9 Vertebral Artery Ostium Stenosis

10.1055/b-0038-162138

9 Vertebral Artery Ostium Stenosis

Leonardo Rangel-Castilla, Adnan H. Siddiqui, and Peter Nakaji

Abstract

The proximal vertebral artery (VA), including VA ostium (VAO) stenosis is the second most common site of stenosis among the blood vessels supplying the brain, and despite the potential consequence of brainstem and cerebellum strokes, this location has not received enough attention. The incidence of extracranial VA atherosclerotic occlusive diseases affects 25 to 40% of patients with cerebrovascular diseases. Symptoms are not specific but usually involve cerebellar, brainstem, and cranial nerve deficits. MRI of the brain and CT angiography of the head and neck should be obtained in patients on whom the diagnosis of posterior circulation ischemia is suspected. The gold standard imaging modality to diagnose VAO stenosis is cerebral angiography. Medical treatment and risk factor management are similar to that of other cerebrovascular disease, including strict diabetes and hypertension control, statins, and antiplatelet therapy. More aggressive management is necessary for patients refractory to medical therapy. Surgical and endovascular interventions include VA transposition and VAO angioplasty and stenting. Outcomes of patients with VAO stenosis treated with open vascular or endovascular techniques are very encouraging. The success rates of both modalities are similar ranging from 93 to 98%. There is a higher incidence or recurrence following endovascular angioplasty and stenting; however, the use of drug-eluting stents and dual-balloon angioplasty has decreased the rate of in-stent stenosis at long-term follow up.

Introduction

Posterior circulation ischemia accounts for 25 to 30% of all ischemic infarctions. Despite medical treatment with anticoagulation or anti-platelet therapy, the annual stroke rate for patients with symptomatic intracranial basilar artery stenosis is 10.7% and for those with symptomatic intracranial vertebral artery (VA) stenosis, it is 7.8%. After the carotid bifurcation, the proximal VA is the most common site of stenosis among the blood vessels supplying the brain. Despite their potential devastating consequences, ischemic events (i.e., transient ischemic attack or stroke) in this location have not received enough attention. Recent studies have shown that such events are associated with a high risk of stroke or early recurrent stroke. The diagnosis and management of posterior circulation ischemia is particularly challenging.

Major controversies in decision making addressed in this chapter include:

Whether or not treatment is indicated.
Timing for intervention.
Open vascular versus endovascular treatment.

Whether to Treat

Atherosclerotic occlusive disease of the extracranial VA is a common finding on diagnostic imaging. Its incidence in the general population is unknown but is estimated to affect approximately 25 to 40% of patients with cerebrovascular disease. Unlike the carotid circulation, for which the natural history of stenosis is well understood, the natural history of vertebrobasilar insufficiency is less well known. Patients with symptomatic vertebrobasilar artery stenosis are treated with medication alone. However, the effects of novel agents, including antiplatelet agents and statins, on altering the natural history of these lesions have not been elucidated. Endovascular stenting or microsurgical intervention may improve the natural history of VA stenosis with concomitant VA ostium (VAO) stenosis refractory to medical treatment.

The presence of symptomatic vertebrobasilar stenosis and the risk of recurrent vertebrobasilar ischemia stroke have not been addressed until recently. Prospective hospital-based studies have shown that 16.6% of patients had at least 50% vertebrobasilar stenosis. Taking the first event as an index event, the risk of recurrent stroke is 30.5% in patients with at least 50% stenosis versus 8.9% in individuals without stenosis ( 1 , 2 in algorithm ).

**Algorithm 9.1** Decision-making algorithm for vertebral artery ostium stenosis.

Anatomical Considerations

Each VA usually arises from the first portion of the subclavian artery or aortic arch. The artery is conventionally divided into four segments: V1, origin to transverse foramen of C6; V2, from the transverse foramen of C6 to the transverse foramen of C2; V3, from C2 to the dura; and V4, from the dura to the confluence of the VAs to form the basilar artery. The normal luminal diameter of the VA is 3 to 5 mm; however, asymmetry is common. Unilateral hypoplasia (<2 mm) in the extracranial VA (most commonly on the right side) is seen in 2 to 12% of healthy individuals and in 25% of patients with posterior circulation ischemia. A luminal diameter of less than 2 mm is suggestive of the presence of atherosclerosis. The posterior inferior cerebellar artery arises from the intracranial portion of the VA; in 9 to 20% of the general population, it has an extracranial origin.

Pathophysiology/Classification

Thromboembolism, with or without hemodynamic compromise, from the site of vertebrobasilar and VAO stenosis seems to be the predominant cause of ischemic symptoms. Posterior circulation lacunar infarcts result from the occlusion of small perforating arteries secondary to thromboembolism or hemodynamic compromise. However, some patients have associated findings of large artery atherosclerosis or a cardioembolic source; it is unclear whether these findings are purely coincidental or the cause of the infarction. VA stenosis can be classified as intracranial stenosis, extracranial stenosis, tandem lesions, and VAO stenosis in terms of location relative to stroke risk and management complexity. Patients with tandem intracranial/extracranial stenosis have a high risk of stroke, and these cases are more complex to manage.

Workup

Clinical Evaluation

The VA and basilar arteries supply the brainstem, cerebellum, inferior temporal lobe, occipital lobe, and thalamus; therefore, posterior circulation ischemia can give rise to a broad range of symptoms. The most frequent symptoms include dizziness, unilateral limb weakness, dysarthria, headache, and nausea/vomiting. Owing to the lack of specificity of the symptoms, a confident diagnosis can often be made only after obtaining imaging studies of the brain. Neurological findings on physical examination are nonspecific. These most frequently include unilateral limb weakness, gait ataxia, unilateral limb ataxia, dysarthria, and nystagmus. Cranial nerve dysfunction can be observed, including horizontal gaze paresis, internuclear ophthalmoplegia, ptosis, dysphagia, and deafness. The cranial nerves involved most commonly are the third and sixth cranial nerves.

Imaging

Computed tomography (CT) and CT perfusion imaging are less specific and sensitive to posterior circulation strokes than anterior circulation strokes. Magnetic resonance imaging (MRI), particularly diffusion-weighted imaging, is more sensitive than CT and CT perfusion imaging to diagnose acute stroke. Duplex ultrasound is less sensitive for detecting VA stenosis than carotid artery stenosis. CT angiography (CTA) of the extracranial and intracranial portions of the VA is essential (▶ Figs. 9.1 and 9.2 ). The “gold standard” imaging modality is cerebral angiography (▶ Figs. 9.1 and 9.2 ). The study should include both VAs and common carotid arteries (CCAs). Angiograms of the VAs should be obtained from subclavian injections while an inflated cuff is on the patient′s arm. If there is no evidence of VAO stenosis or plaque on the extracranial VA angiograms, intracranial VA angiograms can be obtained from a direct VA injection.