Abstract
Objective
To investigate the safety and long-term effect of using the Wingspan stent for severe symptomatic atherosclerotic basilar artery stenosis (≥70%).
Materials and methods
Between July 2007 and April 2013, we had 91 consecutive patients (age range 41–82 years old) with symptomatic severe basilar stenosis (70–99%) who underwent Wingspan stenting at our center. All patients had stenosis-related temporary ischemic attack or strokes. We analyzed the demographic data, pre- and post-procedural cerebral angiography, technical success rate, peri-procedural complications, and clinical and imaging follow-ups.
Results
The Wingspan stenting procedure was successful in all patients: The stenosis was reduced from 82.2% ± 5.8% pre-stenting to 15.9% ± 5.7% post-stenting. The 30-day peri-operative rate for stroke or death was 14.3%, which included ischemic stroke in 12 cases (12/91 = 13.2%) and subarachnoid hemorrhage in one case (1/91 = 1.1%), with a fatal or disabling stroke rate of 2.2%. Among the 77 patients with clinical follow-up assessment within 7–60 months (mean 31.3 ± 15.1 months) after stenting, four patients (5.2%) had posterior ischemia, including one patient with disabling ischemic stroke (1.3%) and three patients (3.9%) with temporary ischemic attack. The 2-year cumulative stroke rate was 16% (95% CI: 8.2–23.8%). Among 46 patients with imaging assessments at 3–45 months (mean, 9.5 ± 8.3) post-stenting, six (13.0%) patients had restenosis, including two (2/46 = 4.3%) with symptomatic restenosis.
Conclusions
The benefit of stenting for patients with severe basilar artery stenosis (> 70%) may lie in lowering the long-term fatal and disabling stroke rate; and as long as the peri-operative stroke rate can be kept at a relatively lower level, patients with severe basilar stenosis can benefit from basilar artery stenting.
Keywords: Adverse effects, atherosclerotic stenosis, basilar artery, imaging, intracranial stenting, long-term effect, restenosis, stenosis, stenting procedures, stroke, temporary ischemic attack, Wingspan stent
Introduction
In patients with symptomatic intracranial atherosclerosis, single-agent treatment with aspirin or warfarin alone is associated with a 2-year ischemic stroke rate of 17–20%.1 The fatal or disabling stroke risk involving symptomatic vertebrobasilar stenosis is very high2,3; and severe vertebrobasilar stenosis portends a stroke and death rate of 8.5–22.8% per year, despite medical therapy.1,4–6 The extracranial-intracranial bypass technique for vertebrobasilar insufficiency failed to demonstrate any advantage over medications, with a relatively high complication rate.7
Intracranial stenting has emerged as a therapeutic option for stroke prevention, in patients with symptomatic and severe intracranial stenosis (≥ 70%).8–10 Nonetheless, the recent publication of the Stenting and Aggressive Medical Management for Preventing Recurrent Stroke (SAMMPRIS) study8,11 demonstrates a higher peri-operative stroke rate than medications alone, and did not favor the use of the Wingspan stent (Stryker Neurovascular, Fremont, CA, USA) for intracranial stenosis; however, the study enrolled only Caucasians, rather than Asians, whom may have had different clinical profiles regarding stroke risk and a different response to stenting. Moreover, the SAMMPRIS study was criticized for the operators’ lack of stenting experience, inclusion of patients whom had not failed medical therapy prior to receiving endovascular intervention, and an inadequate antiplatelet or anticoagulant therapy; because most of the peri-operative strokes occurred in the stenting arm, within 24 hours following stenting.12,13 New devices and complex treatment methods usually necessitate a learning curve; and may result in poor clinical results in the early period, as demonstrated by early coronary and carotid stenting, which are now standard methods for treating coronary and carotid arterial diseases.12,14,15
This study was done to investigate the safety and effect of the Wingspan stent in treating Chinese patients with severe (≥ 70%) basilar atherosclerotic stenosis at a large-volume center.
