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Journal of the American College of Cardiology © 2010 by the American College of Cardiology Foundation Published by Elsevier Inc.


Vol. 55, No. 6, 2010 ISSN 0735-1097/10/$36.00 doi:10.1016/j.jacc.2009.08.069

Interventional Cardiology

Endovascular Stenting for Vertebral Artery Stenosis J. Stephen Jenkins, MD, Samir N. Patel, MD, Christopher J. White, MD, Tyrone J. Collins, MD, John P. Reilly, MD, Paul W. McMullan, MD, Mark A. Grise, MD, Arthur G. Grant, MD, Stephen R. Ramee, MD New Orleans, Louisiana Objectives

The aim of this study was to demonstrate the safety and long-term durability of catheter-based therapy for symptomatic vertebral artery stenosis (VAS).


Symptomatic VAS carries with it a 5-year 30% to 35% risk of stroke. The 2-year mortality approaches 30% for medically managed strokes involving the posterior circulation. Surgical bypass is rarely performed, due to high morbidity and mortality. Endovascular revascularization with primary stenting offers an attractive treatment option for these patients.


One-hundred five consecutive symptomatic patients (112 arteries, 71% male) underwent stent placement for extracranial (91%) and intracranial (9%) VAS from 1995 to 2006. Fifty-seven patients (54%) had bilateral VAS, 71 patients (68%) had concomitant carotid disease, and 43 patients (41%) had a prior stroke.


Procedural and clinical success was achieved in 105 (100%) and 95 (90.5%) patients, respectively. One-year follow-up was obtained in 87 (82.9%) patients, of which 69 patients (79.3%) remained symptom-free. At 1 year, 6 patients (5.7%) had died and 5 patients (5%) had a posterior circulation stroke. Target vessel revascularization occurred in 7.4% at 1 year. At a median follow-up of 29.1 months (interquartile range 12.8 to 50.9 months), 13.1% underwent target vessel revascularization, 71.4% were alive, and 70.5% remained symptom-free.


In experienced hands, stenting for symptomatic VAS can be accomplished with a very high success rate (100%), with few periprocedural complications, and is associated with durable symptom resolution in the majority (approximately 80%) of patients. We conclude that endovascular stenting of vertebral artery atherosclerotic disease is safe and effective compared with surgical controls and should be considered first-line therapy for this disease. (J Am Coll Cardiol 2010;55:538–42) © 2010 by the American College of Cardiology Foundation

Approximately 80% of strokes are ischemic in origin, of which 20% to 25% are located in the posterior circulation involving the vertebrobasilar system (VBS) (1–3). The prognosis for patients with atherosclerotic occlusion or thrombosis of the VBS is poor, with 80% to 100% mortality (4). Medically refractory, symptomatic VBS disease carries a 5% to 11% incidence of stroke or death at 1 year (5– 8). Transient ischemic attacks (TIA) due to extracranial VBS disease are associated with a stroke rate of 30% at 5 years (8 –10). Although the incidence in the general population of vertebral artery stenosis (VAS) is unknown, patients with atherosclerotic peripheral arterial disease (PAD) have a 40% incidence of VAS (11). Patients with symptomatic VBS ischemia have a 25% to 40% incidence of VAS (12). The From the John Ochsner Heart and Vascular Institute, Ochsner Clinic Foundation, New Orleans, Louisiana. Dr. White is a principal investigator in the CABANA trial (Boson Scientific), and is on the advisory board of Baxter Cellular Therapy. Dr. Ramee is an investor/cofounder of SquareOne, Inc. Manuscript received April 17, 2009; revised manuscript received August 7, 2009, accepted August 10, 2009.

