Residency · Residency · Vascular Surgery

Vertebrobasilar Insufficiency and Subclavian Steal

Overview

Vertebrobasilar insufficiency (VBI) describes ischemic symptoms that arise in the posterior circulation territory of the brain, which includes the brainstem, cerebellum, and occipital cortex. Subclavian steal syndrome occurs when there is stenosis or occlusion of the proximal subclavian artery, leading to retrograde blood flow in the ipsilateral vertebral artery as it diverts blood to supply the arm. Most patients with subclavian steal exhibit asymptomatic flow reversal, known as the subclavian steal phenomenon, which typically does not produce clinical symptoms. Treatment is generally reserved for those who are symptomatic.

Anatomy of the Posterior Circulation

The vertebral arteries originate from the subclavian arteries at the V1 segment and travel through the transverse foramina of the cervical vertebrae C6 to C1 (V2 segment). They then curve around the atlas (V3 segment) and enter the cranium via the foramen magnum (V4 segment). The two vertebral arteries join at the pontomedullary junction to form the basilar artery, which supplies critical structures such as the brainstem, cerebellum, occipital cortex, thalamus, and the posterior limb of the internal capsule. The posterior communicating arteries connect the posterior circulation (basilar artery) to the anterior circulation (internal carotid artery) through the Circle of Willis. Anatomically, the left vertebral artery is dominant in approximately 50% of individuals, the right vertebral artery is dominant in about 25%, and both are codominant in the remaining 25%.

Vertebrobasilar Insufficiency

Etiology

The most common cause of vertebrobasilar insufficiency is atherosclerosis, which typically affects the origin of the vertebral artery (V1 segment). Vertebral artery stenosis at this origin is present in 20-25% of patients who have carotid artery disease. Other causes include vertebral artery dissection, fibromuscular dysplasia (FMD), and external compression from cervical spondylosis or atlantoaxial subluxation. Subclavian steal can also contribute to VBI. Rarely, vertebral artery aneurysms or arteritis may be responsible.

Clinical Presentation

Patients with vertebrobasilar insufficiency most commonly present with dizziness or vertigo, although these symptoms are nonspecific. Drop attacks, characterized by sudden falls without loss of consciousness, are another hallmark. Visual disturbances such as bilateral visual loss, diplopia, or homonymous hemianopsia may occur. Cerebellar dysfunction manifests as ataxia and gait instability. Brainstem involvement can cause dysarthria and dysphagia, while bilateral motor or sensory symptoms may present as weakness or numbness on both sides. Syncope or near-syncope episodes are also possible. It is important to note that isolated dizziness is rarely caused by VBI; clinicians should look for accompanying brainstem or posterior fossa symptoms.

Diagnosis

Duplex ultrasound is useful for assessing vertebral artery flow direction and velocity, allowing identification of vertebral artery stenosis and flow reversal. Computed tomography angiography (CTA) and magnetic resonance angiography (MRA) provide anatomic visualization of the vertebral arteries, subclavian arteries, and intracranial circulation, with MRA preferred for vertebral artery assessment due to the absence of calcium artifact. Catheter angiography remains the definitive diagnostic tool, typically reserved for cases where intervention is planned. Transcranial Doppler (TCD) can assess basilar artery flow and intracranial collateral status.

<image>Anatomical diagram of the vertebrobasilar circulation showing the vertebral arteries (V1-V4 segments), basilar artery, posterior cerebral arteries, and Circle of Willis connections, with the common sites of atherosclerotic disease at the vertebral artery origin and subclavian artery highlighted</image>

Subclavian Steal Syndrome

Pathophysiology

Subclavian steal syndrome results from stenosis or occlusion of the proximal subclavian artery before the origin of the vertebral artery. During arm exercise, increased blood demand in the arm creates a pressure gradient reversal, causing blood to flow retrograde down the ipsilateral vertebral artery to supply the arm. This diversion "steals" blood from the posterior cerebral circulation. The left subclavian artery is more commonly affected, occurring two to three times more frequently than the right, likely due to its direct origin from the aortic arch and greater susceptibility to atherosclerosis.

Classification

The subclavian steal phenomenon refers to asymptomatic flow reversal detected on duplex ultrasound, which is very common and found in up to 5% of vascular lab patients; it rarely requires treatment. Subclavian steal syndrome, in contrast, involves flow reversal accompanied by posterior circulation symptoms and is much rarer. Vertebral artery flow reversal progresses through stages: Stage I (latent) shows systolic deceleration in the vertebral artery; Stage II (partial or alternating) exhibits systolic flow reversal with antegrade diastolic flow; and Stage III (permanent) demonstrates complete flow reversal throughout the cardiac cycle.

