Endovascular treatment of the vertebral artery origin stenosis by using the closed-cell, self-expandable Carotid Wallstent

Abstract

Background

Endovascular treatment has been considered a good alternative to surgery for symptomatic vertebral artery origin stenosis (VAOS) due to the high risk of morbidity associated with surgery. The purpose of this study was to evaluate the feasibility and efficacy of insertion of the closed-cell, self-expandable Carotid Wallstent for the treatment of VAOS.

Methods

The records of 72 patients with VAOS refractory to adequate medication who were treated by endovascular treatment with the Carotid Wallstent from December 2006 to November 2018 were retrospectively evaluated.

Results

Of the 72 patients, 43 presented with transient ischemic attacks. Forty-seven patients (65.3%) manifested other brachiocephalic stenoses; of these, 40 patients had occlusion, hypoplasia, or stenosis of the contralateral vertebral artery. Overall technical success (defined as 20% or less residual stenosis) was 100%. Procedure-related complications (n = 8, 11.1%) included sudden asystole (n = 1), acute in-stent thrombosis (n = 3), minor stroke (n = 3), and stent shortening (n = 1). All complications were resolved without permanent neurological deficit. Angiographic follow-up (mean, 13.0 months) was achieved in 49 patients and revealed in-stent restenosis in 1 patient (2.0%) and stent malposition by shortening in 2 patients (4.1%). Follow-up records were available in 57 patients (mean 15.6 months). Three of the 57 patients (n = 3, 5.3%) had recurrent symptoms of vertebrobasilar ischemia and none was retreated.

Conclusions

Endovascular treatment of symptomatic VAOS using the closed-cell, self-expandable Carotid Wallstent is technically feasible and effective in alleviating patient symptoms and for improving vertebrobasilar blood flow.

Introduction

Vertebral artery origin stenosis (VAOS) decreases posterior cerebral perfusion, causing vertebrobasilar insufficiency, or induces embolic infarction in the posterior cerebral circulation.^1,2 Data from the Oxford Vascular Study and New England Registry reveals that 26–33% patients with posterior stroke have severe stenosis (>50%) or occlusion of vertebral artery (VA) origin.^3,4 Despite medical treatment in patients with symptomatic VAOS, the rate of stroke recurrence remains 25% at 90 days.⁵ Surgical revascularization for VAOS is another therapeutic option, but is associated with a high risk of morbidity.

Stent-assisted angioplasty for VAOS has been introduced as a promising option and is widely used in clinical practice.⁶ The Vertebral Artery Ischaemia Stenting Trial showed that stenting in extracranial stenosis appears safe with low rate of complications, while higher complication rates have been noted for intracranial stenosis at 7–10%.⁷ Vertebral ostial stents of different designs and configurations are commercially available. They are classified as either closed-cell or open-cell, depending on the stent design. The closed-cell Carotid Wallstent design, with smaller free cell areas, covers a greater percentage of the vascular wall within the stented region and may better contain fractured plaque and debris after angioplasty, resulting in a lower number of post-procedural events than open-cell design. Additionally, the fully connected Carotid Wallstent is more resistant than open-cell stents to recoil forces that cause stent fracture, due to its geometry and interconnected design. Several small case series and reports document the results of VAOS stenting using open-cell stents, but there have been no reports documenting the use of the closed-cell, self-expandable Carotid Wallstent for VAOS. In this study, we reported 72 consecutive patients with VAOS treated with the Carotid Wallstent.

Methods

Study population

We analyzed 72 patients treated between December 2006 and November 2018 with the closed-cell, self-expandable Carotid Wallstent for symptomatic VAOS refractory to adequate medication. Patients were defined as having a medically refractory condition if they had persistent symptoms attributable to posterior circulation ischemia despite adequate best medical treatment with dual antiplatelet agents. Brain diffusion-weighted imaging (DWI), computed tomography, and computed tomography angiography were performed on admission. Patients with significant VAOS (>50%) as evaluated from the digital subtraction angiogram (DSA) were included in this study. Symptomatic VAOS was defined as the occurrence of one or more transient ischemic attacks and/or strokes in the vertebrobasilar artery territory within six months. Clinical charts were reviewed for demographic features, clinical characteristics, degrees of stenosis before and after stent placement, regimen of antiplatelet and anticoagulation agents, procedure-related complications, and clinical and angiographic outcomes at follow-up.