Joint Study of Extracranial Arterial Occlusion examined 3,800 patients who presented for angiography due to symptomatic cerebrovascular disease and found a 40% incidence of VAS and a 10% incidence of complete occlusion of 1 vertebral artery (13). Although VAS is highly prevalent in patients with PAD, its association with symptoms of vertebrobasilar insufficiency (VBI) is both under-recognized and underdiagnosed (14). Symptoms associated with VBI, such as dizziness, ataxia, visual disturbances, and motor-sensory deficits, might be dismissed as nonspecific findings. Noninvasive imaging of the ostial and proximal vertebral artery, the most frequent site of vertebral atherosclerotic obstructive disease is difficult and often incomplete (15). Although initial antithrombotic and antiplatelet therapy is warranted, arch and 4-vessel angiography, computed tomographic angiography, or magnetic resonance angiography is indicated if symptoms continue despite maximal medical therapy (13). Three surgical revascularization techniques for symptomatic vertebral disease have been described. These open surgical procedures include: 1) transection of the vertebral

Jenkins et al. Vertebral Artery Intervention

JACC Vol. 55, No. 6, 2010 February 9, 2010:538–42

artery above the stenosis with reimplantation into the ipsilateral subclavian or carotid artery; 2) vertebral artery endarterectomy; and 3) vein patch angioplasty. The combined morbidity and mortality rates of VAS surgical therapy range from 10% to 20% and have dampened enthusiasm for this option (10,16 –19). Management of VAS has shifted to percutaneous techniques with the evolution of endovascular device technologies. Sundt et al. (20) reported the first vertebral artery intraoperative transluminal angioplasty in 1980. Since then, multiple case reports and clinical series have described the use of balloon angioplasty and stenting to treat vertebrobasilar atherosclerotic disease (15,21–29). In this article, we report acute and long-term outcomes in 105 consecutive symptomatic patients (112 arteries) undergoing endovascular stenting of VAS over an 11-year period. Methods Patient population. Between December 1995 and May 2006, 105 consecutive symptomatic patients (112 arteries) underwent endovascular stenting of extracranial (91%) and intracranial (9%) atherosclerotic vertebral artery disease (Tables 1 and 2). The population was predominantly male (71%) with mean age of 67.8 ! 11 years (range 43 to 94 years). Patients were diagnosed with VAS by clinical assessment coupled with imaging techniques. The diagnosis was confirmed by independent neurological evaluation by a member of the stroke team not participating in the intervention. All patients had failed management with antiplatelet therapy. Symptoms included vertigo, visual changes, syncope, ataxia, drop attack, or stroke/TIA (Table 1). Patient Characteristics Table 1 Patient Characteristics Patients (n " 105) Age (yrs)

67.8 ! 11


74 (70.5)

Indication for procedure Vertigo

69 (65.7)

Visual disturbance

34 (32.4)


12 (11.4)


9 (8.6)


8 (7.6)

Drop attack

5 (4.8)

Comorbidities Coronary artery disease

69 (65.7)


89 (86.4)


29 (28.4)


83 (83.0)

History of tobacco use

51 (52.6)

Concurrent carotid disease

71 (68.9)

Concurrent subclavian disease

26 (29.2)

Bilateral vertebral disease

57 (54.3)

Prior CVA

43 (41.0)

Values are mean ! SD or n (%). CVA " cerebrovascular accident; TIA " transient ischemic attack.


