Vertebral Artery Atherothrombosis 

Updated: Jun 23, 2021
Author: Mark D Morasch, MD, RPVI; Chief Editor: Brian H Kopell, MD 

Overview

Practice Essentials

The most common disease affecting the vertebral artery is atherosclerosis. Less commonly, the extracranial vertebral arteries can be affected by pathologic processes such as trauma, fibromuscular dysplasia, Takayasu disease, osteophyte compression, dissections, and aneurysms. True extracranial aneurysms are virtually always found in the setting of a connective tissue disorder (CTD), whereas false aneurysms may or may not be related to a CTD but usually follow arterial dissection.

Crawford and coworkers first described the technique of trans-subclavian endarterectomy of the vertebral artery.[1]  Transposition of the proximal vertebral artery to the common carotid was described by Clark and Perry in 1966 through a similar approach.[2]  During the 1970s, the saphenous vein was first used to bypass vertebral artery origin stenoses.[3]  Eventually, transposition techniques were found to be superior solutions for proximal vertebral disease and have supplanted endarterectomy and bypass as the reconstruction options of choice.

The approach to the distal vertebral artery was first described by Matas and Henry and was used for the treatment of traumatic injury.[4, 5] During the late 1970s, venous bypass and skull base transposition procedures to revascularize the distal vertebral artery were developed using a similar approach.[6, 7, 8]

Etiology and presentation

Arterial-to-arterial emboli can arise from atherosclerotic lesions, from intimal defects caused by extrinsic compression or repetitive trauma, and rarely from fibromuscular dysplasia, aneurysms, or dissections. Although fewer patients suffer from embolic phenomena than those with hemodynamic ischemia, actual infarctions in the vertebrobasilar distribution are most often the result of embolic events. Patients with embolic ischemia often develop multiple and multifocal infarcts in the brain stem, cerebellum, and, occasionally, posterior cerebral artery territory. Patient presentation is dissimilar to those with hemodynamic symptoms.

Patients who experience emboli have varied presentations. In patients with posterior circulation ischemia secondary to microembolism and appropriate lesions in a vertebral artery, the potential source of the embolus needs to be eliminated regardless of the status of the contralateral vertebral. These patients are considered candidates for surgical or endoluminal correction of the offending lesion regardless of the condition of the contralateral vertebral artery. With the exception of the patient presenting with a vertebral artery aneurysm, surgical or endovascular intervention is not indicated in asymptomatic patients who harbor suspicious radiographic findings.

Ischemia affecting the temporo-occipital areas of the cerebral hemispheres or segments of the brain stem and cerebellum characteristically produces bilateral symptoms. The classic symptoms of vertebrobasilar ischemia are dizziness, vertigo, diplopia, perioral numbness, alternating paresthesia, tinnitus, dysphasia, dysarthria, drop attacks, ataxia, and homonymous hemianopsia. (See the image below.)

Symptoms of vertebrobasilar ischemia. Symptoms of vertebrobasilar ischemia.

When patients present with 2 or more of these symptoms, vertebrobasilar ischemia is likely the cause. Nevertheless, symptoms associated with posterior circulation ischemia are often dismissed as nonspecific findings. Because of the often vague nature of patient presentation, clinicians may be reluctant to pursue a pathologic diagnosis or to recommend treatment for potentially correctable vertebral artery lesions.

Numerous medical conditions may cause or mimic vertebrobasilar ischemia, thus confounding the selection of patients in need of posterior circulation treatment. These include inappropriate use of antihypertensive medications, cardiac arrhythmias, anemia, brain tumors, benign vertiginous states, basilar artery migraine, and postsubarachnoid hemorrhage vasospasm. (See the image below.)

Nonischemic conditions that may mimic vertebrobasi Nonischemic conditions that may mimic vertebrobasilar ischemia.

In general, the ischemic mechanisms can be broken down into those that are hemodynamic and those that are embolic. Hemodynamic symptoms occur as a result of transient "end-organ" (brainstem, cerebellum, and/or occipital lobes) hypoperfusion and can be precipitated by postural changes or transient reduction in cardiac output. Ischemia from hemodynamic mechanisms rarely results in tissue infarction. Symptoms from hemodynamic mechanisms tend to be short lived, repetitive, almost predictable, and more of a nuisance than a danger.

For hemodynamic symptoms to occur in direct relation to the vertebrobasilar arteries, significant occlusive pathology must be present in both of the paired vertebral vessels or in the basilar artery. In addition, compensatory contribution from the carotid circulation via the Circle of Willis must be incomplete. Alternatively, hemodynamic ischemic symptoms may follow proximal subclavian artery occlusion and the syndrome of subclavian/vertebral artery steal.

In later years of life, vertebral artery stenosis is a common arteriographic finding, and dizziness is a common complaint. The presence of both cannot necessarily be assumed to have a cause-and-effect relationship. Surgical reconstruction is not indicated in an asymptomatic patient with stenotic or occlusive vertebral lesions. These patients are well compensated, usually from the carotid circulation through the circle of Willis.

The minimal anatomic requirement to justify vertebral artery reconstruction for a patient with hemodynamic symptoms is (1) stenosis of more than 60% diameter in both vertebral arteries if both are patent and complete or (2) the same degree of stenosis in the dominant vertebral artery if the opposite vertebral artery is hypoplastic, ends in a posteroinferior cerebellar artery (PICA), or is occluded. A single, normal vertebral artery is sufficient to adequately perfuse the basilar artery, regardless of the patency status of the contralateral vertebral artery.