Endovascular procedure

A complete neurological history was taken, and a complete examination performed on all patients by a neurologist or neurosurgeon. In all patients, magnetic resonance imaging with magnetic resonance angiography was performed before cerebral angiography. Aortic arch and cerebral angiographies were performed in all patients to evaluate the extra- and intracranial arteries. The rate of stenosis was calculated manually and automatically on the DSA (Multistar or Axiom Artis; Siemens, Munich, Germany) according to North American Symptomatic Carotid Endarterectomy Trial criteria.

In all patients, the therapeutic procedure was performed during a second angiography session, and they received dual antiplatelet medication including 75 mg of clopidogrel and 100 mg of aspirin each day over five days or a loading dose of 300 mg of clopidogrel and 300 mg of aspirin at least 12 h before endovascular treatment. All patients were fully awake for neurological evaluation during the procedure. All angiographic procedures were performed using a transfemoral approach under electrocardiogram and blood pressure monitoring and arterial oxygen saturation. An 8-Fr guiding catheter (Envoy; Cordis Corporation, Fremont, California, USA) or 6-Fr Shuttle sheath connected to a continuous saline flush was positioned in the proximal subclavian artery. In case of buckling of the guiding catheter into the aorta during an attempt to place the balloon or stent, we placed a 0.035 in. guidewire into the distal subclavian artery through the guiding catheter throughout the procedure to stabilize the guiding catheter in an appropriate position. Pre-procedural angiographic images were then obtained in orthogonal planes that best defined the stenotic segment. The diameter of the parent artery distal to the lesion was automatically or manually measured by monoplane or biplane DSA. The stent diameter was chosen based on the distal VA diameter, and a slightly oversized (0.5–1.0 mm) stent was used to enable complete apposition to the vessel wall. The appropriate length was selected to allow complete coverage of the plaque within the VA as well as extension 5 mm distal to the plaque and 3–4 mm proximal to the vertebral ostia in the subclavian artery. In case of the tortuous V1 segment, the longer-length stent was applied to induce vessel to straightening. Prior to the therapeutic procedure, patients were systemically administered heparin, in addition to a bolus injection of 3000 IU heparin. An additional bolus of 1000 IU heparin was administered every hour to maintain an activated coagulation time of >200 s throughout the procedure. Via the guiding catheter, a microwire 0.014 in. in diameter was used to cross the stenotic segment of the VA and was placed distal to the lesion. Over this wire, a distal embolic protection device (EPD) (Spider device, ev3, Plymouth, Minnesota, USA) was placed into the distal VA passing the stenotic segment. And then, a semi-compliant coronary or peripheral angioplasty balloon was navigated to the site of stenosis for the purpose of pre-stent balloon angioplasty. After predilation, a self-expandable stent (Carotid Wallstent; Boston Scientific Corporation, USA) was advanced over the microwire and positioned across the stenotic lesion using roadmapping imaging and external stent markings. The stent was then deployed slowly by unsheathing it under the roadmapping image. In all cases, the proximal end of the stent was tried to be located in the middle of the subclavian artery, so that it overhangs within the lumen of the subclavian artery to prevent foreshortening distal to plaque and provide complete ostial plaque coverage. In case of stent shortening or stent malposition, an additional Carotid Wallstent was implanted to cover the entire stenotic lesion. If a remnant in-stent stenosis was found upon post-stenting angiography, the stent-delivery system was removed, a semi-compliant balloon was placed in the stenotic lesion, and angioplasty was performed within the stent by gradual balloon inflation to prevent vascular dissection or rupture. Practically, post-stent balloon angioplasty was performed in almost all cases. Repeat angiography was performed after 20 min to check for possible complications including contrast extravasation or reocclusion of the vessel. After the procedure, hemostasis of the femoral artery was achieved using an occlusion device. Immediately after the procedure, a complete neurological examination was performed by a neurologist or neurosurgeon, and all patients underwent non-enhanced brain CT for the evaluation of possible hemorrhagic complications. Brain DWI was performed on the first post-procedural day. After the procedure, 100 mg aspirin and 75 mg clopidogrel (Plavix; Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership, USA) were administered daily. Additionally, 2850 IU of low-molecular-weight nadroparin calcium (Fraxiparine; GlaxoSmithKline, France) was also administered subcutaneously two to three times a day for at least three days. Clopidogrel resistance test was performed using a VerifyNow P2Y12 assay shortly after the stenting. In patients who were poor responders to clopidogrel, signaled by VerifyNow P2Y12 assay, cilostazol was administrated.