Materials and methods
The ethics committee of our hospital approved this study; and all patients provided signed informed consent for the stenting procedure between July 2007 and April 2013. The inclusion criteria for stenting were ≥ 70% stenosis of the basilar artery, with symptomatic ischemic stroke or a transient ischemic attack (TIA), 18–85 years of age, length of each stenosis ≤ 15 mm; and with at least one atherosclerotic risk factor (arterial hypertension, diabetes mellitus, hyperlipidemia and smoking). The exclusion criteria included: nonatherosclerotic stenosis, intracranial hemorrhage in the territory of the stenosis within 1 month, potential source of cardiac embolism, concurrent intracranial pathology (tumors, aneurysms or arteriovenous malformation) and contraindication to antiplatelet therapy. We included 91 consecutive patients with severe symptomatic basilar stenosis (70–99%) for Wingspan stenting at our center (Table 1).
Table 1.
Baseline data.
| Variables | |
|---|---|
| Age (yrs) | 61.3 ± 9.2 |
| Hypertension | 79 (86.8%) |
| Diabetes | 36 (39.6%) |
| Hyperlipidemia | 40 (44.0%) |
| Smoking | 34 (37.4%) |
| Coronary heart disease | 12 (13.2%) |
| Stroke history | 27 (29.7%) |
| Final event to stenting (d) | 20.4 ± 14.4 |
d: days; yrs: years.
Percutaneous transluminal angioplasty and stent placement was performed, using the Wingspan system. Access was achieved through the common femoral artery, using a 6F guiding catheter or long-sheath system. Heparinization was instituted, to a targeted activated coagulation time of 250–300 s. After conventional catheter-based angiography, a microcatheter (SL-10, Boston Scientific, Boston, MA, USA; or Prowler-10, Cordis, Miami Lakes, FL, USA) was navigated across the target lesion, using a 0.014-inch microwire. The microcatheter was then exchanged over a 0.014-inch microwire for a Gateway angioplasty balloon, with the microwire tip placed at the relatively straight segment of P2 of the posterior cerebral artery. The Gateway balloon diameter was sized to 80–90% of the ‘normal’ parent artery, proximal or distal to the stenosis; and a balloon was selected to match the stenosis length.
After the balloon was sent to the proper site of stenosis, angioplasty was performed with slow-graded inflation of the balloon, to a pressure of 6 atm, for approximately 10–20 s. Following angioplasty, the balloon was removed and the conventional angiography performed, to observe the improvement of the stenosis. Then, the Wingspan delivery system was advanced over the exchange wire, across the target stenosis. The stent diameter was chosen to exceed the diameter of the normal parent artery by 0.5–1.0 mm, and the length was sized to completely cover the entire stenotic segment. The stent was deployed after it was positioned perfectly. If the residual stenosis was ≤ 30%, compared with the normal diameter proximal to the lesion, and no occlusion was present in the distal arterial branches, the microcatheter and the guiding catheter would be withdrawn to end the procedure.
Before stenting, all patients had antiplatelet agents (aspirin 100 mg/day and clopidogrel 75 mg/day) for at least 3–5 days. In emergency cases, aspirin (300 mg) and clopidogrel (300 mg) were administered once, within 24 h prior to stenting. Nimodipine was intravenously administered for 2 h before stenting, for blood pressure control. Immediately after stenting, computed tomography (CT) was performed to check for possible intracranial hemorrhage. Nimodipine was maintained for 1–3 days, to control the patients’ blood pressure at the lower limit. Low-molecular-weight heparin (4000–6000 U per 12 h) was injected subcutaneously, if no intracranial hemorrhage presented. The dual antiplatelet regimen was maintained for 6 months, and then aspirin therapy (325 mg/day) was prescribed for all patients indefinitely after treatment. At the same time, all patients were educated regarding control of other atherosclerotic risk factors.
All patients were followed within 30 days post-stenting, for any stroke or death. At 3 and 6 months after discharge, clinical evaluation of the patients was performed, including the modified Rankin Scale (mRS) score and the National Institute of Health Stroke Scale (NIHSS) score. Follow-up was scheduled at 12 months post-stenting; and once annually, afterwards. A head CT, magnetic resonance imaging (MRI) or digital subtraction angiography (DSA) were performed for the patients whom had possible recurrent stroke.
We assessed the NIHSS and mRS scores during hospitalization and at endpoint events. The primary endpoint was ischemic stroke or death within 30 days; and beyond 30 days, up to 2 years after stenting. The secondary endpoint was the disabling or fatal stroke rate through the study; and the status of the stented segment on imaging at 1 or 2 years, in terms of changes in luminal diameter.
