Figure 89-17. Carotid body tumor located at the bifurcation of the internal and external carotid artery.

VERTEBROBASILAR DISEASE

Anatomy

The vertebral arteries are paired arteries that arise from the subclavian arteries. Rarely, variants can

occur, the most common being a direct origin of the left vertebral artery arising from the aortic arch.

The vertebral artery is composed of four segments: V1 is the origin of the vessel up to the C6 transverse

process, V2 is the segment that runs within the vertebral foramina to the level of C2, V3 is the next

segment above C2 before it enters the base of the skull, and V4 is the intracranial portion of the artery

before it joins with the contralateral side forming the basilar artery.

Clinical Findings

7 The vertebral and basilar arteries make up the posterior circulation to the brain and pathology can

lead to posterior circulation ischemia. This system provides blood flow to the brainstem, cerebellum,

and posterior lobes of the brain. About one-fourth of ischemic strokes involve the posterior

circulation.44 Vertebrobasilar ischemia is a commonly misdiagnosed clinical syndrome, mostly due to

the more subtle and broad symptoms associated with them in comparison to the anterior circulation.

The importance of correct diagnosis cannot be stressed enough as the mortality rate for posterior

circulation strokes is 20% to 30% higher than for anterior circulation strokes.45 Symptoms related to the

vertebrobasilar system are bilateral in nature. Symptoms include diplopia, vertigo, drop attacks,

dysphagia, ataxia, disequilibrium, and paresthesias.

Pathogenesis

The cause of vertebral artery disease can either be embolic or from low flow, with low flow causes

predominating. Embolic phenomena are difficult to recognize and are more commonly from the heart,

aorta, and brachiocephalic vessels. Proximal atherosclerotic lesions can embolize, and are more likely to

lead to irreversible ischemia and infarction, and thus are more debilitating. Additionally, multiple foci

of ischemia are common. Overall, approximately 20% of posterior circulation strokes arise from an

arterial source. 44

Low flow accounts for around 30% of posterior circulation strokes.44 Low flow is more likely to cause

transient symptoms and is due to inadequate collateral circulation. Anything that alters the flow to the

posterior circulation can elicit these symptoms (end organ hypoperfusion), most likely rapid postural

changes, or alteration of the cardiac output. As opposed to embolic phenomena, low flow is unlikely to

cause infarction. Unlike embolism, manifestation of symptoms from hypoperfusion requires either

bilateral disease or unilateral disease with poor collateral circulation from the contralateral vertebral

artery and/or circle of Willis.

Differential Diagnosis

Atherosclerosis is the main cause of vertebrobasilar pathology. There are other etiologies that include

dissection, trauma, FMD, aneurysms, and Takayasu disease. Given the subtle symptomatology, there are

a variety of other organ systems that can mimic symptoms. Syncope or presyncope is sometimes

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confused with vertebrobasilar symptoms. This can be caused by a multitude of causes such as cardiac

arrhythmias, vasovagal events, neurologic, psychiatric, or unexplained. Patients often describe visual

changes that can be mistaken for diplopia, such as myopia or presbyopia, cataracts, floaters, amaurosis

fugax, and a variety of other visual complaints. Disequilibrium and vertigo can be caused by many

etiologies, and can be confused for postural instability, hearing loss, and nystagmus. In addition, a

variety of metabolic disorders can mimic vertebral artery disease.

Diagnostic Evaluation

DUS is extremely useful in the identification of vertebral artery disease, however, is more difficult than

the examination of the extracranial carotid arteries. This is due to the location and depth of the vessel,

and evaluation of the vessel between C2 and C6 is difficult. Direct visualization of the cervical vertebral

artery can identify proximal stenosis and reversal of flow. Examination of the bilateral pulses and blood

pressure can further help identify significant differences between the arms, which would suggest

proximal disease.

CTA and MRA are useful imaging modalities and allow careful examination of the vessels throughout

their course, identify disease, and elucidate collateral circulation. MRI also allows precise identification

of embolism and the diagnosis of a stroke. Angiography is considered the “gold standard.” This allows

careful examination of the vertebral arteries including the origin, however, multiple views are often

needed for correct diagnosis. Information about collateral circulation is also shown via contralateral and

anterior circulation.

Distribution of Disease

The V1 segment of the vertebral artery is the most common area of involvement with 92% of patients

having atherosclerotic disease at the origin of the vertebral artery.46 Extrinsic compression via

osteophytes is common in the V2 segment, as is trauma, aneurysms, and dissections. V3 lesions are most

likely caused by trauma and dissections due to the mobility of this section of the artery. V4 is

infrequently the site of vertebral artery disease, but may be affected by trauma or dissection.

Open Surgical Treatment

Open reconstruction of vertebral artery disease depends on the location of disease. For a V1 lesion,

transposition of the vessel to the common carotid artery is preferred. Another option is a bypass from

either the common carotid or subclavian artery to the vertebral artery distal to the disease with either

graft or saphenous vein. A less commonly performed procedure is the subclavian artery endarterectomy.