Follow-up clinical and angiographic outcomes

The time between stenting and the last clinical follow-up ranged from 7 to 42 months (mean, 15.6 months). In order to assess clinical outcomes, we defined a five-grade scale as follows: I, excellent (neurological improvement without neurological complications); II, good (no neurological improvement and no neurological complications); III, fair (transient neurological complications); IV, poor (neurological deterioration and permanent neurological complications); and V, death associated with the procedure. Follow-up angiography was performed 3–34 months after stenting (mean, 13.0 months). Angiographic in-stent restenosis was defined as more than 50% stenosis seen in the follow-up DSA.

Results

Patient demographic data and characteristics are provided in Table 1. The study group comprised 72 patients, 58 men (80.6%) and 14 women (19.4%). Their ages ranged from 47 to 86 years (mean, 65.6 years). Cerebrovascular accident risk factors, based on the patients’ medical records, included hypertension (n = 57), diabetes (n = 33), prior stroke (n = 11), smoking (n = 28), and coronary artery disease (n = 7). The main symptoms at presentation were stroke (n = 29) and transient ischemic attack (n = 43). All patients had VAOS which was considered to be directly responsible for the symptoms. In 47 patients (65.3%), other extra- and/or intra-cranial arterial stenoses were detected. In 40 patients (55.6%), contralateral VA abnormalities were detected, including hypoplasia (n = 9), severe stenosis greater than 50% (n = 12), and occlusion (n = 19). A total of 78 Carotid Wallstents were implanted in 72 patients, and dual stenting was required in six patients due to stent malposition or stent shortening. The sizes of the stents used are as follows: there were 60 of 5 × 30 mm stent, 15 of 7 × 30 mm stent, and 3 of 7 × 50 mm stent.

Table 1.

Patient demographic data and characteristics.

Number of patients	72
Male	58 (80.6%)
Female	14 (19.4%)
Age
Range	47–86
Mean	65.6
CVA risk factor
Hypertension	57 (79.2%)
Diabetes mellitus	33 (45.8)
Coronary artery disease	7 (9.7%)
Smoking	28 (38.9%)
Prior stroke	11 (15.3%)
Main symptoms
Stroke	29 (40.3%)
TIA	43 (59.7%)
Contralateral VA abnormalities	40 (55.6%)
Hypoplasia	9 (12.5%)
Severe stenosis (greater than 50%)	12 (16.7%)
Occlusion	19 (26.4%)

CVA: cerebrovascular accident; TIA: transient ischemic attack; VA: vertebral artery.