Statistical analysis
The baseline data, imaging data and stenting results of all patients were presented as means (±SD) for continuous variables and numbers, for categorical data; and these data were tested with the t test, χ2 test or Fisher exact test, as appropriate. The cumulative probability of an event (any stroke or death within 30 days; or stroke in the same territory, after 30 days) over time was estimated using the Kaplan-Meier (product limit) method. The value for significance was set at p < 0.05.
Results
We treated 91 patients with severe basilar stenosis with intracranial Wingspan stenting, including 66 male patients and 25 female patients with an age range of 41–82 years (mean, 61.3 ± 9.2), as shown in Table 1. The presenting symptoms were TIA in 47 patients and ischemic stroke in 44 patients; and the stenosis involved the basilar middle segment in 57 patients, the lower segment in 32 patients and the upper segment in only two patients (Table 2).
Table 2.
Basilar artery stenosis characteristics and imaging.
| Variables | |
|---|---|
| Pre-stenting perforator infarct | 43 (47.3%) |
| Pre-stenting non-perforator infarct | 14 (15.4%) |
| Pre-stenting non-posterior infarct | 34 (37.4%) |
| Stenosis length | 7.4 ± 1.8 |
| > 10 mm | 10 (11.0%) |
| 5–10 mm | 77 (82.4%) |
| < 5 mm | 4 (6.6%) |
| Stenosis location | |
| Mid-basilar segment | 57 (62.6%) |
| Upper basilar segment | 2 (2.2%) |
| Lower basilar segment | 32 (35.2%) |
| Pre-stenting stenosis (%) | 82.2 ± 5.8 |
| Post-stenting residual stenosis (%) | 15.9 ± 5.7 |
The stenting procedure was successful in all 91 patients (100%). The mean stenotic rate was improved from the presenting 82.2% (±5.8%) to the post-stenting 15.9% (± 5.7%), as shown in Table 2. During the 30-day peri-operative period, 12 cases (12/91 = 13.2%) had ischemic stroke, while one patient (1/91 = 1.1%) had a subarachnoid hemorrhage (Table 3), resulting in a stroke or death rate of 14.3% (13 in 91 cases). Among these 13 cases, one died and another had severe paralysis, resulting in a fatal or disabling stroke rate of 2.2% (2 in 91 cases). Eight patients had slight neurological sequelae; but the remaining three patients recovered completely, at 1 month post-stenting. Among the 12 patients with ischemic stroke, eight cases were associated with perforator stroke and four cases with intra-stent thrombosis (the balloon was slightly larger in two cases, and the other two were related to relatively longer stenting times). The only subarachnoid hemorrhage was probably related to hyperperfusion after the stenting.
Table 3.
Perioperative 30-day strokes in 13 patients.
| Stroke within 30 days | Cases (n) | Prognosis | |
|---|---|---|---|
| Ischemic stroke | In-stent thrombosis | 4 | Death in one patient Disabling in one patient (mRS 5 at 1 mo) No apparent neurologic symptoms in two patients |
| Perforator stroke | 8 | With neurologic dysfunction, mRS 1 in two cases, 2 in five cases and 3 in one case. | |
| Hemorrhagic stroke | Subarachnoid hemorrhage | 1 | Without any symptoms at discharge |
Mo: month; mRS: modified Rankin Scale.
Analysis of factors affecting the perioperative stroke rate demonstrated that the stenosis length, degree and location in the middle basilar segment were significant (p < 0.05), whereas the operator’s experience was not (p > 0.05); if the 91 cases were divided into three periods that included the early 30, middle 30 and recent 31 cases (Table 4 and Table 5). Significantly (p < 0.05) more stroke events were present in the longer and more severe stenoses (Table 4), as well as in stenosis located in the middle basilar segment (Table 5).
Table 4.
Correlation of continuous factors with ischemic stroke.
| Factor | Non-ischemic stroke | Ischemic stroke | p |
|---|---|---|---|
| Age (yrs, mean) | 61.2 ± 9.3 | 62.3 ± 9.3 | 0.685 |
| Stenosis length (mm, mean) | 7.2 ± 1.8 | 8.9 ± 1.4 | 0.002 |
| Stenosis degree (%, mean) | 81.4 ± 5.7 | 87.5 ± 4.0 | 0.001 |
| Final event to stenting (days, mean) | 21.3 ± 15.2 | 14.5 ± 4.2 | 0.127 |
mm: millimeters; yrs: year.
