Extracranial veterbral artery stenosis

From WikiCNS
Jump to: navigation, search


Checkmark.gif This article has been reviewed by the NeuroWiki Editorial Board


Atherosclerotic occlusive disease of the extracranial VA, which is present in approximately 25 to 40% of the population, is an important cause of posterior circulation ischemia.183,184 The V1 (proximal) segment of the VA, extending from the origin of the VA at the subclavian artery to the entrance into the transverse vertebral foramen, is the most common site for atherosclerotic occlusive disease in the VA.These ostial lesions can serve as not only embolic sources but also flow-limiting stenoses that can produce posterior circulation ischemia. However, the natural history, clinical features, and optimal therapy for atherosclerotic lesions of the extracranial VA are not clearly defined for multiple reasons. First, these lesions may not be well visualized by ultrasonography and may require digital subtraction angiographic or MR angiographic imaging for definitive diagnosis. Second, symptoms of posterior circulation ischemia, such as dizziness and ataxia, may be misinterpreted as non-specific symptoms, leading to misdiagnosis.185,186 Third, no prospective randomized trial has been performed to determine which therapy is optimal for symptomatic stenosis of the extracranial VA.

Surgery of these lesions is technically difficult and associated with significant morbidity and mortality.Medical therapy consisting of antiplatelet agents, systemic anticoagulation, avoidance of orthostatic hypotension, and elevation of mean arterial blood pressure remains empiric. In the last decade, angioplasty with or without stenting has been performed as an alternative treatment for extracranial VA stenosis.188-190 In this section, the authors will discuss indications for these procedures, along with associated technical features and success and complication rates.

Indications For Vertebral Artery Angioplasty and Stenting

The authors do not recommend routine performance of VA angioplasty with or without stenting for asymptomatic patients with atherosclerotic stenosis of the extracranial VA. There are situations, however, for which angioplasty and/or stenting may be indicated for asymptomatic stenosis, such as for stenosis at the VA origin in a patient with a dominant or single VA. Further data is needed regarding the natural history of extracranial VA stenosis as well as the long-term durability of these procedures. Chastain et al. have reported uncomplicated angioplasty and stenting of extracranial VA stenosis in 11 asymptomatic patients.191 These patients were known to have poor intracranial collateral circulation. However, long-term angiographic and clinical follow-up is needed to determine the efficacy of these procedures in this select group of patients.

At this time, the authors recommend reserving angioplasty with or without stent placement for atherosclerotic extracranial VA stenosis when the patient’s symptoms fail to respond to medical therapy. Angioplasty with or without stenting may be recommended instead of medical therapy for symptomatic patients who have physiological evidence of hypoperfusion or inadequate intracranial collateral flow demonstrated by imaging modalities such as PET, SPECT, or Xenon-enhanced CT. Antiplatelet and anticoagulation therapies may reduce embolic events resulting from VA stenosis but are unlikely to augment flow distal to these lesions. Wityk et al. reviewed the clinical features and radiographic findings of patients with either occlusion or high-grade stenosis involving the V1 segment who were enrolled in the New England Medical Center Posterior Circulation Registry and found that 16% had TIAs resulting from hemodynamic instability.184 The advantages of a combination angioplasty and stenting procedure over angioplasty alone include prevention of elastic recoil and early restenosis.


The basic principles of preprocedural treatment with antiplatelet medication, intraprocedural heparinization, and guide catheter placement for vertebral angioplasty and stenting are similar to those used for extracranial carotid and peripheral arterial interventions. Although femoral access is used for most cases, brachial or radial access can be used to perform VA angioplasty and stenting for those cases in which femoral access is unavailable. Occasionally, the VA origin is angled to favor delivery of a stent from a brachial or radial approach. The stenotic lesion is typically crossed with a 0.014-inch guidewire and dilated with a slightly undersized, noncompliant balloon (inflated 3-3.5 mm) before stent placement. After angioplasty, a stent is deployed using the road-mapping function of the angiography unit for guidance. Poststent angioplasty may be performed if significant residual stenosis remains. Precise placement of the stent in the ostium of the VA requires multiple angiographic projections to visualize the ostium as the artery arises posteriorly and superiorly from the subclavian artery. Poor placement of the stent may lead to inadequate coverage of the ostium, resulting in residual ostial stenosis or “watermelon seeding” (forced migration of the stent as a result of asymmetric pressure applied by the vessel onto the stent wall). Alternatively, too much overhang of the stent below the ostium and into the parent lumen may make access into the VA challenging for post-stent angioplasty.

Stent selection

Selection of the stent depends on the location and anatomy of the VA stenosis. In general, ostial lesions are prone to elastic recoil after angioplasty. As a result, a stent with adequate radial strength is required to achieve adequate dilation. Hand-mounted Palmaz (Johnson & Johnson) and balloon-expandable stents have been used for ostial lesions. Newer flexible coronary stents are available. Lesions in the V1 or V2 segment (those located within the transverse foramina at the C1-C6 spinal levels) may be treated with balloon-expandable (Tetra, Guidant Inc) or self-expanding (Magic Wallstent; Boston Scientific Scimed, Maple Grove, MN) stents. Caution should be taken when using self-expanding stents for lesions involving the ostium because the exact length and placement of the stent cannot always be predicted. Stents with a special coating (such as heparin, rapamycin, or taxol) to reduce intimal hyperplasia and distal protection devices may play a role in cases of VA origin stenosis in the future. At present, there is insufficient data to determine their effectiveness in this setting.