Embolic causes of vertebrobasilar ischemia may not be as well recognized. As many as one third of vertebrobasilar ischemic episodes are caused by distal embolization from plaques or mural lesions of the subclavian, vertebral, and/or basilar arteries.[6, 8]  Arterial-to-arterial emboli can arise from atherosclerotic lesions, from intimal defects caused by extrinsic compression or repetitive trauma, and rarely from fibromuscular dysplasia, aneurysms, or dissections. Although fewer patients suffer from embolic phenomena than hemodynamic ischemia, actual infarctions in the vertebrobasilar distribution are most often the result of embolic events. Patients with embolic ischemia often develop multiple and multifocal infarcts in the brain stem, cerebellum, and, occasionally, posterior cerebral artery territory. Patient presentation is dissimilar to those with hemodynamic symptoms.

Patients who experience emboli have varied presentations. In patients with posterior circulation ischemia secondary to microembolism and appropriate lesions in a vertebral artery, the potential source of the embolus needs to be eliminated regardless of the status of the contralateral vertebral artery. These patients are considered candidates for surgical or endoluminal correction of the offending lesion regardless of the condition of the contralateral vertebral artery. With the exception of the patient presenting with a vertebral artery aneurysm, surgical or endovascular intervention is not indicated in asymptomatic patients who harbor suspicious radiographic findings.

Treatable vertebral artery disease may be underdiagnosed when compared to carotid disease. Patients with vertebrobasilar ischemia do represent a significant cohort of patients. Twenty-five percent of all transient ischemic attacks and ischemic strokes involve areas of the brain supplied by the vertebrobasilar circulation. For patients who experience vertebrobasilar transient ischemic attacks, disease identified in the vertebral arteries portends a 30-35% risk for stroke over a 5-year period.[9, 10, 11]  Medical refractory disease of the vertebrobasilar system carries a 5-11% risk of stroke or death at 1 year.[12]  Consequently, mortality associated with a posterior circulation stroke is high, ranging from 20-30%, and this disease entity should not be ignored.[13, 14, 15, 16]

Diagnosis

Diagnosis of vertebrobasilar ischemia begins with an accurate assessment of the presenting symptom complex. A 20 mm Hg systolic pressure drop on rapid standing is the criterion for a diagnosis of orthostatic hypotension causing low-flow in the vertebrobasilar system. An ambulatory 24-hour electrocardiogram (Holter monitor) should be performed in patients with hemodynamic ischemia because arrhythmias are a common cause of symptomatology due to decreased cardiac output associated with the arrhythmia. Echocardiography is useful to rule out significant valvular pathology that could cause brainstem hypoperfusion. 

Once a suspicion of vertebrobasilar ischemia has been entertained, only a few studies clearly ascertain vertebral anatomy.

Duplex ultrasonography is an excellent tool for detecting lesions in the carotid artery but has significant limitations in detecting vertebral artery pathology. The usefulness of duplex ultrasound lies in its ability to confirm reversal of flow within the vertebral arteries and to detect changes in flow velocity consistent with proximal stenosis. It can also diagnose great vessel pathology and confirm subclavian steal.[17]  There is great interest in ultrasound imaging of the vertebral artery for stent placement to treat vertebral artery stenosis. Changes in waveforms are helpful in detecting the pathologic processes that involve the proximal and distal neurovascular circulation.[18, 19, 20]  

Contrast-enhanced magnetic resonance angiography (MRA) with 3-dimensional (3D) reconstruction and maximum intensity projection (MIP) can provide full imaging of the vessels, including the supra-aortic trunks, the carotid and vertebral arteries, and the circle of Willis. MRI provides accurate and noninvasive visualization of the vertebral and basilar arteries and surrounding structures of the posterior fossa. Transaxial MRI can detect acute and chronic posterior fossa infarcts, which is enhanced by MRA with 3D reconstructions and MIP imaging, 

Selective subclavian and vertebral angiography remains the best test for preoperative evaluation of patients with vertebrobasilar ischemia. Catheter angiography may be necessary to prove pathology. Patients with suspected vertebral artery compression, usually by osteophytes, should undergo dynamic angiography.

Treatment

With appropriate diagnosis and surgical correction, complete resolution of hemodynamic and embolic symptoms can be achieved. Location of disease dictates the type of surgical reconstruction required. Patients with symptomatic vertebrobasilar ischemia who cannot be treated with surgery or endoluminal therapy may be treated with antiplatelet agents or long-term anticoagulation to prevent thrombosis. 

Using stents for treating a lesion of the distal V3 segment is an option for the prevention of stroke. However, the relatively small diameter of  a hypoplastic vertebral artery and the tortuous course and atherosclerotic stenosis in V1 or V2 have been known to be obstacles to conventional vertebral stenting.[21]

The main option for treating ostial lesions (V1 segment) is transposition of the proximal vertebral artery onto the common carotid artery.

Elective surgical reconstruction is very rarely undertaken within the V2 segment; however, ligation (at the C1-C2 level) and bypass to the distal (V3 segment) vertebral artery may be indicated. Extrinsic lesions can be corrected to relieve kinking or compression of the artery. The most common indication for exposure of the V3 segment of the artery is for control of hemorrhage. An alternative for traumatic injuries to the V2 segment includes coil embolization.

