Management of Vertebral Artery Dissections and Vascular Insufficiency

Approximately 80% of strokes are ischemic in origin, of which as many as 25% involve the vertebrobasilar system.1 The vertebrobasilar system is composed of the vertebral arteries (VAs) and the basilar artery, and it typically supplies blood to the brainstem, cerebellum, thalamus, and occipital and posterior temporal lobes. Outcomes of posterior circulation transient ischemic attacks (TIAs), or stroke, depend on the location of the lesion. Medically refractory, symptomatic atherosclerotic disease of the vertebrobasilar system is associated with a 5 to 11% risk of stroke at 1 year2,3; TIAs related to extracranial vertebrobasilar system disease are associated with a 30% risk of stroke at 5 years.4–6 Patients with symptomatic intracranial atherosclerosis have a 1-year stroke risk of 11% in the subserved vascular territory.7 If the stenosis is greater than 70%, the risk of stroke increases to 19%. The Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) trial demonstrated that aspirin is not inferior to warfarin in terms of risk reduction for recurrent stroke in patients with symptomatic intracranial disease.3 In their large posterior circulation registry, Caplan and colleagues reported that 22% of patients with a vertebrobasilar TIA or stroke had a poor functional outcome at 30 days.8 Thrombosis of the basilar artery is associated with an extremely poor prognosis, with death or dependence in as many as 80% of cases.9

Vertebrobasilar insufficiency, the clinical syndrome caused by impaired perfusion of the vertebrobasilar system, is characterized by dizziness, ataxia, discoordination, visual disturbances, and sensorimotor deficits. These symptoms can easily be dismissed as nonspecific; consequently, vertebrobasilar insufficiency is underrecognized and frequently misdiagnosed.10

Surgical treatment options for atherosclerosis of the VA include vessel transection distal to the occlusive lesion and reimplantation into the ipsilateral carotid or subclavian artery or an endarterectomy of the VA. Surgical access to the VA, particularly the ostium, is difficult, and the complication rate associated with surgical management is 10 to 20%.5,11,12 The relatively high complication rates of surgical treatments for occlusive disease of the vertebrobasilar system, coupled with the failure of medical therapy to reduce the risk of stroke in select groups of patients, has led to strong interest in the development of endovascular treatment modalities for this disease.

Initial attempts at revascularization of the VAs involved the application of technology developed for the coronary arterial system. Fundamental differences in the vascular anatomy between the vertebrobasilar system and the coronary system (i.e., increased tortuosity of the VAs) necessitated the modification of coronary microcatheters, angioplasty balloons, and stents for use in the vertebrobasilar system. Indeed, the lessons learned in interventional cardiology in the management of atherosclerotic disease of the coronary arteries ultimately proved applicable to the intracranial circulation, including the vertebrobasilar system.

Percutaneous transluminal angioplasty (PTA) has been used successfully in the treatment of peripheral and coronary arterial disease since its initial description by Dotter and Junkins in 1964.13 Intracranial angioplasty was first described by Sundt and colleagues who successfully employed the technique to treat severe basilar artery stenosis causing progressive symptoms despite maximal medical therapy.14 The technique was then repeated with mixed results and was initially associated with what many investigators deemed as an unacceptably high procedural complication rate.15–17 Major complications from intracranial angioplasty include vasospasm, arterial trauma, vessel perforation, and embolic stroke. Increased complication rates for intracranial angioplasty and stenting compared with the coronary system probably reflect the relative fragility of the intracranial vessels and the potential for substantial neurological morbidity from even tiny foci of ischemia, especially brain tissue supplied by brainstem perforators.

Initially, coronary angioplasty balloons were used off-label to perform intracranial PTA alone. As in the coronary arterial system, angioplasty alone in the VA for the treatment of atherosclerotic disease has a very high restenosis rate, approaching 100% in some series.18 As balloon-mounted stents became the mainstay of the endoluminal treatment of coronary artery disease, these devices were adopted for the treatment of intracranial atherosclerotic disease. Technological modifications were necessary to allow navigation of the more tortuous intracranial circulation with more flexible catheters and improved stent delivery systems. Initial attempts at treatment of intracranial atherosclerotic disease with stenting resulted in acceptable periprocedural rates of morbidity and mortality but with relatively high rates of technical failure. Angioplasty as a standalone, initial treatment modality for atheromatous disease of the VA has therefore largely been abandoned. However, angioplasty alone may be performed for in-stent stenosis when the pathoetiology is presumed to be intimal hyperplasia rather than progression of atherosclerotic disease.

Approximately 30% of patients who experience strokes involving the vertebrobasilar circulation have a lesion in the V1 segment of the VA.19 The contrast between the relatively easy endovascular access to the VA ostium and the high morbidity rate associated with an open surgical exposure has led to an interest in stenting high-grade lesions.

As in the coronary stenting experience, the application of drug-eluting stents (DESs) for the treatment of occlusive disease of the VA origin reduces rates of restenosis as has been shown in numerous studies. DESs are not currently employed in the intracranial circulation. Restenosis rates for bare metal stents for symptomatic intracranial and extracranial stenosis have been reported at 35%.20 In the coronary system, that DES significantly reduced restenosis rates from 30% to 4 to 8% at a 9-month follow-up21,22 prompted interest in applying DES to the cerebrovascular arteries. In the setting of VA origin stenosis, Ogilvy and colleagues compared DES (sirolimus and paclitaxel-eluting) with bare metal stents.23 For individuals with >60% symptomatic or >70% asymptomatic VA origin stenosis and an occluded or hypoplastic contralateral VA or significant carotid occlusion, DES reduced angiographic restenosis rates from 38% (9/24) to 17% (2/12). Twenty-nine percent (7/24) of people in the bare metal stenting group required angioplasty for in-stent stenosis, whereas no patients in the DES arm required angioplasty.23 Although long-term follow-up is needed, these and other preliminary data suggest that it may be reasonable to expect similar reductions in in-stent stenosis in the vertebrobasilar system as have been experienced in the coronary system. Placement of a DES in the setting of in-stent stenosis after placement of a bare metal stent has been reported as an effective treatment.24

Although no reports of arterial toxicity have been reported with DES in the cerebrovascular system, reports of delayed hypersensitivity resulting in late thrombosis have been reported in coronary vessels.25 The optimal duration of treatment with antiplatelet agents after implantation of DES has not been established. Our practice is to continue dual antiplatelet therapy, which is individually tailored based on platelet inhibition assays. Angiography is typically performed 3 months after stent placement. If no evidence of in-stent stenosis is seen, the patient is continued on a single antiplatelet agent indefinitely, unless there is a contraindication.

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