Vertebral artery disease
I. Definition and natural history
Up to 20% of ischaemic cerebrovascular events involving the posterior circulation are related to VA disease. While fibromuscular dysplasia, trauma, dissection, osteophyte compression, Takayasu arteritis, and aneurysms can affect the VA, atherosclerosis remains the primary aetiology for VA stenotic/occlusive lesions. The majority of vertebrobasilar embolic events originate from the heart, aorta or a proximal vessel (e.g. subclavian artery).
Observational studies suggest that a recently symptomatic 50–99% VA stenosis may be associated with a 30% risk of stroke over a 5-year period.The risk of recurrent stroke is highest in the early period after onset of symptoms. The 90-day stroke risk from first clinical event is 25% in patients with a VA stenosis versus 7% in those without. The risk of recurrent stroke is higher (33%) with intracranial versus extracranial VA stenoses (16%), with the highest risk within the first few weeks after symptoms onset. The natural history of asymptomatic VA stenoses is unknown.
II. Imaging
CTA and MRA have a higher sensitivity (94%) and specificity (95%) than DUS (sensitivity 70%).Vertebral ostial stenoses are overestimated by MRA,while CTA underestimates the degree and prevalence of ostial vertebral arteries stenoses. Despite these limitations, digital subtraction angiography is rarely required for diagnostic purposes. However, digital subtraction angiography may be necessary in patients with symptomatic vertebral artery disease who are potentially candidates for revascularization. In patients with known VA stenoses, it is reasonable to use DUS to assess stenosis progression and to follow patients after revascularization therapies.
III. Management of vertebral artery disease
Although no prospective RCTs have evaluated different drug therapies in patients with VA disease, aspirin (or clopidogrel if aspirin is not tolerated) and statins are recommended irrespective of symptoms. Most patients with asymptomatic VA disease do not require any revascularization.
In patients with ischaemic events despite antiplatelet therapy, revascularization may be considered. Surgery of extracranial vertebral stenoses (with transposition to common carotid artery, trans-subclavian vertebral endarterectomy, distal venous bypass) can be performed with low stroke/death rates in experienced surgical teams. However, in centres with limited expertise of complex VA reconstructions, open surgery has been mostly replaced by endovascular interventions. A systematic review identified 993 patients who were mostly symptomatic, of whom 72% had ostial vertebral stenoses. Overall, 980 were treated with stent implantation with a technical success rate of 99.3% and a 30-day stroke rate of 1.1%. At 24 months, 1.1% had suffered a recurrent vertebrobasilar stroke. Restenosis rates at 24 months were 11% in patients treated with drug-eluting stents and 30% if bare-metal stents were used.
The Vertebral Artery Stenting Trial (VAST) randomized patients with vertebrobasilar symptoms within the preceding 30 days and an extra- or intracranial VA stenosis greater than 50% to stenting plus BMT (n = 57) or BMT alone (n = 58). VAST was suspended after recruiting 115 patients because of regulatory issues. Thirty-day vertebrobasilar stroke or death occurred in 5% of patients randomized to stenting and 2% in the medical arm. At 3 years, 12% of stented patients had recurrent vertebrobasilar stroke, compared with 7% in the medical arm. These results do not support routine endovascular interventions for symptomatic VA stenoses, unless symptoms recur despite optimal medical therapy.
Recommendations for management of vertebral artery stenoses:
| Recomendations | Class | Level |
| In patiens with symptomatic extracranial vertebral artery stenoses, revascularization may be considered for lesions >= 50% in patients with recurrent ischaemic events, despite optimal medical management | IIb | B |
| Revascularization of asymptomatic vertebral artery stenosis is not indicated, irrespective of the degree of severity. | III | C |