Reconstruction of the distal (V3 segment) vertebral artery is usually performed at the C1-C2 level. The techniques most often used to reconstruct the distal vertebral artery at this level include (1) saphenous vein bypass from the common carotid, subclavian, or proximal vertebral artery; (2) transposition of the external carotid or hypertrophied occipital artery to the distal vertebral; and (3) transposition of the distal vertebral artery to the side of the distal internal carotid artery.[22]

More distal pathology can be accessed surgically above the level of the transverse process of C1. Surgical exposure at the suboccipital segment requires resection of the C1 transverse process and part of its posterior arch. Reconstruction at this level is limited to saphenous vein bypass from the distal internal carotid artery.

The use of drug-eluting balloons (DEB) in peripheral artery disease has shown a reduction in the number of stents as well as their length after percutaneous transluminal angioplasty (PTA). Endovascular treatment is the first therapeutic option for subclavian artery occlusive lesions and generally provides positive results.[23]

Pathophysiology

The most common disease affecting the vertebral artery is atherosclerosis. Less common pathologic processes include trauma, fibromuscular dysplasia, Takayasu disease, osteophyte compression, dissections, and aneurysms. Vertebrobasilar insufficiency is an inadequate flow of blood through the posterior circulation of the brain, which is supplied by the 2 vertebral arteries that merge to form the basilar artery. The vertebrobasilar vasculature supplies blood flow to areas of the brain such as the brainstem, thalamus, hippocampus, cerebellum, occipital and medial temporal lobes.[24, 25, 26]  (See the images below.)

Selective angiogram of a right vertebral artery ps Selective angiogram of a right vertebral artery pseudoaneurysm.
An arteriogram demonstrating aneurysmal degenerati An arteriogram demonstrating aneurysmal degeneration of a left vertebral artery in the V2 segment.
True vertebral artery aneurysm (9 cm). True vertebral artery aneurysm (9 cm).

Indications for Surgery

Once the diagnosis of vertebrobasilar ischemia has been confirmed with appropriate imaging, surgical correction may be considered. The mere presence of vertebral artery stenosis in an asymptomatic patient is rarely an indication for surgery. Surgical reconstruction is based on the specific etiology. The indication for surgery in patients with hemodynamic symptoms depends on the ability to demonstrate insufficient blood flow to the basilar artery.

A single normal-caliber vertebral artery can supply sufficient blood flow into the basilar artery regardless of the status of the contralateral vessel. In this particular subset of patients, surgical intervention is indicated only in the presence of a severely stenotic (>75%) vertebral artery and an equally diseased or occluded contralateral vessel. Surgical reconstruction is not indicated in an asymptomatic patient with the aforementioned radiographic findings because these patients are well compensated from the carotid circulation through the posterior communicating vessels.

In contrast, patients with symptomatic vertebrobasilar ischemia due to emboli are candidates for surgical correction of the offending lesion regardless of the condition of the contralateral vertebral artery. As in the hemodynamic group, surgical intervention is not indicated in asymptomatic patients with suggestive radiographic findings.

In a study by Min Wu et al of predictors of 3-month and 1-year mortality In patients with vertebrobasilar artery occlusion who received endovascular treatment, the 24-hr Glasgow Coma Scale score and mechanical ventilation were found to be common predictors of 3-month and 1-year mortality, and intracranial  hemorrhage was an additional predictor of 1-year mortality.[27]

Relevant Anatomy

The posterior circulation, or vertebrobasilar system, supplies blood to the brainstem, cerebellum, and occipital lobes via paired vertebral arteries. The vertebrals converge beyond the base of the skull and form the basilar artery at the base of the pons.[28, 26] The vertebral artery is arbitrarily segmented into the following 4 parts:

  • V1 extends from the origin of the vertebral artery, where it arises from the subclavian artery up to the point at which the artery enters the C6 transverse process. The origin of the vertebral from the subclavian is the most common site for a hemodynamically significant atherosclerotic stenosis.

  • V2 lies within the cervical transverse processes (C6-C2) and is buried deep within intertransversarium muscle. The V2 segment is the site of a wide variety of disorders. External compression is most likely to occur in this segment because of osteophytes, the edge of the transverse foramina, or the intervertebral joints. Positional changes, such as rotation or extension of the neck, usually trigger compression of the vertebral artery in this segment. The V2 segment is also the most frequent site of true aneurysmal degeneration, fibromuscular diseases, and embolizing atherosclerotic plaques.

  • V3 is the extracranial segment that lies between the transverse process of the C2 and the base of the skull, where the artery enters the foramen magnum and penetrates the dura matter. This segment is infrequently affected by atherosclerosis but is vulnerable to direct trauma and stretch injuries.

  • V4 is the intracranial portion beginning at the atlanto-occipital membrane and terminating at the formation of the basilar artery. The V4 segment is devoid of adventitia; as such, open or endovascular intervention in this segment should be approached with extreme caution.

Dissections commonly occur at the base of the skull where V3 transitions to V4. This likely occurs because, here, the vertebrae allow for maximal cervical mobility near where the artery loses some of its integrity.

The anterior spinal artery arises from branches off each of the vertebral arteries just before they converge to form the basilar artery. Pontine and cerebellar arteries arise from the basilar artery before it bifurcates into the paired posterior cerebral arteries. One vertebral artery may end in a posterior inferior cerebellar artery rather than join the basilar artery.