Table 5.
Correlation of categorical variables with ischemic stroke.
| Factor | Patients without events, (n) | Patients with events (n) | p value |
|---|---|---|---|
| Gender | |||
| Male | 58 (87.9%) | 8 (12.1%) | 0.730 |
| Female | 21 (84.0%) | 4 (16.0%) | |
| Pre-stenting events | |||
| Stroke | 38 (86.4%) | 6 (13.6%) | 1.000 |
| TIA | 41 (87.2%) | 6 (12.8%) | |
| Hypertension | |||
| No | 12 (100%) | 0 (0%) | 0.355 |
| Yes | 67 (84.8%) | 12 (15.2%) | |
| Diabetes | |||
| No | 47 (85.5%) | 8 (14.5%) | 0.758 |
| Yes | 32 (88.9%) | 4 (11.1%) | |
| Hyperlipemia | |||
| No | 45 (88.2%) | 6 (11.8%) | 0.759 |
| Yes | 34 (85.0%) | 6 (15.0%) | |
| Hyper-hemocyanin | |||
| No | 68 (85.0%) | 12 (15.0%) | 0.348 |
| Yes | 11(100%) | 0 (0%) | |
| Coronary heart disease | |||
| No | 71 (89.9%) | 8 (10.1%) | 0.193 |
| Yes | 9 (75.0%) | 3 (25.0%) | |
| Smoking history | |||
| No | 51 (89.5%) | 6 (10.5%) | 0.353 |
| Yes | 28 (82.4%) | 6 (17.6%) | |
| Symptomatic Stroke history | |||
| No | 54 (84.4%) | 10 (15.6%) | 0.340 |
| Yes | 25 (92.6%) | 2 (7.4%) | |
| Prestenting mRS scores | |||
| 0 | 31 (93.9%) | 2 (6.1%) | 0.199 |
| 1–3 | 48 (82.8%) | 10 (17.2%) | |
| Concurrent with anterior lesions | |||
| No | 45 (88.2%) | 6 (11.8%) | 0.759 |
| Yes | 34 (85.0%) | 6 (15.0%) | |
| Stenosis location | |||
| Middle basilar segment | 46 (80.7%) | 11 (19.3%) | 0.049 |
| Lower basilar segment | 31 (96.9%) | 1 (3.1%) | |
| Pre-stenting perforator infarct | |||
| No | 44 (91.7%) | 4 (8.3%) | 0.216 |
| Yes | 35 (81.4%) | 8 (18.6%) | |
| Operator experience | |||
| A | 26 (86.7%) | 4 (13.3%) | 1.000 |
| B | 26 (86.7%) | 4 (13.3%) | |
| C | 27 (87.1%) | 4 (12.9%) |
Lesions affecting upper basilar artery 1/3 segment were only in two cases.
The p value indicates the Fisher exact test.
A: Wei-Xing Bai; B: Tian-Xiao Li; C: Zi-Liang Wang; TIA: transient ischemic attack.
Clinical follow-up assessment was performed in 77 patients (84.6%) 7–60 months (mean, 31.3 ± 15.1 months) after stenting. Excepting one patient who died in the peri-operative period and another patient with severe paralysis who had no follow-up evaluation, we lost 12 patients to follow-up. Before intracranial stenting, the mRS ranged from 0–3 (mean, 1.18 ± 1.14); and at the post-stenting follow-up, the mRS for the 77 patients ranged from 0–4 (mean, 1.13 ± 1.04), with no significant difference (p > 0.05) compared to before stenting. During the follow-up, we had four patients (4/77 = 5.2%) with posterior ischemia, including one disabling ischemic stroke (1.3%) and three TIAs (3/77 = 3.9%); and one patient whom died from bone fracture complications, 2 years later. Of the four patients with posterior ischemia (except for one patient who had no imaging check-up), three patients had had DSA showing no restenosis in one patient, smaller than 50% restenosis in another patient, and over 50% at the proximal end of the stent in the remaining patient. Within 2 years after stenting, only one patient had ischemic stroke; the 2-year cumulative stroke rate (including 30-day stroke and deaths, and beyond 30-day ischemic stroke, in the same area) was 16% (95% CI 8.2–23.8%), as seen in Figure 1.
Figure 1.