Procedural complications and results of treatment are shown in Table 2. The technical success rate of stent deployment and recanalization (defined as 20% or less residual stenosis) was 100%. The mean pre-procedural stenosis was 82.5% (range, 55–95%), and the mean stenosis immediately after stent placement was 6.3%. Procedure-related complications included sudden asystole (n = 1) during balloon angioplasty for remnant in-stent stenosis, acute in-stent thrombosis (n = 3), symptomatic minor stroke due to embolic infarction (n = 3), and stent shortening (n = 1). In the patient who underwent a sudden asystole during balloon angioplasty, the procedure was immediately stopped, and a neurological examination was performed while keeping the airway. After a few minutes, the patient recovered with a normal sinus cardiac rhythm and without neurological abnormality. The acute in-stent thrombosis seen in three patients was lysed with intra-arterial administration of abciximab or tirofiban. Three other patients with symptomatic minor stroke were discharged without significant neurological deficit after antiplatelet and anticoagulation medication. Besides these three patients with symptomatic stroke, DWI at 24 h poststenting disclosed asymptomatic distal embolization in three other patients. Stent shortening occurred immediately after stenting in one patient, resulting in stent malposition. In this patient, an additional Carotid Wallstent was implanted to cover the entire stenotic lesion (Figure 1). All procedure-related complications were thus resolved.

Table 2.

Procedural complications and treatment results.

Procedure-related complications	8 (11.1%)
Acute in-stent thrombosis	3 (4.2%)
Embolic infarction	3 (4.2%)
Asystole	1 (1.4%)
Stent shortening	1 (1.4%)
Postprocedural clinical outcome
Excellent	55 (76.4%)
Good	14 (19.4%)
Fair	3 (4.2%)
Poor	0
Death	0
Follow-up angiographic results	49 (68.1%)
In-stent restenosis	1 (2.0%)
Stent shortening	2 (4.1%)
Stent fracture	0
Follow-up clinical results	57 (79.2%)
Stroke	1 (1.8%)
TIA	2 (3.5%)

Figure 1.

A 52-year-old man presented with vertebrobasilar insufficiency: (a, b) both subclavian angiograms show focal severe stenosis (90%) of both VA origins; (c) anteroposterior radiography after stent deployment reveals malposition of the Carotid Wallstent not covering VA origin (arrow); (d) anteroposterior radiography demonstrates second Wallstent navigation within first stent; (e) immediate post-procedural angiogram reveals complete recanalization of the VA origin without remnant stenosis; (f) left subclavian angiogram obtained 34 months after stenting demonstrates asymptomatic, mild (20%) in-stent restenosis due to intimal hyperplasia.

After procedure, clinical outcomes were as follows: symptomatic relief in 55 patients (clinical grade I, 76.4%), neurological stability in 14 patients (clinical grade II, 19.4%), and transient neurological complications in 3 patients (clinical grade III, 4.2%). There were no cases in clinical grades IV and V. Of 72 patients, 57 (79.2%) had follow-up (mean 15.6 months; range, 7–42 months). Three of 57 patients (5.3%) with follow-up had recurrent symptoms of vertebrobasilar ischemia at 6, 8, and 14 months (mean 9.3 months) after the initial treatment. One patient of these three patients with clinical recurrences was diagnosed with a minimal embolic infarction of the vertebrobasilar territory at 14 months after the initial treatment and underwent new DSA that did not demonstrate greater than 50% restenosis. The other two patients had recurrent dizziness at six and eight months, respectively, but both refused further evaluation.

In 49 patients (68.1%), angiographic follow-up (mean 13.0 months; range, 3–34 months) was performed. In 48 of these 49 patients (98.0%), there was no significant in-stent restenosis. In the remaining one patient with in-stent occlusion, the contralateral VA origin was stenotic; this was treated with an additional Carotid Wallstent to improve vertebrobasilar flow. In two patients (4.1%), stent shortening without in-stent restenosis was detected in the follow-up DSA (Figure 2). No stent fracture had occurred in any of the patients evaluated by follow-up angiography. Representative case is shown in Figure 3.

Figure 2.