For lesions or bleeding in the V2 location, typically proximal and distal ligation suffices. A bypass to the

V3 segment can be performed if it is felt that there is not enough collateral circulation. Options for the

V3 segment include bypass using saphenous vein to the C1–2 segment. The external carotid artery can

also be swung over and act as a conduit, after all branches are taken. Reconstruction for the V4 segment

is technically demanding, and requires exposure of the suboccipital segment via resection of the C1

transverse process.

Results are limited to case series and mainly reports from a single surgeon, with a low risk of stroke

and death <1%.47 Other complications include nerve injury (vagus and recurrent laryngeal nerve),

Horner syndrome, and lymphatic leak. The risk of reconstruction of the distal vertebral artery has a

higher risk of stroke and death rate (3%) than proximal lesions.48 Symptoms are alleviated in 71% to

80% of patients, with 10-year patency of 82% to 91%.48,49

ENDOVASCULAR TREATMENT

8 Endovascular management of vertebral artery disease has gained favor due to the relative ease of

repair in contrast to the open repair. The risks that plague any cerebrovascular endovascular

intervention hold true for vertebral artery disease with the risk of embolization, stroke, thrombosis,

dissection, and restenosis. Distal protection can be used to decrease the risk of embolization by way of

an EPD. Angioplasty alone is fraught with high rates of restenosis and the need for reintervention at

close to 50%.50 Additionally, the stroke rate appears to be quite high at 6.4% at 30 days.51 There are

small randomized trials comparing intervention with medical management.

Brachiocephalic Disease

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Anatomy

The aorta arises as it emerges from the aortic valve. The ascending and transverse arch are separated

into the aortic root (aortic valve, three sinuses, and the coronary arteries), tubular portion, and

transverse arch. Most commonly, the aortic arch has three main trunks. These three trunks arise in

order from proximal to distal; innominate artery, left common carotid artery, and left subclavian artery.

There are a few variations that exist relating to these main branch vessels. Most commonly, the

innominate and left common carotid artery come off the arch in one common ostia, the “bovine arch.”

This variant is found in 8% of whites and up to 25% of blacks.52 Another common variant is the

presence of an aortic origin for the left vertebral artery found in 6% of the population that arises

between the left common carotid artery and the left subclavian artery. An aberrant right subclavian

artery occurs when the origin for the right subclavian artery comes off the aorta distal to the left

subclavian artery and courses posteriorly behind the arch, and occurs approximately 0.5% to 1% of the

time.53–55

CLINICAL FINDINGS

Atherosclerosis is the most common disease that affects the brachiocephalic vessels. The clinical scenario

depends on the location of disease and how many vessels are involved. Up to 40% of the time multiple

vessels are involved.56 The clinical picture depends on multiple factors. Disease of the subclavian artery

typically causes embolization, arm claudication or easy fatigability. Occlusive disease involving the

subclavian artery typically manifests as pain and fatigue with continued arm use. With more severe

cases, rest pain and tissue loss can occur. Involvement of the origin of the subclavian artery can cause

subclavian steal, vertebrobasilar insufficiency, or myocardial ischemia if proximal to a functioning LIMA

coronary bypass (subclavian coronary steal). Rarely, hemiparesis or aphasia can occur. Involvement of

the innominate artery can lead to a stroke, TIA, or similar symptoms to subclavian artery involvement.

Common carotid disease can lead to TIA or stroke. Multivessel disease can present as a combination of

all these symptoms.

DIFFERENTIAL DIAGNOSIS

Atherosclerosis is the most common cause of brachiocephalic occlusive disease. The typical picture in

atherosclerosis is an ostial lesion. Vasculitides, such as Takayasu and Giant cell arteritis, can affect the

brachiocephalic arteries (Fig. 89-18). There are infectious processes that can affect the brachiocephalic

vessels. Syphilis and tuberculosis are the most common infectious causes of brachiocephalic disease,

albeit rare, and can lead to aneurysm degeneration of the brachiocephalic artery, and most commonly

the subclavian arteries. Penetrating and blunt trauma can affect the brachiocephalic vessels. Thoracic

outlet obstruction, often related to cervical ribs, can cause subclavian artery aneurysms. These

aneurysms can lead to embolism and distal ischemia.

Figure 89-18. Duplex ultrasonography showing thickening along the common carotid artery and narrowing of the lumen,

consistent with Takayasu arteritis.

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DIAGNOSTIC EVALUATION

A comprehensive physical examination is prudent for the identification of brachiocephalic disease.

Absence of pulses in the extremities can signify proximal disease in either the subclavian or innominate

arteries. Blood pressure measurement can identify subtle differences between the arms, with a

significant finding being greater than 20 mm Hg between sides. Auscultation can identify carotid and

subclavian bruits.