The location of disease will dictate the type of surgical reconstruction that is required. With rare exceptions, most reconstructions of the vertebral artery are performed to treat an origin stenosis (V1 segment) or stenosis, dissection, or occlusion of its intraspinal component (V2 and V3 segments).

Contraindications

As discussed previously, a single normal-caliber vertebral artery can supply sufficient blood flow into the basilar artery regardless of the status of the contralateral vessel. In this particular subset of patients, surgical intervention is indicated only in the presence of a severely stenotic (>75%) vertebral artery and an equally diseased or occluded contralateral vessel. Surgical reconstruction is not indicated in an asymptomatic patient with the aforementioned radiographic findings, because these patients are well compensated from the carotid circulation through the posterior communicating vessels.

Patients with symptomatic vertebrobasilar ischemia who are not amenable to surgery or investigational endoluminal therapy may be treated medically with long-term anticoagulation to prevent thrombosis.

 

Workup

Imaging Studies

A precise diagnosis of vertebrobasilar ischemia begins with an accurate assessment of the presenting symptom complex. This must be followed by efforts to exclude other causes for patient symptoms. These other medical conditions include inappropriate use of antihypertensive medications, cardiac arrhythmias, anemia, brain tumors, and benign vertiginous states. A thorough investigation generally includes a workup for inner-ear pathology and ruling out cardiac arrhythmias, internal carotid artery stenosis/occlusion, and the inappropriate use of medications.

Any systemic mechanism that decreases the mean pressure of the basilar artery may be responsible for hemodynamic symptomatology. Affected individuals may or may not have concomitant vertebral artery stenosis or occlusion. Certain prescription medications can mimic vertebrobasilar ischemia; as such, patient medications require a thorough review. Excessive use of antihypertensive medications is the most common cause of posterior circulation symptoms and can also cause hemodynamic posterior circulation ischemia by decreasing the perfusion pressure and inducing severe orthostatic hypotension.

The evaluation of patients with posterior circulation ischemia should include numerous specific steps. The precise circumstances associated with development of symptoms should be ascertained. Symptoms often appear on standing in older individuals with poor sympathetic control of their venous tone, which causes excessive pooling of blood in the veins of the leg. This is particularly common in patients with diabetes who have diminished sympathetic venoconstrictor reflexes. A 20 mm Hg systolic pressure drop on rapid standing is the criterion for a diagnosis of orthostatic hypotension causing low-flow in the vertebrobasilar system. In such cases, the pressure drop triggers the symptoms of posterior circulation ischemia.

A cardiac abnormality is another common cause of brainstem ischemia, especially in the elderly, and thorough evaluation should include monitoring for arrhythmias and a thorough assessment heart valve function. An ambulatory 24-hour electrocardiogram (Holter monitor) should be performed in patients with hemodynamic ischemia because arrhythmias are a common cause of symptomatology due to decreased cardiac output associated with the arrhythmia. Patients with ischemia secondary to arrhythmias often report the association of palpitations with the appearance of symptoms. Echocardiography is useful to rule out significant valvular pathology that could cause brainstem hypoperfusion.

Investigation must be undertaken to exclude inner-ear pathology, including rare cerebellar-pontine angle tumors. In addition, neurologic evaluation should be considered to rule out benign vertiginous states.

Because patients often present with a combination of cerebral hemispheric and posterior symptoms, investigation of the great vessels and the carotid circulation is usually warranted. An important aspect of the history is identifying triggering events such as positional or postural changes. This is followed by a thorough physical examination, which includes palpation, auscultation, pulse exam, and comparative arm blood pressures (recumbent and standing).

Physical examination can alert the physician to the possibility of a subclavian steal in patients with brachial pressure differences greater than 25 mm Hg or with diminished or absent pulses in one arm. The diagnosis of reversal of vertebral artery flow can be made accurately by noninvasive indirect methods and demonstrated directly by duplex imaging of the reversal of flow in the vertebral artery.

Patients may relate their symptoms to turning or extending their heads. Frequently, the mechanism is extrinsic compression of the vertebral artery, usually the dominant or the only one, by arthritic bone spurs.[7] To differentiate this mechanism from dizziness or vertigo secondary to labyrinthine disorders that appear with head or body rotation, the patient should attempt to reproduce the symptoms by turning the head slowly and then repeating the maneuver, but this time briskly, as when shaking the head from side to side. In labyrinthine disease, the sudden inertial changes caused by the latter maneuver result in immediate symptoms and nystagmus. Conversely, in extrinsic vertebral artery compression, a short delay occurs before the patient fears for his or her balance.

Once a suspicion of vertebrobasilar ischemia has been entertained, only a few studies clearly ascertain vertebral anatomy.

