms was found to benefit patients in reducing risk of severe morbidity and mortality, although 5-year evidence from ISAT and 3-year evidence from the BRAT showed no benefit in outcomes in patients with aneurysms of the anterior circulation treated by either modality. In the setting of rupture, early intervention to secure the aneurysm allows for critical care and neurosurgical physicians to prevent rehemorrhage, aggressive treatment of vasospasm, and prevention of delayed cerebral ischemia.
In cases of incidental or unruptured aneurysms, the decision for treatment is often based on many factors. The International Study of Unruptured Intracranial Aneurysms (ISUIA) was the first large-scale, prospective study looking at the natural history of unruptured aneurysms as well as the risks of treatment. Although prior studies found rupture risks as high as 32%, ISUIA along with the Unruptured Cerebral Aneurysm Study from Japan found lower risks of rupture for most aneurysms. Factors found to increase the risk of rupture were size (greater than 7 mm), unusual shape or protrusion coming from aneurysm dome, posterior circulation location, previous personal history of SAH, and SAH in a first-degree relative. Another arm of ISUIA compared risks of treatment with risks of the natural history, finding the morbidity and mortality for surgical and endovascular treatment greatly exceeding the 7.5-year risk of rupture in patients without a prior history of SAH in aneurysms smaller than 10 mm. The impact of ISUIA has led some centers to recommend treatment of aneurysms of the anterior circulation, including AComAAs, larger than 7 mm and to conservatively manage smaller lesions. A recent study of 932 patients, however, found AComA and distal ACA aneurysms greater than 4 mm to have risks of rupture similar to posterior circulation these aneurysms should be considered for treatment.
Endovascular treatment of anterior communicating artery aneurysms
History
Although initially performed through a craniotomy, reports of aneurysm embolization were described as early as 1962. With poor results of this method of embolization, coupled with advancements in microsurgical clip reconstruction, embolization did not become popular until the early 1990s. At this time, advances in catheter technology had already been made to make cerebral catheterization safer.
In 1991, Guglielmi reported the experimental results and clinical application of electrolytically detachable platinum coils for aneurysm embolization. Initially, endovascular treatment was geared toward the treatment of posterior circulation lesions, such as basilar apex aneurysms, because surgery for these lesions was associated with higher morbidity then their anterior circulation counterparts. In the largest series of endovascularly treated aneurysms of its time, only 43% of the aneurysms treated were of the anterior circulation. With more than 97% of the aneurysms treated in ISAT found in the anterior circulation, greater benefit was generalized to aneurysms arising from the AComA.
After the publication of ISAT, the field of endovascular neurosurgery expanded, with technological advancements allowing physicians to treat aneurysms thought previously uncoilable. These include BACE, SACE, embolization with Onyx HD-500 (eV3 Neurovascular, Irvine, California), flow-diverting stents, and, most recently, the Woven EndoBridge (WEB) aneurysm embolization system (Sequent Medical, Aliso Viejo, California). Furthermore, microcatheter techniques have evolved and coil technology has improved to aid in primary aneurysm coiling. These advancements have assisted in the treatment of patients who may not be surgical candidates but harbor aneurysms, which were historically difficult to treat endovascularly. Table 1 summarizes the results of studies dedicated to the treatment of AComAAs treated endovascularly over the past 10 years.
