Vertebral artery revascularization

INTRODUCTION — Many pathologic processes, including atherosclerosis, trauma, fibromuscular dysplasia, dissections, and aneurysm, among others, can lead to symptoms referable to the vertebral artery. Atherosclerotic vertebral artery disease is often underdiagnosed as a cause of posterior circulation ischemia because of the frequently vague nature of patient presentation. Clinicians may be reluctant to pursue pathologic diagnosis or to recommend treatment, but revascularization of the vertebral artery should be considered in symptomatic patients for whom medical therapy has failed. Intervention is not indicated in asymptomatic patients.

Both surgical and endoluminal approaches are options for treating vertebral artery pathology, with the choice between the two often determined by the anatomic location of the lesion. Clinicians must carefully balance the risks of surgery versus the limitations of endoluminal intervention before proceeding. Open techniques for revascularization of the vertebral artery have proven clinical durability and acceptable surgical morbidity in experienced hands. Endovascular techniques, which have gained momentum over the last decade, are clinically feasible but have yet to deliver on durability benchmarks set by open surgical revascularization. As such, vertebral artery stenting should be reserved for select centers with high-volume experience that have established acceptable outcomes in both clinical success and safety.

The indications, evaluation and preparation, and methods of vertebral artery revascularization are reviewed here.

ANATOMIC CONSIDERATIONS — The vascular supply to the brain is divided into the anterior and posterior circulations originating from the carotid and vertebral arteries, respectively (figure 1). The circle of Willis connects the anterior and posterior circulations but is completely intact and symmetric in only approximately 20 percent of individuals [1]. The anatomic variability of the collateral circulation helps explain the variability of clinical presentations of patients with vertebral artery disease.

The vertebral arteries most commonly originate from the subclavian arteries. They originate directly from the aortic arch in 3 to 5 percent of individuals [2]. The vertebral arteries are commonly asymmetric in diameter, and it is not uncommon for one vertebral artery to be atretic, a finding that is slightly more common on the left than the right [3]. In some patients, an atretic vertebral artery can perfuse an isolated ipsilateral posterior inferior cerebellar artery.

The vertebral artery traverses the neck anterior to the scalene muscle, enters the vertebral foramina of the sixth cervical vertebra, and exits the transverse foramina of the second cervical vertebra. The vertebral arteries are traditionally divided into four segments (figure 2).

●The V1 segment originates at the posterior surface of the first segment of the subclavian artery and extends to the transverse foramina of either the fifth or sixth cervical vertebrae.

●The V2 segment courses through the bony canal of the transverse foramina from C6 to C2 and is buried deep within intertransversarii muscle.

●The V3 segment continues as the artery exits the transverse foramina at C2 and ends as the vessel passes through the foramen magnum and penetrates the dura matter. At this site, the vertebrae allow for maximal cervical mobility, which, in combination with a loss of some of the vertebral artery structural integrity, makes this region vulnerable to injury and dissection.

●The V4 segment is entirely intracranial, beginning at the atlantooccipital membrane and terminating as the two vertebrals converge to form the basilar artery. The V4 segment is vulnerable to direct trauma and stretch injuries. The V4 segment is devoid of adventitia; as such, any intervention in the segment should be approached with extreme caution.

VERTEBROBASILAR DISEASE

Etiology — Atherosclerosis is the most common disease affecting the vertebral artery. Less common pathologic processes include trauma, fibromuscular dysplasia, Takayasu's disease, osteophyte compression, vertebral artery dissection, and other arteritides. Aneurysms of the vertebral artery can also occur. True extracranial aneurysms are virtually always found in the setting of a connective tissue disorder (image 1) [4]. False aneurysms may or may not be related to a connective tissue disorder but usually follow arterial dissection (spontaneous, trauma) [5]. Dissections commonly occur at the base of the skull. (See "Posterior circulation cerebrovascular syndromes" and "Cerebral and cervical artery dissection: Clinical features and diagnosis" and "Blunt cerebrovascular injury: Mechanisms, screening, and diagnostic evaluation".)

Ischemia of the posterior cerebral circulation related to atherosclerotic vertebral artery disease appears to be less common compared with pathologies involving the anterior circulation. However, vertebral artery disease may be underdiagnosed in comparison with carotid disease and is potentially treatable. Patients with vertebrobasilar ischemia 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. Disease of the vertebrobasilar system that is refractory to medical management carries a 5 to 11 percent risk of stroke or death at one year [6]. For patients who experience vertebrobasilar transient ischemic attacks, disease identified in the vertebral arteries is associated with a 30 to 35 percent risk for stroke over a five-year period [7-9]. Mortality associated with a posterior circulation stroke is high, ranging from 20 to 30 percent [6,10-12].