A 60-year-old man presented with dizziness and vertigo: (a) left subclavian angiogram shows complete occlusion of the left VA origin; (b) right subclavian angiogram shows focal severe stenosis of the right VA origin; (c, d) radiography and angiogram immediately following Carotid Wallstent placement reveal complete recanalization of the VA origin with appropriate positioning of the stent (arrows); (e, f) right subclavian angiogram obtained eight months after stenting demonstrates proximal migration of the stent (arrows) due to stent shortening without in-stent restenosis.

Figure 3.

A 69-year-old man presented with acute infarction in vertebrobasilar territory: (a) DWI shows acute infarction in the left cerebellar hemisphere and both occipital lobes; (b) left subclavian angiogram shows focal severe stenosis (90%) of the left VA origin; (c) anteroposterior radiography demonstrates balloon angioplasty for remnant in-stent stenosis after Carotid Wallstent placement at the VA origin; (d) immediate post-procedural angiogram reveals complete recanalization of the VA origin with mild remnant stenosis; (e, f) compared with pre-stenting VA angiogram, angiographic perfusion after stenting is much improved.

Discussion

Whether the main cause of posterior circulation ischemic disease is VAOS is an extremely important question; even in patients presenting with posterior circulation ischemic symptoms, it is not always clear that VAOS is the main source of the ischemia. However, Caplan et al.³ reported that among 407 patients in the New England Medical Center Posterior Circulation Registry, the most common site of symptomatic lesions was the extracranial VA. Wityk et al.² reported that 20 of these 407 patients presented with direct artery-to-artery embolic infarction caused by unilateral VAOS. Some authors have stated that hemodynamic impairment is the most important mechanism of infarct formation when embolic cardiac sources are excluded.⁸ Caplan et al.³ documented that hypoperfusion, relating to an occlusive disease of the VA origin, typically causes brief spells of dizziness, veering, visual blurring, and ataxia.

The Carotid Wallstent is a closed-cell, self-expandable, smooth mesh interconnected construction made of elgiloy (a cobalt-chrome alloy) with a small free cell surface. In contrast, an open-cell stent has non-interconnecting struts with a larger free cell surface. The potential advantages of the closed-cell Carotid Wallstent are an increased scaffolding ability and increased resistance against the chronic recoil force at the focal stenotic portion. The closed-cell Carotid Wallstent with its small free cell area and smooth and regular surface may offer better scaffolding than that provided by open-cell stents.⁹ Increased scaffolding ability may prevent atherosclerotic plaque from prolapsing through the stent and becoming vascular emboli, resulting in improved plaque coverage and impaction. In addition, it may decrease the possibility of delayed embolism by plaque protrusion though stent struts in comparison with open-cell stents. In our series, embolic infarction occurred in three patients (4.2%) just after the stenting procedure, but delayed embolic infarction was not detected. Although open-cell stents with their superior flexibility have some advantages over closed-cell stents due to peculiarities of the VA anatomy, they also have lower scaffolding ability.⁹

The VA ostial segment is characterized by large amounts of elastin and smooth muscle, both of which could produce high recoil forces after angioplasty.^10,11 VA stenosis occurs primarily at the ostium of the vessel. At the VA ostium, the tortuosity and small caliber of the vessel, the acute angle from the much larger-caliber subclavian artery, and kinking due to cervical movement may contribute to a greater propensity for recoil after stenting.¹² Straightening of a tortuous vessel by stenting generates a force tending to return the vessel to its original state, and this force may cause recoiling after stenting.¹³ Lederman et al.¹⁴ reported that patients with treated vessels smaller than 4.5 mm had a 36% restenosis rate, compared with 12% in patients with vessels larger than 4.5 mm. Tsunoda et al.¹⁵ estimated that in right coronary artery ostial restenosis, as much as 33% of luminal loss is due to chronic stent recoil, and that in-stent restenosis occurred in areas of stent recoil. As in the right coronary artery ostium, in-stent restenosis due to the chronic recoil force may also occur in the VA ostium. Therefore, VAOS with the above-mentioned recoil forces requires a stent designed specifically to overcome strong recoil forces.⁹ Even though there are no data to support the superiority of a specific stent design, it is considered that a closed-cell, self-expandable stent such as the Carotid Wallstent is more resistant to localized chronic recoil forces than open-cell stent, due to its specific geometry and fully interconnected construction.^16,17 The strong recoil forces at the VA ostium may cause stent fracture. Kim et al.¹⁸ reported two cases of stent fractures after placement of open-cell stents for the treatment of VAOS. These stent fractures were associated with restenosis. Stents with an open-cell design show superior conformability and flexibility, because there are only a few points connecting the cells of the stent.¹⁹ Despite these advantages, the open-cell stent may be vulnerable to localized chronic recoil forces because of the disintegration of loosely attached cells. In this study, using the Carotid Wallstent, no stent fracture was detected during post-procedural and follow-up angiography.