Ultrasonography

Duplex ultrasonography is an excellent tool for detecting lesions in the carotid artery, but it has significant limitations when used to detect vertebral artery pathology. Direct visualization of the second portion of the vessel is difficult because of its intraosseous course through the transverse processes of C2 to C6. The usefulness of duplex ultrasound lies in its ability to confirm reversal of flow within the vertebral arteries and detect flow velocity changes consistent with a proximal stenosis. In addition, this imaging may diagnose great vessel pathology and confirm subclavian steal.[17]

Zhang et al, in a study of the use of color Doppler ultrasound in 54 patients with intervertebral stenosis, found that color Doppler can reliably identify intervertebral stenosis and can be used as a preliminary reference for evaluating the condition.[19]

In a study of  218 cases of stenosis with vertebral artery origins in 139 patients, by Rice et al, ultrasound showed a sensitivity of 85.7%  and specificity of 99.5%for occlusion.  A mean flow velocity (MFV) cutoff value of 44 cm/s corresponded to 77% sensitivity and 70% specificity to detect vertebral artery origin stenosis >50%, and an MFV cutoff value of 60 cm/s corresponded with 70% sensitivity and 82% specificity to predict 70-99% stenosis. A peak systolic velocity (PSV) of 97 cm/s corresponded with a 72% sensitivity and 70% specificity to detect >50% stenosis, and a PSV cutoff value of 110 cm/s corresponded with 80% sensitivity and 72% specificity to predict 70-99% stenosis.[20]

MRI

Contrast-enhanced magnetic resonance angiography (MRA) with 3-dimensional (3D) reconstruction and maximum intensity projection (MIP) imaging techniques provide full imaging of the vessels, including the supra-aortic trunks, the carotid and vertebral arteries, and the circle of Willis. MRA does tend to "overcall" stenoses, especially those lesions found at the origin of the vertebral artery in the V1 segment. MRI allows for accurate and noninvasive visualization of the vertebral and basilar arteries, as well as the surrounding posterior fossa structures.

Brain stem infarctions are often missed by CT scan because they tend to be small and the resolution of the CT scan in the brain stem is poor. Transaxial MRI is also invaluable in detecting acute and chronic posterior fossa infarcts, as depicted in the first image below. This has been enhanced by the development of MRA with 3D reconstructions and MIP imaging, as depicted in the second image below.

Magnified view of MRI of the brain. The arrow deno Magnified view of MRI of the brain. The arrow denotes the site of a posterior fossa infarction.
Magnetic resonance angiography (MRA) with 3-dimens Magnetic resonance angiography (MRA) with 3-dimensional reconstruction of the extracranial and intracranial vertebral and carotid arterial system. The arrow denotes the right vertebral artery.

Arteriography

Selective subclavian and vertebral angiography remains the best test for preoperative evaluation of patients with vertebrobasilar ischemia. The most common site of disease, the vertebral artery origin, may not be well imaged with ultrasonography, MRA, or CT angiography, and catheter angiography may be necessary to prove pathology. Lesions at the origin of the vertebral artery, which are often the result of "spill-over" from the subclavian vessel, can, in some cases, only be displayed using oblique projections that are not part of standard arch evaluation.

Patients with suspected vertebral artery compression, usually by osteophytes, should undergo dynamic angiography, which incorporates provocative positioning. This is performed either with the patient sitting up, by means of bilateral brachial injections, or with the patient supine in the Trendelenburg position with the head resting against a block. In these positions, which exert axial compression of the cervical vertebrae, the angiographer should obtain the specific rotation or extension of the head that provokes the symptoms. When the patient is rendered symptomatic, the arteriographic injection demonstrates the extrinsic compression that developed with the head rotation or extension.[29]

Delayed imaging should be performed to demonstrate reconstitution of the extracranial vertebral arteries through cervical collaterals, such as the occipital artery or the thyrocervical trunk.[22] Because of this collateral network, the distal vertebral and basilar arteries usually remain patent despite a proximal vertebral artery occlusion. A patent V3 segment can be exploited as a distal target for reconstruction. (See the image below.)

Selective angiography of the left subclavian arter Selective angiography of the left subclavian artery demonstrating collateral flow to a patent distal left vertebral artery via the thyrocervical trunk.
 

Treatment

Surgical Therapy

Previous experience has shown that with appropriate diagnosis and surgical correction, complete resolution of hemodynamic and embolic symptoms can occur predictably. Vertebral artery reconstruction can be performed successfully with fewer ischemic complications than carotid artery surgery and with durable long-term results.[30, 31] The location of disease dictates the type of surgical reconstruction required.

Patients with symptomatic vertebrobasilar ischemia who cannot be treated with surgery or endoluminal therapy may be treated medically with antiplatelet agents or with long-term anticoagulation to prevent thrombosis.

The main option for treating offending ostial lesions (V1 segment) is transposition of the proximal vertebral artery onto the common carotid artery.

A retrospective study of 30 patients with dominant atherosclerotic ostial vertebral artery stenosis confirmed the feasibility of deploying drug-eluting balloon mounted stents (DES) for endovascular treatment of ostial vertebral artery stenosis, with low periprocedural risk and low medium-term rates of restenosis. One technical complication (stent migration) and 3 (10%) minor periprocedural complications occurred. Complications included one asymptomatic ischemic infarct in the posterior circulation, one femoral artery thrombosis, and one post-procedure altered mental status secondary to contrast induced neurotoxicity.[32]

Elective surgical reconstruction is very rarely undertaken within the V2 segment; however, ligation (at the C1-C2 level) and bypass to the distal (V3 segment) vertebral artery may be indicated. Extrinsic lesions can be corrected to relieve kinking or compression of the artery. The most common indication for exposure of the V3 segment of the artery is for control of hemorrhage. An alternative for traumatic injuries to the V2 segment includes coil embolization.