Mechanisms of ischemia — In general, the mechanisms of ischemia can be divided into those that are hemodynamic and those that are embolic.

Hemodynamic — 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. Any systemic mechanism that decreases the mean pressure of the basilar artery may be responsible for hemodynamic symptomatology (table 1). Symptoms from hemodynamic mechanisms tend to be short-lived, repetitive, almost predictable, and more of a nuisance than a danger. Ischemia from hemodynamic mechanisms rarely results in tissue infarction. Such affected individuals may or may not have concomitant vertebral artery stenosis or occlusion.

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 (figure 1). Alternatively, hemodynamic ischemic symptoms may be due to proximal subclavian artery occlusion and the syndrome of subclavian/vertebral artery steal. (See "Subclavian steal syndrome", section on 'Introduction' and "Upper extremity atherosclerotic disease" and "Upper extremity atherosclerotic disease", section on 'Subclavian steal'.)

Symptoms upon standing are common 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 mmHg systolic pressure drop on rapid standing is a criterion for a diagnosis of orthostatic hypotension causing low flow in the vertebrobasilar system. In these cases, the pressure drop triggers the symptoms of posterior circulation ischemia. In some patients, the cause of the drop in mean arterial pressure can be corrected simply by readjusting their antihypertensive regimen, by the administration of antiarrhythmic drugs, or by inserting a cardiac pacemaker. In patients with orthostatic hypotension, the problem may not respond to medical treatment and only the reconstruction of a diseased or occluded vertebral artery will render the patient asymptomatic in the face of persistent oscillations of blood pressure secondary to poor sympathetic venous tone.

Rheologic factors, such as increased viscosity (polycythemia) and decreased oxygen-carrying capacity (anemia), may exacerbate or cause posterior circulation ischemia in patients with severe vertebral artery occlusive disease.

Embolism — 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. The majority of posterior circulation strokes that result from arterial embolization occur as a result of intracranial arterial pathology. It is estimated that up to one third of episodes of vertebrobasilar ischemia are caused by distal embolization from plaques or mural lesions of the subclavian, vertebral, and/or basilar arteries [13]. Those of extracranial origin usually arise from one of the vertebral arteries with atherosclerosis at the origin the most common source. Rarely, the innominate or subclavian vessels are the source [13].

Patients with embolic mechanisms have varied presentations, and events are completely unpredictable. Infarctions in the vertebrobasilar distribution are most often the result of embolic events even though fewer patients have an embolic compared with hemodynamic mechanism for vertebrobasilar ischemia. Patients with embolic ischemia often develop multiple and multifocal infarcts in the brain stem, cerebellum, and, occasionally, posterior cerebral artery territory.

INDICATIONS — Indications for vertebral revascularization depend upon the etiology of disease. (See "Posterior circulation cerebrovascular syndromes", section on 'Extracranial vertebral arteries'.)

●Hemodynamic symptoms and bilateral significant vertebral artery stenosis – For patients with persistent hemodynamic symptoms, the minimal anatomic requirement to justify vertebral artery revascularization is a greater than 60 percent diameter stenosis in both vertebral arteries if both are patent and complete, or a >60 percent unilateral stenosis in the dominant vertebral artery if the contralateral 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.

●Symptomatic embolism suspected to be from a vertebral lesion – For patients with posterior circulation ischemia due to microembolism and an appropriate lesion in a vertebral artery, the potential source of the embolus needs to be eliminated. A patient would be considered a candidate for revascularization if symptoms persist or recur despite optimal medical therapies (eg, antithrombotic agents, statins, and other risk factor treatment), regardless of the status of the contralateral vertebral artery. (See "Overview of secondary prevention for specific causes of ischemic stroke and transient ischemic attack", section on 'Extracranial vertebral artery stenosis'.)

●Vertebral artery aneurysm – Symptomatic vertebral artery aneurysm should be repaired, as well as asymptomatic aneurysm larger than 1.5 cm.

Contraindications — With the exception of the patient presenting with a vertebral artery aneurysm (discussed in the prior section), surgical or endovascular interventions are not indicated for asymptomatic patients.