However, closed-cell stents have the disadvantage of stent shortening during or after deployment when compared to open-cell stents. Aikawa et al.²⁰ documented carotid artery stenting in 28 patients and observed that the mean stent deviation at the proximal ends was greater than at the distal ends. The greater shift at the proximal end can be explained by the difference in vessel diameter between the proximal and distal sides and by the fact that the apposition and fixation of the stent to the vessel begins at the distal part of the stent. The authors suggested that to cover the entire stenotic lesion, placement of the center of the stent more proximal to the virtual central line, or the use of a longer stent, might be more effective. A report by Yoon et al.²¹ suggested that to prevent stent shortening, it might be necessary to place the center of the stent at or above the stenotic portion when closed-cell design stents are used. Even though there are no specific reports of stent shortening after stenting for VAOS, the reported mechanism of stent shortening following carotid artery stenting may be applied to VAOS stenting as well. Therefore, in our study, we placed the center of the stent proximal to the virtual central line and placed the proximal end of stent at the central portion in the subclavian artery, with a long enough stent to cover the entire stenotic lesion. However, stent malposition by shortening occurred immediately after stent deployment in one patient, and delayed stent shortening was detected on follow-up angiography in two other patients. In the case of stent shortening during the procedure, an additional Carotid Wallstent was used because the implanted stent did not cover the entire stenotic lesion. Fortunately, the two cases of delayed stent shortening were not associated with in-stent restenosis.

Authors have documented that the technical success rate for placing an open-cell stent at the VAOS is high, with a very low complication rate.^22–25 In our study, overall technical success (defined as 20% or less residual stenosis) was achieved in all 72 patients (100%). There was no significant difference in technical success rates between closed-cell and open-cell stents in the treatment of VAOS. Further, in the case of carotid angioplasty and stenting, there are no studies supporting the superiority of a specific carotid stent cell design with respect to outcomes.²⁶

In this study, procedure-related complications occurred in eight patients (11.1%). These included in-stent thrombosis (n = 3) and symptomatic distal embolization (n = 3). Schillinger et al.²⁶ documented a “scissor effect” of the Carotid Wallstent, referring to the fact that the angle between the stent struts changes during expansion and foreshortening of the Carotid Wallstent, thereby resulting in potentially cutting off parts of atherosclerotic plaque and mobilizing embolic materials. In this study, all three in-stent thrombosis were fortunately resolved with an intraarterial injection of abciximab or tibofiban. Meanwhile, signal intensity abnormalities on DWI at 24 h poststenting were observed in six patients (8.3%), including three patients with symptoms. Dabus et al.²³ reported that VA origin plaques are hard, smooth, and concentric, are less prone to ulceration or intraluminal hemorrhage, and therefore carry less risk of embolism than carotid bifurcation plaques. Therefore, even though the “scissor effect” may have existed during the procedure, no significant neurological complications related to procedure were detected probably due to the characteristics of VA origin plaques and the use of EPD. Furthermore, using a small profile EPD such as the Spider FX enhances navigation, especially in tortuous and critically stenosed cases. Although the evidence that EPDs reduce the incidence of clinical events in carotid artery stenting remains inconclusive, this technique has been widely adopted in clinical practice and has been applied to stenting for VAOS as well.²⁷ Studies such as the one by Qureshi et al.²⁸ used EPDs during angioplasty and stenting of VAOS and showed an overall reduced rate of peri- and postprocedure stroke.