Lesion characteristics. One Abbreviations hundred five arteries were treated and Acronyms with stents (Table 2). Seven PAD ! peripheral arterial (6.7%) patients underwent treatdisease ment of both vertebral arteries. TIA ! transient ischemic Angiographic evaluation. Aorattack tic arch and 4-vessel angiograVAS ! vertebral artery stenosis phy, including carotid and vertebral artery angiography, was VBI ! vertebrobasilar insufficiency performed in all patients. Intracranial imaging to define the anVBS ! vertebrobasilar system terior circulation, posterior circulation, and the circle of Willis was included in all studies. Technique. All patients received aspirin (325 mg once daily) and ticlodipine (250 mg twice daily) or clopidogrel (75 mg once daily) before the procedure. All patients received 5,000 to 10,000 U of heparin after arterial access to maintain an activated clotting time !250 s. Selective engagement of the vertebral artery was performed with an appropriate-shaped 6-F coronary guiding catheter. A 0.014-inch steerable coronary guidewire was advanced across the stenosis, and no embolic protection devices were used in this series of patients. The reference vessel diameter was determined with quantitative angiography before balloon angioplasty and stent placement (Table 2). After stent deployment, completion angiography was performed. Minimal or no sedation was used during the procedure, and continuous neurological monitoring was performed. Post-procedure antiplatelet therapy included dual antiplatelet therapy (aspirin and thienopyridines) for a minimum of 1 month and continued at the treating physicians’ discretion. Definitions. Technical success was defined as residual stenosis "30% without in-hospital stroke or death. Clinical success was defined as technical success with VBS symptom resolution. Target vessel revascularization was defined as repeat intervention of the target vessel driven by clinical symptoms with a !70% stenosis. Major complications included death and stroke. Follow-up. Outpatient clinic visits were encouraged at regular intervals, and symptom status was assessed. Noninvasive imaging with duplex ultrasound was at the physician’s discretion and was often performed in conjunction with outpatient clinic visits. Repeat angiography was performed if repeat revascularization was being considered for recurrent symptoms with suspicion of restenosis on noninvasive imaging. The incidence of mortality and the date of death were determined via the Social Security Death Index. Statistical analysis. Categorical data were presented as percentages, and continuous variables were presented as mean ! SD. Survival rates were calculated with the KaplanMeier Product Limit method.


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JACC Vol. 55, No. 6, 2010 February 9, 2010:538–42

Procedural Table 2 Data Procedural Data

Procedural (n ! 105) (n ! 105) Table 4 Complications Procedural Complications

Artery treated (n " 112)


0 (0)

Left vertebral

63 (56.3)

Transient ischemic attack

1 (1.0)

Right vertebral

49 (43.7)

Dissection (flow-limiting)

1 (1.0)

Hematoma/bleeding requiring transfusion

2 (1.9)

Access site complications

1 (1.0)

All complications

5 (4.8)


7 (6.3)

Segment treated (n " 117) V1

97 (82.9)


7 (6.0)


2 (1.7)


11 (9.4)

Stent type (n " 133) Balloon-expandable bare-metal



follow-up of 29.1 months, 71.4% of all treated patients were alive. The overall patient survival is shown in Figure 1.


Balloon-expandable drug-eluting


Stent diameter Stent length

Values are n (%).

4.1 ! 0.7 13.4 ! 6.4

Stenosis (%)* Pre-intervention

89.2 ! 9.1


1.4 ! 4.8

Values are n (%) or mean ! SD. *Angiographic visual estimation.

Results Procedural outcome. Technical success was achieved in all 112 arteries (100%) (Table 3). There was 1 VBS stroke that developed within the first month after the procedure. Clinical success was achieved in 95 (90.5%) of 105 symptomatic patients (Table 3). Of the 10 patients who did not achieve clinical success, 1 developed a VBS stroke 3 days after hospital discharge and 9 had persistent symptoms. Periprocedural complications before hospital discharge occurred in 5 (4.8%) patients (Table 4). Follow-up. Of a total of 105 patients (112 arteries), 5 patients (5 arteries) were lost to follow-up. Clinical follow-up was obtained in 100 (95.2%) patients (107 arteries) at a median of 29.1 months (interquartile range 12.8 to 50.9 months), with 87 (82.9%) patients (94 arteries) having at least 1-year follow-up. At 1 year, 6 patients (5.7%) had died, and 5 patients (4.8%) experienced a VBS stroke. Target vessel revascularization occurred in 13.1% (14 of 107 arteries) at 29.1 months (Table 3). Survival. Although there were no in-hospital deaths, there was 1 patient death within 30 days of the procedure secondary to a myocardial infarction. At the median