EVALUATION — Stenotic or occlusive vertebral lesions are common arteriographic findings in later years of life, and dizziness is a common complaint. The presence of both cannot necessarily be assumed to have a cause-effect relationship. Most patients are well compensated, usually from the carotid circulation through the circle of Willis (figure 1). (See "Approach to the patient with dizziness".)

Prior to considering vertebral artery revascularization, the vascular surgeon or interventionalist must correlate symptoms with anatomic pathology, usually together with a neurologist, to ensure that revascularization has a high likelihood of success in relieving the patient's symptoms. (See 'Complications' below.)

●Confirm that the clinical features are consistent with vertebrobasilar insufficiency. Physical examination may support the diagnosis or suggest another etiology. (See 'History and physical' below.)

●Exclude other causes for patient symptoms (table 2).

History and physical — Symptoms associated with posterior circulation ischemia are nonspecific. 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, drop attacks, diplopia, perioral numbness, alternating paresthesia, tinnitus, dysphasia, dysarthria, and ataxia. When patients present with two or more of these symptoms, vertebrobasilar ischemia is likely the cause. The precise circumstances associated with development of symptoms should be determined. (See "Posterior circulation cerebrovascular syndromes".)

Certain prescription medications can mimic vertebrobasilar ischemia; as such, patient medications require 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. (See 'Hemodynamic' above.)

An important aspect of evaluating such a patient 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). Brachial pressure differences greater than 25 mmHg or with diminished or absent pulses in one arm can alert the physician to the possibility of a subclavian steal.

Patients may relate their symptoms to turning or extending their heads. Frequently, the mechanism of extrinsic compression of the vertebral artery is arthritic bone spurs compressing, usually of a dominant or single vertebral artery [14]. To differentiate this mechanism from dizziness or vertigo secondary to labyrinthine disorders that appear with head or body rotation, the patient should be asked 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.

Imaging — Vascular imaging is necessary to identify the vertebral artery lesion. Many patients may present to the vascular surgeon with studies in hand, and if these are of good quality, repeat studies are not needed. We obtain arteriography and duplex ultrasound. If magnetic resonance (MR) angiography is chosen, we will often include MR imaging of the brain.

Vascular imaging — In addition to identifying the site and characterizing the vertebral lesion, investigation of the great vessels and the carotid circulation is usually warranted since patients often present with a combination of cerebral hemispheric and posterior symptoms.

Selective subclavian and vertebral arteriography remains the best test for preoperative evaluation of patients with vertebrobasilar ischemia. The most common site of disease, the vertebral artery origin (V1), may not be well imaged with ultrasound or MR or computed tomographic (CT) arteriography. Conventional catheter-based arteriography may be necessary to detect pathology at this vascular site. Lesions at the origin of the vertebral artery, oftentimes 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 arteriography, 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 Trendelenburg's position with the head resting against a block (femoral access), which mimics the effects of the weight of the head on the spine. In these positions, intended to 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 will demonstrate the extrinsic compression that developed with the head rotation or extension [15].

Delayed imaging should be performed to demonstrate reconstitution of the extracranial vertebral arteries through cervical collaterals, such as the occipital artery (picture 1) or the thyrocervical trunk (image 2). Because of this collateral network, the distal vertebral and basilar arteries will usually remain patent despite a proximal vertebral artery occlusion. A patent V3 segment can be exploited as a distal target for reconstruction.

Contrast-enhanced MR angiography with three-dimensional reconstruction and maximum image intensity (MIP) techniques provides full imaging of the supraaortic trunks, the carotid and vertebral arteries, and the circle of Willis. MR angiography is less invasive than contrast arteriography but tends to overestimate the degree of stenosis, particularly lesions at the origin of the vertebral artery in the V1 segment.

Duplex ultrasound is limited in its ability to detect vertebral artery pathology. The first portion (V1) is shadowed by the overlying clavicle, and the second portion (V2) is difficult to image due to its intraosseous course through the transverse processes of C2 to C6. Although the third and fourth portion can be imaged, a skilled ultrasonography is needed, and these segments are rarely seen in their entirety. The usefulness of duplex ultrasound lies in its ability to detect flow velocity changes consistent with a proximal vertebral stenosis (V1), and reversal of flow within the vertebral arteries confirms subclavian steal, as well as identifying concomitant carotid pathology [16]. (See "Subclavian steal syndrome", section on 'Initial vascular imaging' and "Evaluation of carotid artery stenosis" and "Upper extremity atherosclerotic disease", section on 'Physical examination'.)