Restenosis is a major concern of stent placement in the VA origin. Restenosis rates of 10–43% following open-cell stenting for VAOS have been documented in the literature, even though these case series were small.^12,29 Wehman et al.²⁹ reported that most cases of restenosis occurred 6–12 months after stent placement, and follow-up angiography was essential. Drug-eluting stents (DES) have been recently introduced in VAOS treatment, which prevent in-stent restenosis via eluted chemical drugs (paclitaxel or sirolimus); some studies reported the efficacy of such DES in VAOS treatment.^9,30 However, Ellis et al.³¹ documented that DES also delays endothelial healing and increases the risk of subsequent thrombosis and that the use of DES is an independent risk factor for very late stent thrombosis (six months to three years) in the coronary artery. In this study, follow-up angiography was performed in 49 patients (68.1%) during a median follow-up of 13.0 months (range, 3–34 months). Even though bare-metal stents were used in all cases, only one patient (2.0%) exhibited asymptomatic in-stent restenosis on follow-up angiography. The factors contributing to this low rate of restenosis are unclear, but may be related to the aforementioned characteristics of Carotid Wallstent. We have summarized the reported studies in which more than 10 patients with VAOS were treated with stenting in Table 3.

Table 3.

A summary of the reported studies on stenting in symptomatic vertebral artery origin stenosis.

Reference	n	Used stent	Technical success rate	Periprocedural morbidity	Periprocedural mortality	Significant restenosis	Recurrent stroke
Lin et al.9	11	DES	11/11 (100)	0	0	0/2 (0)	0/11 (0)
Albuquerque et al.12	33	31 BES, 2 SES	33/33 (100)	0	0	13/30 (43.3)	1/33 (3.0)
Akins et al.22	12	7 BMS, 5 DES	12/12 (100)	0	0	3/12 (25)	2/12 (16.7)
Dabus et al.23	28	4 SES, 19 BES, 5 PTA alone	26/28 (92.9)	0	0	3/10 (30)	5/19 (26.3)
Natarajan et al.24	50	35 BES, 15 DES	50/50 (100)	0	0	11/36 (30.6)	2/44 (4.5)
Weber et al.25	38	BES	38/38 (100)	1/38 (2.6)	0	12/26 (46.2)	1/26 (3.8)
Qureshi et al.28	12	3 BMS, 10 DES	11/12 (91.7)	0	0	NA	NA
Park et al.30	20	DES	20/20 (100)	0	0	5/20 (25)	2/20 (10)
Current study	72	Carotid Wallstent	72/72 (100)	3/72 (4.2)	0	1/49 (2.0)	3/57 (5.3)

Values are n/N (%).

DES: drug-eluting stent; BES: bare-metal stent; SES: self-expandable stent; PTA: percutaneous transluminal angioplasty; NA: not available.

Conclusions

Endovascular treatment of VAOS with a closed-cell, self-expandable Carotid Wallstent in patients presenting with medically refractory vertebrobasilar insufficiency symptoms is feasible, safe, and effective in alleviating patient symptoms and for improving vertebrobasilar blood flow. Short-term clinical outcomes after stent placement are also favorable. However, long-term angiographic and clinical follow-up studies are still needed to define the safety, efficacy, and durability of the closed-cell Carotid Wallstent in treating VAOS.

ORCID iDs

Jun-Kyeung Ko https://orcid.org/0000-0002-5652-7659

Chang-Hwa Choi https://orcid.org/0000-0003-2549-4150

Lee Hwangbo https://orcid.org/0000-0002-1323-4450

Tae-Hong Lee https://orcid.org/0000-0001-5911-5214