Procedural Complications

Angioplasty and stenting for stenosis of the extracranial VA is associated with potential complications of transient arterial spasm, dissection, rupture, occlusion, hemorrhage, stroke, and death, in addition to transient neurological complications or TIAs. Angioplasty and stenting of the distal VA may be technically difficult because of the tortuous anatomy, especially in older patients with severe atherosclerotic stenosis. Spasm of the VA may be relieved by the removal of catheters or the administration of IA nitroglycerin. A flow-limiting, hemodynamically significant dissection resulting from angioplasty may need to be treated with a stent to avoid permanent occlusion and a potential thromboembolic event. Higashida et al. reported an 8.8% occurrence of transient neurologic complications among 34 patients in whom proximal VA stenosis (>70% stenosis) was treated with angioplasty alone.192 Rates of transient neurologic complications ranging from 3 to 8% have been reported for combination VA angioplasty and stenting (Table 11).191,193-196 This complication is probably related to a thromboembolic event. Further studies are needed to assess the complications associated with these procedures.


Before VA stenting was introduced, angioplasty alone for symptomatic stenosis of the extracranial VA was reported as a safe alternative to medical therapy. However, vertebral angioplasty has several limitations. First, an ostial stenosis can be very difficult to dilate adequately with angioplasty alone. In addition to immediate elastic recoil, a restenosis rate (defined as >50% residual luminal stenosis) of 8.8% within 2 to 5 months has been reported.192 These data have encouraged the use of stents. Mukherjee et al. reported symptomatic restenosis in 1 (8%) of 12 patients who underwent VA origin angioplasty and stenting.195 Although most studies report a significant benefit of vertebral angioplasty and stenting in alleviating symptoms of posterior circulation ischemia, the series are small, retrospective, and non-randomized. Many of these studies lack long-term clinical and angiographic evaluations. More studies are required to evaluate the efficacy of these procedures.

In one of the largest series of angioplasty for extracranial VA stenosis, Higashida et al. reported a 5% (2 of 38 patients) mortality (1 death within 30 days).192 Two deaths were related to angioplasty of stenotic lesions of the VA located between the C1 and C3 spinal levels. In one case, vessel occlusion leading to stroke resulted in death; in the other, vessel rupture resulted in death several months later. In one of the largest series of combination angioplasty and stenting, Chastain et al. reported 30-day mortality and morbidity rates of 2%, respectively, among 50 patients.191 One patient had a major stroke during a coronary angiogram 4 days after VA revascularization. Another patient died of MI 19 days after the procedure. Although these series are small, combination angioplasty and stenting of the VA appears to be associated with low rates of morbidity and mortality and a reduction in the rates of posterior circulation strokes in the setting of medically refractory posterior circulation ischemia.


  1. Phatouros CC, Higashida RT, Malek AM, Meyers PM, Lefler JE, Dowd CF, Halbach VV. Endovascular treatment of noncarotid extracranial cerebrovascular disease. Neurosurg Clin N Am. 2000;11:331-350.
  2. Wityk RJ, Chang HM, Rosengart A, Han WC, DeWitt LD, Pessin MS, Caplan LR. Proximal extracranial vertebral artery disease in the New England Medical Center Posterior Circulation Registry. Arch Neurol. 1998;55:470-478.
  3. Caplan LR, Amarenco P, Rosengart A, Lafranchise EF, Teal PA, Belkin M, DeWitt LD, Pessin MS. Embolism from vertebral artery origin occlusive disease. Neurology. 1992;42:1505-1512.
  4. Gomez CR, Cruz-Flores S, Malkoff MD, Sauer CM, Burch CM. Isolated vertigo as a manifestation of vertebrobasilar ischemia. Neurology. 1996;47:94-97.
  5. Rocha-Singh K. Vertebral artery stenting: ready for prime time? Catheter Cardiovasc Interv. 2001;54:6-7.
  6. Crawley F, Brown MM, Clifton AG. Angioplasty and stenting in the carotid and vertebral arteries. Postgrad Med J. 1998;74:7-10.
  7. Drescher P, Katzen BT. Percutaneous treatment of symptomatic vertebral artery stenosis with coronary stents. Catheter Cardiovasc Interv. 2001;52:373-377.
  8. Storey GS, Marks MP, Dake M, Norbash AM, Steinberg GK. Vertebral artery stenting following percutaneous transluminal angioplasty. Technical note. J Neurosurg. 1996;84:883-887.


Reprinted with permission from Mohr JP, Choi DW, Grotta JC, Weir B, Wolf PA (eds): STROKE: PATHOPHYSIOLOGY, DIAGNOSIS, AND MANAGEMENT (4th edition), pp. 1475-1520 (chapter 78), Copyright Elsevier 2004. Permission has been granted to reproduce this material in online electronic format for non-exclusive world English rights.

Personal tools