| Author, Year | Study Design | Aneurysms Treated | Complete Obliteration a (%) | Procedure-Related Complications (%) | Procedure Morbidity and Mortality (%) | Key Points | ||
|---|---|---|---|---|---|---|---|---|
| Total | Ruptured | Thromboembolic | Intraoperative Rupture | |||||
| Elias et al, 2003 | Prospective | 30 | 30 | 56.7 | N/A | N/A | N/A | Favorable outcomes achieved in younger, good-grade SAH females. |
| Proust et al, 2003 | Prospective | 37 | 36 | 78.4 | 10.8 | 2.7 | 13.5 | Endovascular treatment may be preferred in AComAAs when the fundus is oriented posteriorly. |
| Birknes et al, 2006 | Retrospective | 123 | 113 | 77.5 | 0.8 | 3.3 | N/A | Predicting successful aneurysm embolization may be dictated by aneurysm morphology. |
| Guglielmi et al, 2009 | Retrospective | 306 | 236 | 45.5 | N/A | 3.0 | 4.5 | There is less risk to perforating blood vessels when treating AComAAs endovascularly compared with surgery. |
| Songsaeng et al, 2010 | Retrospective | 96 | 7 | 62.5 | N/A | N/A | N/A | Statistically significant increased rate of recurrence with unilateral A1 aplasia. |
| Finitsis et al, 2010 | Prospective | 268 | 234 | 29.5 | 8.1 | 4.3 | 9.1 | The risk of aneurysm recurrence was significantly more frequent in ruptured aneurysms and larger aneurysms (>4 mm). |
| Raslan et al, 2011 | Retrospective | 44 | 43 | 72.7 | 6.8 | 11.4 | 11.4 | Long-term occlusion rates can be achieved with SACE in the setting of SAH with no patients requiring retreatment in their series. |
| Choi et al, 2011 | Retrospective | 45 | 45 | N/A | 0 | 2.2 | 0 | Morphologic features of AComAAs (size, neck, dome-to-neck ratio, multiple lobulations, and vessel incorporation) need to be considered in deciding for a surgical or endovascular treatment. |
| Schuette et al, 2011 | Retrospective | 347 | 277 | N/A | N/A | 5.2 | N/A | Smaller AComAAs (<4 mm) and treatment in the setting of SAH pose increased risk for intraoperative rupture |
| Johnson et al, 2013 | Retrospective | 64 | 5 | 70.9 | 0 | 1.6 | 1.6 | SACE was found safe and durable treatment of AComAAs <15 mm. |
| Huang et al, 2013 | Retrospective | 27 | 27 | 74.1 | 0 | 3.7 | 0 | SACE was found safe in the acutely ruptured setting for wide-necked AComAAs. |
a Complete obliteration varies depending on the original study investigators’ metric for measurement. Some studies used the Raymond classification to determine complete occlusion, whereas others used a percentage of angiographic obliteration to define complete obliteration (ie, >90%).
General Techniques and Principles
Several basic principles and steps help ensure safe interventional procedures. Although some institutions perform aneurysm embolization in conscious patients, the authors perform interventional procedures under general endotracheal anesthesia. Prior to starting the procedure, the patient should have 2 peripheral intravenous lines, a Foley catheter, and an arterial line for monitoring of periprocedural blood pressure. Blood pressure monitoring with arterial lines in the immediate postoperative period is beneficial. All sheaths, guide catheters, and microcatheters are continually flushed with heparinized saline. Generally, the authors begin the procedure with a micropuncture needle and ultimately upsize to a 6-French (F) short sheath unless femoral access is tortuous or arch anatomy is unfavorable, in which case, a long sheath or 6F shuttle is used.
Once access is obtained, 70 U/kg of heparin are administered for an activated clotting time (ACT) goal of 250 seconds. The authors use ACT point-of-care testing through the duration of the procedure to ensure adequate anticoagulation. Meticulous attention to ACT can help prevent disastrous thromboembolic and hemorrhagic complications. It is critical that protamine is immediately available in case of intraoperative rupture. An appropriate guide catheter and selector catheter are used to access the vessel of interest. The ICA ipsilateral to the dominant A1 is catheterized. In cases where the A1s are codominant, the A1 with the straightest course to the aneurysm should be catheterized.
For AComAAs, proximal support is paramount. The authors often use the use of the Neuron 070 (Penumbra, Alameda, California) as a guide catheter and advance it as far as the distal petrous or proximal cavernous ICA segment. In cases of significant cervical ICA tortuosity, the authors often use of the Navien catheter (eV3 Neurovascular). Once treatment projections are chosen, 10 mg of intra-arterial verapamil are given to prevent catheter-induced vasospasm. If the guide catheter cannot be advanced to the petrous segment initially, it is advanced to the desired position over a microcatheter that is supported in a distal A2 or M2 segment.
