Endovascular Strategies for Vertebrobasilar Dissecting Aneurysms

Discussion

The natural history of unruptured dissecting aneurysms remains poorly understood.²² Dissection is a dynamic process, and some vertebral dissecting aneurysms may heal spontaneously, whereas others can cause ischemic symptoms or stroke due to stenosis, occlusion of the parent vessel, or involvement of perforators.²² The guidelines for endovascular treatment of unruptured dissecting aneurysms presenting with ischemia, headache, and incidental findings remain controversial. The relatively benign clinical course and outcome reported for unruptured vertebral dissecting aneurysms have resulted in conservative treatment such as anticoagulation being recommended.^18–20 Anticoagulation with a target international normalized ratio of 2.0–3.0 is generally accepted for 3–6 months. However, a recent study demonstrated serial angiographic changes in 88.2% of unruptured vertebral artery (VA) dissections, including subsequent formation of aneurysms that may be amenable to surgical treatment.²² Iihara et al⁷ recommended short-term follow-up angiography (within 3 weeks) after presentation in unruptured vertebral dissecting aneurysms for the purpose of performing active treatment for these aneurysms. Although anticoagulation is critical for preventing thromboembolic events in the initial stages of disease, it may be insufficient to overcome the flow-limiting nature of a dissecting lesion.

A convincing argument for early neurointervention also exists.²³ Naito et al²¹ reported that the risk of bleeding from unruptured VA dissecting aneurysms was higher than previously considered and that endovascular treatment should be considered for unruptured VA dissections associated with relatively large aneurysmal dilations or the double-lumen sign in the acute stage and with growing aneurysmal dilations during the follow-up period, on the basis of 21 patients with unruptured VA dissections.

Our rationale for treatment of unruptured dissecting aneurysm includes aneurysm morphology susceptible to bleeding and chronologic morphologic change of the VA dissection. In addition to these, our indications for endovascular treatment of unruptured dissecting aneurysms extend to acute-onset symptomatic lesions beyond typical indications for treatment. These indications based on variability of morphology in ruptured dissecting aneurysm and sudden-onset symptoms suggest the possibility of the prodromal symptoms warning of a leak. Clinical and radiologic outcomes were favorable in all patients with unruptured vertebral dissecting aneurysms treated by endovascular modalities comprising internal trapping, stents, and stent with coil. No procedural morbidity or mortality occurred in unruptured vertebrobasilar dissecting aneurysms treated with endovascular procedures. Endovascular treatment for dissecting aneurysms by using stents has been proposed, especially in patients with otherwise untreatable dissecting basilar arteries, internal carotid artery pseudoaneurysms, and dissecting VA aneurysms.^24–37 Although endovascular surgery by using stents is effective for dissecting lesions, it usually does not prevent rebleeding,²⁵ and rebleeding can occur after double-stent placement alone.⁹ Recently, we performed stent-only or stent-assisted coil embolization in patients with symptomatic unruptured dissecting aneurysms, without consideration of the PICA relationship. Radiologic outcomes, follow-up radiologic outcomes, and clinical outcomes were satisfactory in those patients.

Ruptured vertebrobasilar dissecting aneurysms have an extremely high rate of early rebleeding (≤70% in some series).⁴ Rebleeding generally occurs within the first 24 hours after rupture onset and is associated with a poor clinical outcome. Considering the aggressive behavior of ruptured vertebral dissecting aneurysms, we believe that the best and most definitive treatment is parent vessel deconstruction. This can be achieved by using either open surgical trapping or endovascular balloon or coil occlusion.^{6–8,32,38,39} Results of multiple series^1,5,40–43 suggest that surgical or endovascular trapping to directly occlude the pathologic artery segment is appropriate in vertebral dissecting aneurysm cases.^1,5,40–43 However, this strategy is not feasible for vertebral dissecting aneurysms involving the PICA not supplied by other vasculature. Proximal occlusion as an alternate strategy for trapping may allow better collateral circulation, especially when lesions involve the PICA origin. However, proximal occlusion is associated with the risk of retrograde flow into the pseudoaneurysm from the contralateral vertebral or basilar artery, with persistence of flow into the aneurysm.⁴⁴ Rabinov et al⁸ reported rebleeding in ruptured vertebral dissecting aneurysms treated by proximal occlusion.