Reconstruction of the distal (V3 segment) vertebral artery is usually performed at the C1-C2 level. The techniques most often used to reconstruct the distal vertebral artery at this level include (1) saphenous vein bypass from the common carotid, subclavian, or proximal vertebral artery; (2) transposition of the external carotid or hypertrophied occipital artery to the distal vertebral; and (3) transposition of the distal vertebral artery to the side of the distal internal carotid artery.[22]

More distal pathology can be accessed surgically above the level of the transverse process of C1. Surgical exposure at the suboccipital segment requires resection of the C1 transverse process and part of its posterior arch. Reconstruction at this level is limited to saphenous vein bypass from the distal internal carotid artery.

Exposure and transposition of the vertebral artery into the common carotid artery

The approach to the proximal vertebral artery is the same as the approach for a subclavian to carotid transposition. The patient is positioned in a slight chair position to decrease venous pressure and to allow optimal visualization of the anatomy at the base of the neck. The incision is placed transversely about a finger’s breadth above the clavicle and directly over the 2 heads of the sternocleidomastoid muscle. Subplatysmal skin flaps are created and dissection is carried down directly between the two bellies of the sternocleidomastoid. The omohyoid muscle is divided with electrocautery. The jugular vein is mobilized laterally, and the vagus nerve is retracted medially with the common carotid artery. The carotid should be exposed proximally as far as possible and well behind the ipsilateral clavicle.

On the left side, the thoracic duct is divided between ligatures. Accessory lymph ducts, often seen on the right side of the neck, are also meticulously identified, ligated, and divided. The entire dissection is confined medial to the prescalene fat pad that covers the scalenus anticus muscle and phrenic nerve. These structures are left unexposed lateral to the field. The vertebral vein emerges from the angle formed by the longus colli and scalenus anticus and overlies the proximal vertebral artery. It is ligated and divided. The vertebral and subclavian vessels are now visible.

Identifying and avoiding injury to the adjacent sympathetic chain is important. The vertebral artery is dissected superiorly up to the level of the tendon of the longus colli and inferiorly to its origin from the subclavian artery, exposing 2-3 centimeters of length. The vertebral artery is freed from the sympathetic trunk resting on its anterior surface without damaging the trunk or the ganglionic rami. After dividing the vertebral artery at its origin, it can be transposed to a position anterior to the sympathetics without causing them harm.

Once the artery is fully exposed, an appropriate site for reimplantation in the common carotid artery is selected. The patient is given systemic heparin. The distal portion of the V1 segment of the vertebral artery is clamped below the edge of the longus colli. The proximal vertebral artery is ligated immediately above the stenosis at its origin using a small monofilament suture as a transfixion stitch. The artery is divided at this proximal level.

The carotid artery is then cross-clamped. An elliptical 5-7 mm arteriotomy is created in the posterolateral wall of the common carotid artery with an aortic punch. The anastomosis is performed in parachute fashion with continuous 7-0 polypropylene suture, avoiding any tension on the vertebral artery, which may easily tear. (See the video below.)

Anastomosis.

Before completion of the anastomosis, standard flushing maneuvers are performed; the suture is tied; and flow is reestablished. (See the image below.)

An arteriogram following a proximal vertebral to c An arteriogram following a proximal vertebral to carotid artery transposition.

Exposure of the V2 segment of the vertebral artery

The V2 segment is rarely surgically accessed because of its interosseous position. Direct exposure usually requires resection of the transverse processes of the cervical vertebrae. As such, control may be best affected with proximal and distal ligation of the artery in V1 and V3 segments or via endoluminal coil embolization.

V3 exposure and distal vertebral artery reconstruction

The skin incision is placed in the upper neck anterior to the sternocleidomastoid muscle similar to the incision used for carotid endarterectomy. The dissection proceeds between the jugular vein and the anterior edge of the sternocleidomastoid, exposing the retrojugular portion of the spinal accessory nerve. The nerve is followed proximally as it crosses in front of the jugular vein and the transverse process of C1. Next, levator scapula muscle is identified by removal of the fibrofatty tissue overlying it. The spinal accessory nerve must be protected from undue stretch during this portion of the dissection.

Once the anterior edge of the levator muscle is exposed, the anterior ramus of C2 is visible. This nerve is easily identifiable and marks the accessible segment of the vertebral artery. With the ramus as a guide, a right-angle clamp is slid under the levator scapula and over the ramus, and the muscle is elevated. The muscle is transected from its insertion on the C1 transverse process. The C2 ramus divides into 3 branches after crossing the vertebral artery. The nerve trunk should be cut before it branches. Once the ramus has been divided, the vertebral artery can easily be identified. Division of the C2 ramus may leave the patient with minor posterior scalp numbness but is otherwise a benign manuever. The artery is freed from the surrounding venous plexus using bipolar cautery.

Once the vertebral artery is exposed circumferentially at this level, the common carotid artery is dissected and prepared as inflow for a bypass graft. The location selected for the proximal anastomosis of the bypass graft should not be too close to the bifurcation because cross-clamping at this level may fracture underlying atheroma. Because the distal anastomosis is completed first, a valveless segment of vein or a radial artery conduit facilitates back-bleeding of the vertebral artery for purposes of flushing debris.