If stenting is planned prior to treatment, dual antiplatelet therapy with aspirin, 325 mg daily, and clopidogrel, 75 mg daily, is initiated 7 days prior to treatment. Clopidogrel therapy is stopped 3 months after stent placement, whereas aspirin therapy is often continued indefinitely. Some patients are unresponsive to clopidogrel inhibition and are at greater risk for suffering a periprocedural thromboembolic event, because the target moiety of platelets, P2Y 12 , has been shown to have a variable response to clopidogrel. The real-time evaluation of platelet inhibition with the VerifyNow P2Y 12 assay is a measure many physicians use to guide therapy. No standard of care has been established, however, regarding the medication regimen to be used in patients found unresponsive to standard clopidogrel inhibition. At the authors’ institution, the daily dose of clopidogrel is doubled, to 150 mg in divided doses, whereas other investigators have advocated the addition of cilostazol or ticlopidine to standard clopidogrel therapy. In settings where a stent needs to be placed without preoperatively medicating, a loading dose of aspirin, 325 mg, and clopidogrel, 300 to 600 mg, is given.
For aneurysms requiring stenting or with significant coil mass exposed at the neck, a heparin infusion, at 8 U/kg/h, is often used overnight to prevent delayed thromboembolic complications. If delayed thromboembolism occurs, an abciximab infusion is initiated for 24 hours and daily clopidogrel dose is increased. A postoperative blood pressure goal of less than 160 mm of Hg is strictly enforced.
Treatment
Primary coiling
The largest study of endovascular versus open surgical treatment of aneurysms was designed for aneurysms that could be coiled primarily. Generally, this technique is reserved for aneurysms with a favorable dome-to-neck ratio (2 or greater). Aneurysms with a neck diameter of 7 mm or greater are often difficult to treat by standard coiling without BACE or SACE. The options for endovascular neurosurgeons and interventionalists have significantly increased in recent years, with greater selection in coils and microcatheters. In general, once a microcatheter is securely within the aneurysm, a framing coil sized to the smallest dimension of the aneurysm or the mean value of the height, width, and depth can be used. Oversizing the first framing coil is thought to cause unnecessary wall tension and is generally avoided.
Contemporary framing coils are designed with larger and smaller loops with the smaller loops intended to break inside the aneurysm and the larger coils to form the basket. Once a farming coil is securely placed, subsequent coils should be filling coils or smaller framing coils. Most standard coils find adequate aneurysm embolization with a packing density of approximately 30%, although some coils boast a more robust percentage of obliteration. Regardless of packing density, respecting the lumen of the parent vessel and not allowing coils to herniate from the aneurysm are basic tenets of aneurysm embolization.
Before ISAT, the published experience of endovascular treatment of cerebral aneurysms was fairly poor. One study found a significant difference of angiographic obliteration of ACA (including AComA) aneurysms compared with microsurgical ligation. The same investigators found better endovascular results in the treatment of posterior circulation aneurysms only. Another early prospective study found better results of aneurysmal obliteration in clipping (93.2%) versus coiling (56.1%) and a lower risk of permanent injury related to treatment of anterior circulation aneurysms including neurologic injury and death (1.7% vs 7.5%). With further experience and improved endovascular techniques and technologies, primary aneurysm coiling is now the preferred method of treatment at most centers when the geometry of the aneurysm is favorable.
When BACE and SACE cannot be performed, the dual catheter technique can be attempted for wide-necked AComAAs. That is, with 2 microcatheters in the aneurysm, coils are alternatively deployed from each catheter while only detaching after 2 coils are fully introduced into the aneurysm and have demonstrated stability in the coil mass. Theoretically, this improves packing density while ensuring the coil mass does not herniate through the fundus of the aneurysm. A similar technique used at the authors’ institution is bringing a second microcatheter into the lumen of the distal A2. When coiling the aneurysm through the primary microcatheter, the second microcatheter serves to protect the A2 from unintended occlusion or stenosis from the coil mass. This is especially helpful when the origin of the A2 is incorporated into the neck of the aneurysm and a balloon or stent is not desired, as in cases of tortuous proximal anatomy or in cases of ruptured aneurysms ( Fig. 6 ).
Related posts:
General Technical Considerations for the Endovascular Management of Cerebral Aneurysms
Pitfalls and Complications Management in the Endovascular Treatment of Aneurysms
Cerebral Vasospasm
Vertebrobasilar Fusiform Aneurysms
Endovascular Management and Treatment of Acute Ischemic Stroke
Endovascular Management of Intracranial Atherosclerosis
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