Discussion In experienced hands, catheter-based treatment with stents for symptomatic VAS can be successfully accomplished in a very high percentage (100%) of patients, with rare major complications (no in-hospital strokes or deaths). Stenting of VAS provides durable symptom resolution in approximately 70% of patients at 2.5 years of follow-up. Although medical therapy for the management of VBS ischemia traditionally includes warfarin anticoagulation or antiplatelet therapy, there is lack of evidence supporting the use of these drugs for this disease or comparing these drugs to other treatment options (17,30 –32). Surgical options remain unattractive, due to the difficulty in gaining access to the origin of the vertebral artery and the increased morbidity and mortality (33). There has been only 1 very small prospective randomized trial that compared VAS stent placement with medical therapy (CAVATAS [Carotid and Vertebral Artery Transluminal Angioplasty Study], n " 16) (33). Eight patients were randomized to medical therapy, and 8 patients under-

Clinical Points and Table 3End Clinical EndLong-Term Points andFollow-Up Long-Term Follow-Up Technical success (n " 112) Clinical success (n " 105)

112 (100) 96 (91.4)

Clinical follow-up (n " 105) All patients Median, months Patients with #1-yr follow-up Asymptomatic at last follow-up (n " 100)

100 (95.2) 29.1 [12.8–50.9] 87 (82.9)

Target vessel revascularization All vessels (n " 107)*

Figure 1

Overall Survival

74 (74.0) 14 (13.1)

Values are n (%) or median [interquartile range]. *Excludes 5 vessels lost to follow-up.

With the Kaplan-Meier Product Limit method, median survival is 10.1 years (121 months) with August 15, 2007, as the censoring date. Of 105 patients, 72.5% were censored and 30 (28.6%) died.

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went successful endovascular stenting, with no strokes or death occurring within 30 days in either group. At mean follow-up of 4.7 years, there were no vertebral strokes in either group. A Cochrane Review identified 173 cases of VAS stenting of 313 cases of vertebral artery intervention (34). Analysis of these 20 studies found a 30-day major stroke and death rate of 3.2% and a 30-day TIA and nondisabling stroke rate of 3.2%. This meta-analysis suggests that vertebral artery stenting is safe and effective, although a selection bias exists. Over the last 2 decades, catheter-based treatment of PAD has become the preferred therapy compared with surgical revascularization. Treatment of VAS has evolved more slowly than endovascular therapies in the iliac, renal, and coronary arteries. A major impediment to treatment has been a nonpayment decision by Medicare in 1984. However, since that time there have been significantly more favorable data supporting the safety, efficacy, and benefit of VAS. Nonpayment for percutaneous vertebral artery therapies is difficult to understand in view of the positive track record for percutaneous transluminal angioplasty and stenting in other vascular territories and the lack of treatment alternatives for a disease with a 2-year mortality for medically treated VBS disease of 30% and a combined surgical morbidity/ mortality of 25%. Therefore, it seems appropriate that this nonpayment decision be revisited. Study limitations. Our data reflect our clinical practice at the Ochsner Clinic Foundation, including dedicated high-volume interventionalists who benefited from the cooperation and support of a team of neurologists and neuroradiologists, and might not be reproducible under less ideal conditions. The major limitation of this study is its retrospective nature, which does not allow direct comparison with other treatment strategies. A minor limitation is the lack of angiographic core laboratory analysis. Conclusions Our results demonstrate the safety and feasibility of treating symptomatic vertebral artery stenotic lesions with endovascular stent therapy. The excellent safety results and durability of symptom-free outcomes support the efficacy of endovascular stent therapy for symptomatic VAS. Vertebral stenting offers a safer and less morbid alternative than open surgery and should become the preferred therapy for symptomatic vertebral artery atherosclerotic obstructive disease. Acknowledgments

The authors are thankful for the cooperation and support of a team of physicians including Kevin McKinley (neurology), Robert Felberg (neurology), and Robert Dawson (neuroradiology). The authors also thank Mr. James O’Meara and


Mr. Darren Barre for assistance with the manuscript preparation and data collection. Reprint requests and correspondence: Dr. J. Stephen Jenkins, Department of Cardiology, Ochsner Medical Center, 1514 Jefferson Highway, New Orleans, Louisiana 70121. E-mail: jsjenk@


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Endovascular Stenting for Vertebral Artery Stenosis 2010