DUS is typically the first imaging modality used for the identification of disease. DUS can evaluate the

carotid arteries with direct visualization of the majority of the extracranial system. It is often difficult to

visualize the proximal vessels as they arise from the aortic arch; however, indirect findings can suggest

disease. A decrease in the waveform amplitude and slope (tardus-parvus waveform) can signify

significant proximal disease. Additionally, reversal of flow in a vertebral artery can signify innominate

or proximal subclavian artery disease and a steal syndrome.

Other modalities include CTA and MRA (Fig. 89-19). These modalities provide excellent imaging of

the aorta and brachiocephalic branches. The images, especially when used with 3D reconstructions,

avoid the use of angiography for diagnosis and allow careful planning for surgical treatment. Thorough

examination of the arterial flow to the brain and collateral circulation is prudent prior to surgical

intervention. Gated CT in coordination with the patient’s electrocardiogram allows careful identification

of the mobile ascending aorta and arch and decreases motion artifact. Angiography is the “gold

standard,” although it has associated risks such as stroke, embolization, and arterial injury. Another

option is transesophageal echocardiogram which can be used to rule out proximal extension of a

dissection, or ascending, arch, and descending aortic pathology.

Figure 89-19. Magnetic resonance angiography (MRA) with brachiocephalic vessel disease. There is a critical stenosis of the

innominate artery and left common carotid artery. There is also a severe proximal left subclavian artery stenosis.

INDICATIONS FOR REPAIR

In general, repair is indicated for symptomatic disease. Asymptomatic disease should be monitored for

progression of disease and medical management of risk factors. A stroke or TIA should prompt repair

due to the continued risk of embolization or low flow state. A low threshold for repair should be given

to those with an internal mammary bypass and proximal subclavian artery disease. Upper extremity

tissue loss, rest pain, and significant exertional pain are indications for repair.

OPEN SURGICAL TREATMENT

There are two general categories for open surgical repair of brachiocephalic disease. Those are

transthoracic and extra-anatomic revascularization. Transthoracic repair requires a median sternotomy

and direct revascularization. This modality is ideal for low-risk patients and those with multilevel

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disease. In the case of the treatment of Takayasu arteritis, debranching off the ascending aortic arch to

the healthy involved vessels is best to avoid diseased arterial segments. Options for repair include aortic

endarterectomy, bypass grafts, and arch replacement with bypass. Results are excellent with 10-year

patency around 90%.57,58 Complications include mortality and stroke rates of 3% to 8% and MI rates of

1.5% to 3%.57–59

9 Based on the patient’s comorbidities and surgical risk, extra-anatomic revascularization carries the

benefit of the avoidance of the risk associated with a median sternotomy. In recent years with the

introduction of endovascular techniques for repair of aortic and brachiocephalic pathologies, extraanatomic procedures are used in conjunction for hybrid repair in high-risk patients. Options for repair

include a carotid–carotid bypass, axilloaxillary bypass, carotid–subclavian bypass and carotid–subclavian

transposition. The transposition avoids the use of a conduit; however, is contraindicated in those with a

previous left mammary bypass graft due to intolerance of proximal clamping. Results are excellent with

10-year patency greater than 80%.56 Mortality rates are lower than those that underwent transthoracic

repair at less than 1%, with slightly lower stroke and MI rates.56,60

Figure 89-20. A: Critical stenosis of the innominate artery with distal wire access for endovascular management. B: Placement of a

balloon-expandable stent for treatment of the innominate artery stenosis. C: Final angiographic run showing complete resolution

of stenosis.

ENDOVASCULAR TREATMENT

As with carotid stenting, the option for endovascular treatment of brachiocephalic disease depends of

the aortic anatomy, anatomical variants, baseline renal function, arch type, lesion characteristics, and

proximity to branch vessels (Fig. 89-20).

Options for repair include angioplasty and stenting. This does require intraprocedural anticoagulation

and antiplatelet therapy after repair. Results of repair do not appear to compare to open repair,

however, there is a paucity of data regarding long-term results. One-year patency appears to be around

90% and 5-year patency drops to 77% to 89%.61–63 Given these results, surveillance is required and

follow-up procedures for assisted patency are required.

Care must be given to avoid embolization to the vertebral arteries when intervening on the

subclavian arteries or the internal carotid arteries when intervening on the innominate or common

carotid arteries. This is usually accomplished with a filter being placed distal to the target area of

revascularization with a 0.014-in–based system. Separate access or use of the 0.014 wire with a rapid

exchange system allows protection during intervention. However, the risk of embolization is low and

risks associated with filter placement should be weighed.

References

1. Lozano R, Naghavi M, Foreman K, et al. Global and regional mortality from 235 causes of death for

20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010.

Lancet 2012;380:2095–2128.

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