Cerebral imaging — If the patient's symptoms are clearly ischemic and associated with an appropriate lesion on vascular imaging, cerebral imaging may not be needed. But if there is any question, investigation must be undertaken to exclude posterior fossa stroke, inner-ear pathology, and rarer cerebellar-pontine angle tumors. In addition, neurologic evaluation to rule out benign vertiginous states should be considered.

Transaxial MRI images can readily diagnose both acute and chronic posterior fossa infarcts. 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.

Cardiac evaluation — A cardiac abnormality may be the next most common cause of brainstem ischemia, especially in older adults, and thorough evaluation should include monitoring for arrhythmias and a thorough assessment of heart valve function. These studies are often performed prior to referral and, if negative, are not repeated. If not already performed, and the etiology of the symptoms remains in question, an ambulatory 24 hour electrocardiogram (Holter monitor) should be performed in patients with hemodynamic ischemia as arrhythmias are a common cause for 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 can be obtained selectively to rule out significant valvular pathology that could cause brainstem hypoperfusion.

TREATMENT

Approach

Open surgery versus endovascular treatment — Vertebral artery revascularization should be performed only at select centers with high-volume experience with established acceptable outcomes in both clinical success and safety. In general, stroke and death rates are comparable for open versus endovascular approaches; the main issue is durability. Surgery is more durable, but there are a limited number of surgeons with sufficient experience with open techniques, such that vertebral artery stenting has become the more prevalent method of revascularization by default. Until the indications for its routine application become clearer, vertebral artery angioplasty/stenting should be reserved for select cases.

The results of open vertebral reconstruction should be considered the benchmark by which endovascular treatment should be compared. Combined death and stroke rates for open surgery range from 1 percent for proximal reconstruction to 4 percent with distal bypass [17-20]. Risk is increased for patients who undergo a combined vertebral and carotid artery revascularization. Long-term outcomes of open revascularization are generally excellent, with high stroke-free survival rates, and patency rates as high as 90 percent at 10 years [21].

Although vertebral artery angioplasty with or without stenting appears to be a safe approach that avoids the morbidity associated with vertebral artery surgery, most available data are limited to small, single-center reviews with limited follow-up [22-25]. Despite high rates of technical success, angioplasty of the vertebral artery disease is associated with high rates of restenosis, ranging between 13 and 50 percent in the available reports. Adjuvant stent placement may add to the clinical durability but also adds to potential morbidity (eg, stent malposition, stent fracture (picture 2)). Drug-eluting stents, used effectively in other vascular beds to minimize the development of neointimal hyperplasia and prevent restenosis have also been tried in the vertebral artery; however, the mean patient follow-up time is less than one year in most of these observational studies [26-39]. Extrapolating from data from the cardiac literature, treatment with drug-eluting stents requires dual antiplatelet therapy for a time to reduce the rates of acute thrombosis. It remains unclear whether stent makeup (drug-eluting versus not) will have a significant impact in the outcomes of patients who undergo interventions of the vertebral artery.

Studies illustrating the outcomes of endovascular treatment are as follows:

●A subset of 16 patients treated represents the only data on vertebral stenting from a randomized trial. The Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS 2001) compared endovascular therapy with best medical care for symptomatic vertebral stenosis [40]. There were no 30 day strokes or deaths in either group, although two of eight patients who underwent endovascular treatment experienced transient ischemic symptoms. At a mean follow-up of 4.5 years, there were no posterior circulation strokes in either group. Another trial also comparing percutaneous vertebral intervention with medical therapy, the Vertebral Artery Stenting Trial (VAST), is underway [41].

●A systematic review identified 313 endovascular interventions for vertebral artery stenosis, with just over half of the interventions using a stent. The rate of technical success was 95 percent. The periprocedural (30 day) rate of transient ischemic attack or stroke was 3.2 percent; the mortality rate was also 3.2 percent [42].

●In a later series of 105 patients treated for symptomatic vertebral artery disease, radiographic improvement (residual stenosis ≤30 percent) was achieved in all patients. The periprocedural complication rate (transient ischemic attack, flow-limiting dissection, hematoma, and catheter access site problems) was 4.8 percent, and the periprocedural mortality rate was 1 percent [43]. At one year of follow-up, six patients had died and five had experienced a vertebrobasilar stroke. At approximately 2.5 years of follow-up, 70 percent of patients remained symptom free, but 13 percent of patients had restenosis requiring retreatment.