The patient is administered intravenous heparin. The vertebral artery is elevated gently and controlled using a small J-clamp. This isolates a short segment for an end-to-side anastomosis. The vertebral artery is opened longitudinally over a short length adequate to accommodate the spatulated end of the bypass conduit. The end-to-side anastomosis is completed with continuous 8-0 monofilament suture. A vascular clamp is placed in the vein graft proximal to the anastomosis, the J-clamp is removed, and flow is reestablished through the vertebral artery.

The proximal end of the graft is passed behind the jugular vein and in proximity to the side of the common carotid artery. The common carotid artery is then cross-clamped; an elliptical arteriotomy is made with an aortic punch; and after cutting to appropriate length, the proximal end of the graft is anastomosed end-to-side to the common carotid artery. Before the anastomosis is completed, standard flushing maneuvers are performed. The vertebral artery can be occluded with a clip placed immediately below the anastomosis to create a functional end-to-end anastomosis. This maneuver should be performed to avoid competitive flow or the potential for recurrent emboli.

When no suitable conduit can be identified, the external carotid can be debranched and used as an autograft to the distal vertebral artery. Alternatively, with appropriate exposure and length, the vertebral artery can be transposed, end-to-side, into the internal carotid artery.

Endovascular therapy

Endovascular treatment of vertebral artery disease, usually with stent placement, has gained favor as an alternative to surgery. Endovascular access to the vertebral artery is relatively straightforward. The procedure can be performed under local anesthesia, enabling continuous neurologic monitoring of the patient. 

Endovascular therapy outcomes of procedures performed with general anesthesia and conscious sedation have reported worse outcomes for patients treated with general anesthesia, but the reported results remain controversial as the evidence is generally from small retrospective studies.[33, 34]  Results of randomized, controlled trials have found comparable results for the 2 anesthesia approaches.[35, 36]

Most cases are performed from a femoral approach, although transbrachial and transradial access has also been used. The stenotic lesions are crossed and treated with 0.014-inch or 0.018-inch guidewires and small coronary-diameter balloons and stents. Procedures can be performed with or without the assistance of embolic protection, although most vertebral arteries are too small to accommodate most distal protection devices.

The use of drug-eluting balloons (DEB) in peripheral artery disease has shown a reduction in the number of stents as well as their length after percutaneous transluminal angioplasty (PTA). Endovascular treatment is the first therapeutic option for subclavian artery occlusive lesions and generally provides positive results.[23, 37]

Using stents for treating a lesion of the distal V3 segment is an option for the prevention of stroke. However, the relatively small diameter of  a hypoplastic vertebral artery and the tortuous course and atherosclerotic stenosis in V1 or V2 have been known to be obstacles to conventional vertebral stenting.[21]

In a study by Li et al of 238 patients with ischemic stroke caused by intracranial vertebrobasilar stenosis (IVBS), the rate of severe stroke at 1 year after percutaneous transluminal angioplasty and stenting (PTAS)  was 0%, while that after standardized medical treatment (SMT) was 9.7%[38]

Postoperative details and follow-up

Intraoperative completion imaging using digital angiography is useful and should be considered for all types of vertebral artery reconstruction. Reparable technical flaws may be identified, and repair can prevent reconstruction failure.

Postoperatively, patients should be monitored and should receive long-term antiplatelet therapy (eg, aspirin).

Follow-up care and monitoring are primarily based on clinical assessment of recurrent symptoms. The presence of new symptoms consistent with vertebrobasilar ischemia mandates imaging studies as previously outlined.

 

Complications

The perioperative complication rates differ for proximal versus distal vertebral artery repairs. The technically easier proximal operations have been reported to have a combined morbidity/mortality rate of 0.9%. Distal reconstructions have a combined morbidity/mortality rate of 3-4%.[39]

Risk is generally increased when patients undergo a combination of both vertebral and carotid revascularization. Perioperative complications for proximal V1 reconstruction include immediate thrombosis (1.4%), vagus and recurrent laryngeal nerve palsy (2%), Horner syndrome (8.4-28%), lymphocele (4%), and chylothorax (5%),[40] as well as stroke or hematoma in rare cases. The occurrence of ptosis (drooping of the eyelid) on the operative side is a known complication of proximal vertebral artery reconstructions. This condition is usually temporary and is attributed to a traction injury of the lower cervical sympathetic nerves. For distal reconstructions, complications include stroke, hemorrhage, thrombosis, and nerve injury (spinal accessory nerve).

Periprocedural risks for endoluminal therapies include access complications, distal embolization and stroke, arterial rupture, stent malposition, and vessel thrombosis or dissection. Later, restenosis and stent fracture are not uncommon. Late stent fracture with concomitant in-stent restenosis appears to also be a problem plaguing endoluminal therapies that target lesions at the vertebral artery origin. Anatomically, the vertebral artery originates from the subclavian artery at a near right angle. In addition, the first portion of the subclavian artery has relative mobility, while the vertebral artery becomes fixed as it passes into the transverse foramen of C6. This particular anatomy may create unique mechanical forces that make stent fracture more likely than in other parts of the body. (See the image below.)

Vertebral stent fracture with in-stent restenosis. Vertebral stent fracture with in-stent restenosis.

Outcome and Prognosis

Open surgical intervention

Results following both proximal and distal vertebral artery reconstructions are generally equal to or better than those reported for other forms of cerebrovascular revascularizations. In experienced hands, the combined stroke and death rates are 4% or less. Long-term patency of the reconstructions is excellent. More than 80% of patients experience symptom relief following surgical reconstruction.