The present study indicates that there are considerable pitfalls associated with treating ruptured dissecting aneurysms by using endovascular treatment modalities, trapping and proximal occlusion. First, the length of the segment treated using endovascular techniques is not controllable and is generally longer than anticipated. In the case of a ruptured dissecting aneurysm in the supra-PICA level, the possibility of unwanted coil herniation into the PICA or coil packing below the PICA is always present. Second, radiologic complete occlusion is not always possible, and incomplete occlusion for ruptured dissecting aneurysms treated with trapping or proximal occlusion involves the additional risk of rebleeding. Despite these pitfalls, endovascular procedures can be regarded as a standard treatment for vertebral dissecting aneurysms due to good lesion access and relatively acceptable procedure-related complication rates.

Endovascular stent or stent with coil, the reconstructive technique for the parent vessel, has been applied to dissecting vertebral or basilar aneurysms. As limitations of parent vessel reconstruction with a stent for dissecting vertebral aneurysms, its unproven durability of treatment and the maintenance of antiplatelet medication were reported.⁴⁵ However, in recent studies, outcomes of endovascular treatment by using stents appear favorable.^12,31–37 In our series, outcome of that treatment was favorable as well in unruptured vertebral dissecting aneurysms. The mechanisms of stent placement for vertebral dissecting aneurysms were fundamentally based on sidewall flow models reported by Canton et al⁴⁶ and histologic evidence for endothelialization of the Neuroform stent (Boston Scientific, Natick, Mass) reported by Lopes et al.⁴⁷

These studies suggested that stents for dissecting aneurysms, with their radial force and metal-mesh ratio, may enhance true lumen expansion, flow diversion, and stent endothelialization to achieve aneurysm exclusion and parent artery reconstruction. However, although endovascular surgery by using stents was considered for ruptured vertebral dissecting aneurysms, heparinization and antiplatelet premedication were not performed maximally due to the possibility of rebleeding. Endovascular surgery by using stents for ruptured vertebral dissecting aneurysms requires further investigation and has, thus far, been limited to cases not treatable by using other modalities. For ruptured vertebral dissecting aneurysms that cannot be treated with trapping, combined treatment by using bypass surgery such as occipital artery (OA)-PICA anastomosis and trapping should be considered.

With respect to procedure-related complications, the present study mostly encountered rebleeding and acute PICA-territory infarction. All immediate control angiograms after endovascular procedures revealed contrast filling of the PICA. Kitanaka et al² suggested that sacrifice of the PICA was not always dangerous because of the rich pial anastomoses. However, a retrospective review of the causes of PICA territory infarctions in the 4 supra-PICA dissecting aneurysms indicates that 1 case might have been due to a thromboembolism caused by a coil loop herniation into the PICA origin. PICA territory infarctions in the other 3 cases might have resulted from injury to a critical perforating artery supplying the brain stem and deep cerebellar nuclei or from microthromboembolism due to a coil mass exposed to the PICA.

To perform trapping for ruptured supra-PICA dissecting aneurysms and to sacrifice the PICA in cases with other poor collateral circulation covering the PICA territory, one should consider bypass techniques such as OA-PICA anastomosis to reduce the complication of symptomatic PICA territory infarction. In addition to ischemic complications of the PICA during endovascular procedures, the possibility for occluding the anterior or posterior spinal artery arising from the dissected segment should be invariably considered. Iwai et al⁴⁸ reported that severe ischemic complications such as quadriparesis or respiratory disturbance could occur if the anterior spinal artery originated only from the side of the dissected VA in patients with VA aneurysms located distal to the PICA. Therefore, for planning of trapping vertebrobasilar dissecting aneurysms, these factors should be definitely considered for reducing dismal ischemic complications.