●In the Stenting of Symptomatic Atherosclerotic Lesions in the Vertebral or Intracranial Arteries (SSYLVIA) Trial, 18 patients with vertebral artery disease underwent angioplasty and stenting. Technical success was achieved in all but one patient [44]. There were no periprocedural neurological complications; however, the six-month restenosis rate was 50 percent and over one third of cases were symptomatic [44].

●In a study in which drug-eluting stents were used to treat vertebral artery origin stenoses, the rate of in-stent restenosis was significantly lower for those who received drug-eluting stents compared with conventional stents (38 versus 17 percent) over a mean of 21 months follow-up [28].

●Patients with a recent vertebrobasilar transient ischemic attack or ischemic stroke and vertebral artery stenosis of at least 50 percent have a high risk of future vertebrobasilar stroke. Stenting of vertebral artery stenosis is promising, but of uncertain benefit. We investigated the safety and feasibility of stenting of symptomatic vertebral artery stenosis of at least 50 percent and assessed the rate of vascular events in the vertebrobasilar supply territory to inform the design of a phase three trial.

●A trial randomly assigned 115 patients with a recent transient ischemic attack (TIA) or minor stroke associated with an intracranial or extracranial vertebral artery stenosis of at least 50 percent to stenting plus best medical treatment or best medical treatment alone [45]. Three patients in the stenting group (5 percent) had vascular death, myocardial infarction, or any stroke within 30 days after the start of treatment compared with one patient in the medical treatment group (2 percent). During a median follow-up of three years, seven (12 percent) patients in the stenting group and four (7 percent) in the medical treatment group had a stroke in the territory of the symptomatic vertebral artery.

Approach by segment — The location of disease in the vertebral artery generally dictates the nature of reconstruction. Most reconstructions of the vertebral artery are performed to treat an origin stenosis (V1 segment) or stenosis, dissection, or occlusion of the intraspinal segments (V2, V3).

●V1 segment – The V1 segment can be approached using an open (transposition) or endovascular approach. (See 'Vertebral artery transposition' below and 'Endovascular treatment' below.)

●V2 segment – The second segment of the vertebral artery (V2), which ascends within the foramina of the cervical vertebrae, is the site of a wide variety of pathology; however, due to its interosseus position, the V2 segment is rarely accessed surgically. The most common indication for exposure of the V2 segment is for control of hemorrhage. 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 vertebral artery in V1 and V3 segments or via endoluminal coil embolization. Management of the V2 segment would also include bypass to the V3 segment (image 3). (See 'Distal vertebral artery bypass' below and 'Endovascular treatment' below.)

●V3 segment – Isolated V3 segment disease is uncommon, but if disease extends to the base of the skull, there are no extracranial options for revascularization.

●V4 segment – The V4 segment is vulnerable to direct trauma and stretch injuries but is surgically inaccessible. Revascularization, when undertaken, is predominantly by endovascular means. But because the V4 segment is devoid of adventitia, any intervention should be approached with extreme caution. (See 'Endovascular treatment' below.)

Open surgical repair — Open surgical repair can be performed under general anesthesia (with or without neuromonitoring) or local anesthesia with sedation, much as is done with carotid endarterectomy. (See "Anesthesia for carotid endarterectomy and carotid stenting".)

The first and third segments of the vertebral artery (V1, V3) are easily accessible by an open surgical approach. The second and fourth segments, which are technically difficult to expose, are rarely directly managed using open surgery. Lesions in the V2 segment are managed with bypass to the V3 segment.

●For the proximal vertebral artery (V1 segment), vertebral artery transposition has become recognized as a superior solution and has supplanted endarterectomy [46] and bypass [47] as the reconstruction option of choice [48,49]. The inflow artery must be free of disease to provide good inflow into the vertebral artery.

●When bypass is required to the distal vertebral artery (occluded V2 segment), the distal portion of the reconstruction is completed in the V3 segment at the C1C2 spinal level. The technique most often uses a saphenous vein conduit originating from the common carotid or subclavian artery, which needs to be free of lesions to provide good inflow [50-53]. Alternatively, in the absence of a suitable vein, the radial artery can be used as conduit. During the late 1970s, vein bypass and skull base transposition procedures to revascularize the distal vertebral artery were developed using a similar approach.