Cumulative stroke rate using the Kaplan-Meier method. The 2-year cumulative stroke rate, including all 30-day peri-operative stroke and deaths; and the ipsilateral stroke rate beyond 30 days was 16.0% (95% CI, 8.2–23.8%).
We performed an imaging assessment in 46 patients at 3–45 months (mean, 9.5 ± 8.3) post-stenting, including CT angiography in 18 cases and digital subtraction angiography in the remaining 28 cases. We had six patients (6/46 = 13.0%) with restenosis, including two (2/46 = 4.3%) with symptomatic restenosis.
Discussion
The perioperative safety and long-term preventive effect of recurrent stroke after stenting are the main concerns in performing basilar stenting. Some studies demonstrate better outcomes of stenting in this aspect, including two studies from a large-volume medical center in China.10,16,17 Our current study investigated the Wingspan stent in the treatment of severe basilar stenosis, with the greatest number of patients reported, and it showed a relatively lower 30-day perioperative stroke or death rate, and better effects of long-term stroke prevention.
There are some reasons for high peri-operative ischemic stroke in basilar artery stenting. One possible reason is the vertebro-basilar anatomy, in which endovascular devices in the basilar artery and spasm around the guiding catheter in the instrumented vertebral artery limit the basilar artery blood supply, causing poor perfusion of the basilar artery. Stasis-induced local thrombus may further increase the risk of ischemic injury. This study found that the length, degree and location of stenosis could significantly affect the peri-operative stroke rate, with significantly (p < 0.05) more stroke events being produced in longer and more severe stenosis (Table 4), as well as in stenosis locating in the middle basilar segment (Table 5). The length and degree of stenosis reflect disease severity and emphasize that technical difficulty is associated with ischemic complications.18 The stenosis degree may reflect the larger burden of embolic debris released when stents are navigated through a severe stenotic lumen of an artery, or redistribution of a larger plaque mass over the surface area incorporating the perforator orifice. The location of stenosis in the middle segment of the basilar artery also significantly affects the stroke rate, probably because of the enriched perforating arteries in this segment. The stent struts and redistributed plaque may not immediately block the perforator orifice, but may encroach sufficiently to disturb local hemodynamics of the perforators, thus causing more ischemic injury.
In our study, eight cases of peri-operative ischemic stroke were related to perforator occlusion or insufficiency. Two cases were caused by intra-stent thrombosis, which was probably associated with the bigger balloon used in them. A bigger balloon for pre-dilation may enhance the ‘snow-plowing’ effect on the one hand, and increase injury to the arterial intima and subsequent intra-stent thrombosis on the other hand. These effects can exaggerate ischemic stroke; so the use of a smaller balloon for sub-optimal pre-dilation may be a better choice, to reduce possible ischemic stroke. The remaining two cases of ischemic stroke were possibly caused by a longer operating time and/or non-connection of the perfusion line to the stent system. One case was due to insufficient anesthesia, leading to restlessness of the patient; and the other was caused by tortuous vertebral artery, resulting in a longer operating time. These two cases indicated that the stent system should be connected to the perfusion line and the stent system should not stay in the body too long, to prevent thrombosis before stent deployment.
Our study had a lower perioperative ischemic stroke or death rate (14.3%), compared with that (20.8%) of the basilar artery stenting in the SAMMPRIS study19; which confirmed that patients with basilar stenosis have a 20.8% rate of peri-operative ischemic events, versus 6.7% for other arteries. Experience is one reason to account for the lower peri-operative ischemic event rate. For any new endovascular devices and complex endovascular procedures like the Wingspan stenting, a learning curve is involved for the operator to become efficient. The stenting operators in our study had all completed the learning curve period, with every operator having finished 20 Wingspan stenting procedures before this study. Thus, the procedure as relates to the stroke rate could be greatly decreased.
In the SAMMPRIS study,20 there was no significant difference in the peri-operative 30-day stroke rate in the high-enrolling centers (15.3%) and low-enrolling centers (16.7%), although the 12 high-enrolling centers had only enrolled 112 patients for the Wingspan stenting procedure. Apparently, the operators in the SAMMPRIS study did not finish their learning curve, even if some operators had other experience for compensation, like angioplasty only or intracranial stent-assisted coiling with the Neuroform stent (Stryker, Kalamazoo, Michigan, USA), or balloon-mounted coronary stents. These stents are quite different from the Wingspan stent, which is relatively stiff compared to the Neuroform stent. Some studies report the difficulty to navigate the Wingspan through tortuous vessels into intracranial vasculature.21,22 In our experience, we also had difficulty in three patients, to navigate the Wingspan stent through the tortuous vessels in other intracranial locations. We believe the experience of performing Wingspan stenting could not be replaced by other stenting experience with other stents.