Long-term outcomes of open revascularization for vertebral artery disease are generally excellent, with high stroke-free survival rates and patency as high as 90% at 10 years.[41, 42] Although the number of studies is limited and these reports consist of only medium-sized case series, the results seen with open vertebral reconstruction should be considered benchmarks upon which endoluminal therapy should be compared.

Endovascular intervention

Despite high technical success rates, angioplasty alone appears to have unacceptably high rates of restenosis. Adjuvant stent placement seems to add to the clinical durability but adds inherent morbidity such as malposition and potential stent fracture.

Eighteen patients with extracranial vertebral artery disease in The Stenting of Symptomatic Atherosclerotic Lesions in the Vertebral or Intracranial Arteries (SSYLVIA) Trial underwent angioplasty and stenting. Technical success (determined as less than 50% residual stenosis following treatment), was achieved in 17 (94%) of the 18 patients. There were no periprocedural neurologic complications. The investigators, however, reported 6-month restenosis rates of 50%. These recurrences were symptomatic in 39% of cases.[43]

In their series of 105 patients who underwent endovascular stenting for symptomatic vertebral artery disease, Jenkins et al achieved 100% radiographic improvement (residual stenosis ≤30%). The authors reported immediate (30 day) periprocedural risk of death of 1% and periprocedural complication rate of 4.8%. Complications included transient ischemic attack, flow-limiting dissection, hematoma, and catheter-access-site problems. At 1 year of follow-up, 6 patients had died and 5 had experienced a vertebrobasilar stroke. At approximately 2.5 years of follow-up, 70% of patients remained symptom free, but 13% of patients had restenosis requiring re-treatment.[44]

A Cochrane review identified 313 endovascular interventions for vertebral artery stenosis, with just over half of the interventions using stent placement as part of the treatment of vertebrobasilar stenosis. The 30-day risk of  transient ischemic attack (TIA) or stroke was 3.2%, and the death rate was also 3.2%.[45] The technical success rate was 95%.

As with open surgical techniques, retrospective case series exist for endoluminal therapies for the treatment of vertebral artery disease. In a subset of 16 patients treated in the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS 2001), endoluminal therapy was compared with best medical care for symptomatic vertebral artery stenosis. No 30-day strokes or deaths were reported in either group, although 2 of 8 patients who underwent endoluminal therapy experienced transient ischemic symptoms. Furthermore, with a mean follow-up of 4.5 years, no posterior circulation strokes were noted in either group.[46]

Ogilvy et al reported a series of patients with 21-month follow-up in whom drug-eluting stents were used in vertebral artery origin stenoses. They found that the incidence of in-stent restenosis (>50% diameter) was 38% for patients who received non-drug-eluting stents versus 17% for those who received drug-eluting stents.[47] Other reports also suggest decreased restenosis rates with drug-eluting stents.[48, 49] Treatment with drug-eluting stents requires long-term dual antiplatelet therapy.

The Vertebral Artery Stenting Trial (VAST) investigated the safety and feasibility of stenting of symptomatic vertebral artery stenosis of at least 50%, with 57 patients being assigned to receiving stents and 58 to receiving medical treatment alone. Three patients in the stenting group experienced vascular death, myocardial infarction, or any stroke within 30 days after the start of treatment (5%) versus 1 patient in the medical treatment group (2%). During a median follow-up of 3 years, 7 patients (12%) in the stenting group and 4 (7%) in the medical treatment group had a stroke in the area of the symptomatic vertebral artery. Eleven patients (19%) in the stenting group and 10 (17%) in the medical treatment group ultimately experienced vascular death, myocardial infarction, or any stroke. In total, after complete follow-up, there were 60 serious adverse events (8 strokes) in the stenting group and 56 (7 strokes) in the medical treatment group.[50, 51, 52]

In a study by Min Wu et al of predictors of 3-month and 1-year mortality In patients with vertebrobasilar artery occlusion who received endovascular treatment, the 24-hr Glasgow Coma Scale score and mechanical ventilation were found to be common predictors of 3-month and 1-year mortality, and intracranial  hemorrhage was an additional predictor of 1-year mortality.[27]

Future and Controversies

Atherosclerotic vertebral artery disease is an underdiagnosed cause of posterior circulation ischemia. Revascularization of the vertebral artery is often a viable option and should be considered in symptomatic patients in whom medical therapy has failed. Modern surgical advances have resulted in a safe and durable mode of therapy for patients with documented symptomatic vertebrobasilar ischemia. Both surgical and endoluminal approaches to treating vertebral artery pathology may be considered and the choice between the two is often determined by the anatomic location of the lesion being intervened upon. Such consideration requires a complete understanding of the vertebrobasilar anatomy using appropriate imaging studies.

Open techniques for revascularization of the vertebral artery have proven clinical durability and acceptable surgical morbidity in experienced hands. Endoluminal techniques, which have gained momentum over the past decade, have shown clinically feasible but have yet to deliver on durability benchmarks set by open surgical revascularization. As such, vertebral artery stenting should be reserved to select centers with high volume experience that have established acceptable outcomes in both clinical success and safety. For each individual patient who suffers from medically refractive vertebrobasilar ischemia, practitioners must carefully balance the risks of surgery versus the limitations of endoluminal intervention before recommending intervention.