Aneurysms of the vertebral artery are managed with vertebral arterial ligation above and below the aneurysm at accessible sites with or without distal revascularization (bypass) to the V3 segment.

Vertebral artery transposition — The approach to the proximal vertebral artery is the same as the approach for carotid-subclavian transposition. The patient is positioned in a slight chair position, which decreases venous pressure and will optimize the exposure of the anatomy at the base of the neck.

The incision is placed transversely approximately a finger's breadth above the clavicle and directly over the two 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 ligated and divided. Accessory lymph ducts, often seen on the right side of the neck, should also be 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, which 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 should now be visible. It is important to identify and avoid injury to the adjacent sympathetic chain. 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 to 3 cm of length. The vertebral artery needs to be freed from the sympathetic trunk resting on its anterior surface without damaging the trunk or the ganglionic rami. It can be transposed to the carotid artery in 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 systemically anticoagulated (typically 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 suture and divided. The carotid artery is clamped proximal and distal the chosen site, and an elliptical 5 to 7 mm arteriotomy is created in the posterolateral wall of the common carotid artery with an aortic punch. The anastomosis is performed using a parachute technique with continuous 7-0 polypropylene suture, avoiding any tension on the vertebral artery, which can easily tear. Before completing the anastomosis, standard flushing maneuvers are performed, the suture is tied, the clamps sequentially removed from the carotid and distal vertebral artery, and flow is reestablished.

Distal vertebral artery bypass — For distal vertebral artery bypass, a vertical 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, the 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 will be 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 three 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 maneuver. 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 be away from the bifurcation to avoid disturbing any underlying atheroma. The distal anastomosis will be completed first. A valveless segment of vein (to facilitate backbleeding) or a radial artery conduit can be used. After the patient has been systemically anticoagulated (typically 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 then placed proximal to the anastomosis on the graft, and the J-clamp removed. 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 clamped proximal and distal to the selected site, an elliptical arteriotomy is made with an aortic punch, and, after cutting to the 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 clamps sequentially released, and flow reestablished into the vertebral artery. The vertebral artery can also 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.

The vertebral artery can also 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. Bypasses above the level of C1 (suboccipital) are technically demanding and have been required in only a small number of distal vertebral artery reconstructions.

Intraoperative completion imaging using digital arteriography is useful and should be considered for all types of vertebral artery reconstruction. Identification and repair of technical flaws can prevent reconstruction failure.

Endovascular treatment — Endovascular treatment of vertebral artery disease, usually by placing a stent, has become a popular alternative to surgery, particularly given that endovascular access to the vertebral artery is relatively straightforward. (See 'Open surgery versus endovascular treatment' above.)

Also, the procedure can be performed under local anesthesia, enabling continuous neurologic monitoring of the patient. Most cases are performed using a femoral approach, although transbrachial or transradial access has also been described.

Stenotic lesions are crossed and treated with 0.014 or 0.018 inch guidewires and treated by means of small coronary-diameter balloons and stents. Procedures can be performed with or without the assistance of embolic protection devices [54], and drug-eluting stents have also been used to prevent restenosis [26,55-57]. Periprocedural risks include embolization, rupture, thrombosis, arterial dissection, and stent malposition or fracture. Periprocedural antithrombotic therapy is similar to that used for carotid angioplasty and stenting. (See "Overview of carotid artery stenting", section on 'Dual antiplatelet therapy'.)

COMPLICATIONS — Perioperative/periprocedural mortality associated with vertebral artery intervention (open surgery, endovascular treatment) is overall low (<5 percent) [20,58,59]. Risk is generally increased for patients who require combined vertebral and carotid revascularization.

Complications of open surgery include immediate thrombosis (1.4 percent), vagus and recurrent laryngeal nerve palsy (2 percent), Horner's syndrome (8.4 to 28 percent), lymphocele (4 percent), and chylothorax (5 percent) [20].

As discussed above, in-stent restenosis is common following vertebral artery angioplasty and may be less with stenting [60]. However, late stent fracture predisposes to in-stent restenosis [61].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Occlusive carotid, aortic, renal, mesenteric, and peripheral atherosclerotic disease" and "Society guideline links: Blunt cerebrovascular injury".)