Clinical Presentation

Patients with subclavian steal syndrome experience posterior circulation symptoms such as dizziness, vertigo, syncope, and visual disturbances, typically provoked by arm exercise. Arm symptoms include claudication, fatigue, and a blood pressure difference greater than 20 mmHg between arms. In patients with a left internal mammary artery (LIMA) to left anterior descending artery (LAD) bypass graft, subclavian steal can cause coronary steal syndrome, leading to angina due to retrograde blood flow through the LIMA. Most patients remain asymptomatic, and intervention is reserved for those with symptoms or coronary-subclavian steal.

Diagnosis

A blood pressure differential greater than 20 mmHg between arms serves as a useful screening test. Duplex ultrasound can confirm vertebral artery flow reversal and detect subclavian stenosis or occlusion. CTA and MRA provide anatomic confirmation. It is essential to correlate posterior circulation symptoms with arm exercise to establish the diagnosis.

<image>Diagram illustrating subclavian steal physiology showing normal antegrade vertebral artery flow on the unaffected side, and retrograde vertebral artery flow on the side with proximal subclavian artery stenosis, with blood being diverted from the basilar artery toward the arm during exercise</image>

Treatment

Medical Management

Medical therapy includes antiplatelet agents such as aspirin or clopidogrel, statin therapy, and modification of vascular risk factors including smoking cessation, blood pressure control, and diabetes management. This approach is adequate for most patients with the subclavian steal phenomenon who are asymptomatic.

Endovascular Treatment: Subclavian Artery Stenting

For symptomatic subclavian stenosis, endovascular treatment with subclavian artery stenting is the first-line option. Access is typically obtained via the femoral or brachial artery. The procedure involves balloon angioplasty followed by deployment of a balloon-expandable stent, which is preferred for ostial lesions. Technical success rates exceed 95%, with primary patency rates of 80-90% at five years. Advantages include minimal invasiveness and lower morbidity compared to open surgery. Risks include embolization, which necessitates protection of the vertebral artery, access site complications, and vessel injury. Total subclavian occlusions may require a retrograde approach via brachial or radial access.

Open Surgical Options

Carotid-subclavian bypass involves creating a conduit using a prosthetic graft (PTFE or Dacron) or saphenous vein from the common carotid artery (CCA) to the subclavian artery distal to the stenosis. This procedure is performed through a supraclavicular incision and offers excellent patency rates of 90-95% at five years. However, it should be avoided in patients with ipsilateral carotid artery disease to prevent steal from the carotid circulation.

Subclavian-carotid transposition entails dividing the subclavian artery distal to the stenosis and reimplanting it into the CCA. This technique is preferred when feasible because it avoids prosthetic material and provides excellent long-term outcomes. It is more technically challenging on the left side due to the proximity of the thoracic duct and recurrent laryngeal nerve.

Axillo-axillary bypass is an extra-anatomic procedure connecting one axillary artery to the other and is reserved for cases where carotid-subclavian options are not feasible.

Vertebral Artery Revascularization

Revascularization of the vertebral artery is rarely necessary because most posterior circulation symptoms resolve after subclavian revascularization. Vertebral artery transposition to the CCA can be considered for isolated vertebral artery origin stenosis. Vertebral artery stenting is an emerging but technically challenging option due to the small size and tortuosity of the vessel. Indications for vertebral artery intervention include bilateral vertebral stenosis, failure of medical therapy, and significant stenosis in a dominant vertebral artery.

Clinical Pearls

The subclavian steal phenomenon, characterized by asymptomatic flow reversal, is very common and almost never requires treatment; only symptomatic subclavian steal syndrome warrants intervention. It is important to measure bilateral arm blood pressures in every vascular patient, as a difference greater than 20 mmHg suggests subclavian stenosis. Isolated dizziness is rarely caused by vertebrobasilar insufficiency, so clinicians should look for associated brainstem or cerebellar symptoms. In patients with a LIMA-to-LAD bypass graft, left subclavian stenosis can cause coronary steal and angina, making it essential to assess the left subclavian artery before cardiac surgery. Subclavian stenting is the first-line treatment for symptomatic stenosis, while open surgery such as carotid-subclavian bypass or transposition is reserved for occlusions or failed stenting. When performing carotid-subclavian bypass, ensure the ipsilateral carotid artery is free of significant disease to avoid creating a steal phenomenon from the carotid territory.

References

• Defined S, et al. Subclavian steal syndrome: a review. J Vasc Surg. 2017;66(2):571-577.
• Osiro S, et al. A comprehensive review of the anatomy, imaging, and clinical implications of the subclavian steal syndrome. Neurosurg Rev. 2012;35(3):411-417.
• Naylor AR, et al. ESVS 2023 Guidelines on Carotid and Vertebral Artery Disease. Eur J Vasc Endovasc Surg. 2023;65(1):7-111.
• De Vries AB, et al. Subclavian artery stenosis and vertebral artery disease. Semin Vasc Surg. 2004;17(4):319-326.
• Kieffer E, et al. Subclavian artery reconstruction by carotid-subclavian bypass or transposition. J Vasc Surg. 1994;19(2):257-264.

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