In comparison with the SAMMPRIS study,19 our study’s peri-operative and 2-year cumulative stroke rates (14.3% involving 13 patients and 16% involving 18 patients, respectively) were higher than those in the medical management arm in the SAMMPRIS study (5.8% involving 13 patients and 14.1%, respectively)8,11; however, in our study, 13 patients had stroke in the 30-day perioperative period, while only 5 patients (including one with disabling stroke) had ischemic stroke during the follow-up. Based on the SAMMPRIS data,8,11 the disabling or fatal stroke probability was 1.8% (4 patients) at 30 days, but 7.8% (18 patients) at 2 years for the medical management group. This indicates that basilar stenting can prevent recurrent basilar ischemic stroke, especially a disabling or fatal stroke. The higher stroke rate in the peri-operative period in our study was probably related to the level of stenting experience of the operator.
It has been noted that the posterior circulation has more ischemic strokes than the anterior circulation in stenting, because of the small diameter and angulation of the vertebral and basilar arteries being associated with a high degree of technical complexity; multiple perforating arteries in the basilar artery being possibly occluded by the stent struts and embolic debris released during angioplasty and stenting; and the important brain stem, which can be injured more seriously by even the ‘smallest’ of embolic debris, than other parts of the cerebral hemispheres.23–25 Even so, some good results had been achieved in the vertebrobasilar stenting. In 2010, Jiang et al.26 performed awake stenting under local anesthesia in 43 patients with vertebrobasilar stenosis (20 cases in the basilar artery). Compared with general anesthesia, which may mask procedure-related neurological changes during stenting and contribute to a higher risk of severe complications, local anesthesia for awake stenting allows the timely detection of acute neurological changes and may reduce the risk of major procedural complications. In that Jiang et al.26 case series, they achieved a 7% perioperative stroke rate, much lower than ours. Therefore, careful management of the stenting procedure in the posterior circulation is beneficial to gain a lowering of the perioperative stroke rate.
During the follow-up of 7–60 months (mean, 31.3 ± 15.1), one patient had a disabling stroke (1.3%) and another three had only a TIA (3.9%). In the three patients with TIA, these TIA in two patients were probably caused by restenosis, which were confirmed by medical imaging data. The 2-year cumulative stroke rate was 16%, indicating that basilar stenting can prevent long-term severe recurrent stroke, consistent with other studies.10,27,28
Imaging follow-up was performed in 46 cases (50.5%), with our restenosis rate of 4.3% (2 out of 46 cases) being apparently lower than in other reports.9,29 Some factors may contribute to this low restenosis rate: Bigger balloon for dilatation, low residual stenosis rate after stenting and longer dual antiplatelet therapy. However, having fewer patients for imaging follow-up may lead to the underestimation of restenosis.
Some good results of intra-cranial stenting have also been reported10,16,27,28; and these studies, like ours, were all conducted in a single, large-volume center with experienced stenting operators, which may have contributed to the good results. Based on the current study, the benefit of stenting for patients with severe basilar artery stenosis (>70%) may lie in lowering the patients’ long-term fatal and disabling stroke rate, and as long as the peri-operative stroke rate can be kept at a relatively lower level, patients with this kind of stenosis can benefit from basilar artery stenting.
This was a non-randomized, non-controlled, single-center study; which may overlook some adverse events. In the future, a randomized, controlled study with multiple high-volume centers and more efficient stenting operators involved may be needed to investigate the exact peri-operative and long-term cumulative stroke rates, as compared with intensive medications alone.
In conclusion, the benefit of stenting for patients with severe basilar artery stenosis (> 70%) may lie in lowering the long-term fatal and disabling stroke rate, and as long as the peri-operative stroke rate can be kept at a relatively lower level, we believe patients with severe basilar stenosis can benefit from basilar artery stenting.
Declaration of conflicting interests
The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The authors received no financial support for the research, authorship, and/or publication of this article.
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