SUMMARY AND RECOMMENDATIONS

●The vascular supply to the brain is from the anterior and posterior circulations (figure 1). The vertebral arteries, which supply the posterior circulation, are traditionally divided into four segments (figure 2). A single, normal vertebral artery is sufficient to adequately perfuse the basilar artery. (See 'Anatomic considerations' above.)

●Many pathologic processes, most commonly atherosclerosis, can lead to symptoms of vertebrobasilar ischemia, either due to a hemodynamic or embolic mechanism. For hemodynamic symptoms to occur in direct relation to disease of the vertebrobasilar arteries, significant occlusive pathology must be present in both of the paired vertebral vessels, or in the basilar artery. Arterial to arterial emboli can arise from atherosclerotic lesions, or more rarely from fibromuscular dysplasia, aneurysm, or dissection. (See 'Vertebrobasilar disease' above.)

●Atherosclerosis, which is the most common disease affecting the vertebral artery, is often underdiagnosed as a cause of posterior circulation ischemia given the often vague nature of the clinical presentation. Prior to considering vertebral artery revascularization, the vascular surgeon or interventionalist must correlate symptoms with anatomic pathology identified on vascular imaging (conventional arteriography, magnetic resonance [MR] angiography), usually together with a neurologist, to ensure that revascularization has a high likelihood of success in relieving the patient's symptoms. Other sources for vertebrobasilar symptoms must be ruled out. (See 'Vertebrobasilar disease' above and "Posterior circulation cerebrovascular syndromes".)

●Intervention is not indicated in asymptomatic patients, except for those who have vertebral artery aneurysm. Indications for intervention include (see 'Indications' above):

•Hemodynamic symptoms and bilateral, significant (>60 percent) vertebral artery stenosis

•Symptomatic embolism suspected to be from a vertebral lesion

•Symptomatic vertebral artery aneurysm

•Asymptomatic vertebral artery aneurysm >1.5 cm

●Clinicians must carefully balance the risks of surgery versus the limitations of endovascular intervention before proceeding. Open techniques for revascularization of the vertebral artery have proven clinical durability and acceptable surgical morbidity in experienced hands. Endovascular techniques are clinically feasible but have yet to deliver on durability benchmarks set by open surgical revascularization. Vertebral artery revascularization should be performed only at select centers with high-volume experience with established acceptable outcomes in both clinical success and safety. (See 'Open surgery versus endovascular treatment' above.)

●The location of disease in the vertebral artery generally dictates the nature of reconstruction. Most reconstructions of the vertebral artery are performed to treat an origin stenosis (V1 segment), or stenosis, dissection, or occlusion of the intraspinal segments (V2, V3). The second and fourth segments, which are technically difficult to expose, are rarely directly managed using open surgery. Lesions in the V2 segment are managed with bypass to the V3 segment. Aneurysms of the vertebral artery are managed with vertebral arterial ligation above and below the aneurysm at accessible sites with or without distal revascularization (bypass) to the V3 segment. (See 'Approach by segment' above.)

•The V1 segment can be approached using an open or endovascular approach. The preferred open approach is vertebral artery transposition, provided the inflow vessel (typically the carotid artery) is free from disease. At times, combined carotid/vertebral artery revascularization is needed.

•The V2 segment is rarely accessed surgically. The most common indication for open exposure of this segment is for direct control of hemorrhage, which is difficult and may require vertebral artery ligation. When vertebral artery bypass is required for an occluded V2 segment, the distal vein graft is anastomosed in the V3 segment at the level of C1/C2.

•Isolated V3 segment disease is uncommon, but if disease extends to the base of the skull, there are no extracranial options for revascularization.

•The V4 segment is vulnerable to direct trauma and stretch injuries but is surgically inaccessible. Revascularization, when undertaken, is predominantly endovascular. But because the V4 segment is devoid of adventitia, any intervention should be approached with extreme caution.

●Perioperative/periprocedural mortality associated with vertebral artery intervention (open surgery, endovascular treatment) is overall low (<5 percent). In general, stroke and death rates are comparable for open versus endovascular approaches. Perioperative risk is generally increased for patients who require combined vertebral and carotid revascularization. Complications of open surgery include immediate thrombosis, nerve injury, lymphocele, and chylothorax. In-stent restenosis is common following vertebral artery angioplasty and may be less with stenting, but late stent fracture can occur and also predisposes to in-stent restenosis. (See 'Open surgery versus endovascular treatment' above and 'Complications' above.)