Skip to main content
Advertisement

Main menu

  • Home
  • Content
    • Current Issue
    • Publication Preview--Ahead of Print
    • Past Issue Archive
    • Case of the Week Archive
    • Classic Case Archive
    • Case of the Month Archive
  • For Authors
  • About Us
    • About AJNR
    • Editors
    • American Society of Neuroradiology
  • Submit a Manuscript
  • Podcasts
    • Subscribe on iTunes
    • Subscribe on Stitcher
  • More
    • Subscribers
    • Permissions
    • Advertisers
    • Alerts
    • Feedback
  • Other Publications
    • ajnr

User menu

  • Subscribe
  • Alerts
  • Log in
  • Log out

Search

  • Advanced search
American Journal of Neuroradiology
American Journal of Neuroradiology

American Journal of Neuroradiology

  • Subscribe
  • Alerts
  • Log in
  • Log out

Advanced Search

  • Home
  • Content
    • Current Issue
    • Publication Preview--Ahead of Print
    • Past Issue Archive
    • Case of the Week Archive
    • Classic Case Archive
    • Case of the Month Archive
  • For Authors
  • About Us
    • About AJNR
    • Editors
    • American Society of Neuroradiology
  • Submit a Manuscript
  • Podcasts
    • Subscribe on iTunes
    • Subscribe on Stitcher
  • More
    • Subscribers
    • Permissions
    • Advertisers
    • Alerts
    • Feedback
  • Follow AJNR on Twitter
  • Visit AJNR on Facebook
  • Follow AJNR on Instagram
  • Join AJNR on LinkedIn
  • RSS Feeds
Research ArticleINTERVENTIONAL
Open Access

Effect of Intracranial Atherosclerotic Disease on Endovascular Treatment for Patients with Acute Vertebrobasilar Occlusion

Y.W. Kim, J.M. Hong, D.G. Park, J.W. Choi, D.-H. Kang, Y.S. Kim, O.O. Zaidat, A.M. Demchuk, Y.H. Hwang and J.S. Lee
American Journal of Neuroradiology November 2016, 37 (11) 2072-2078; DOI: https://doi.org/10.3174/ajnr.A4844
Y.W. Kim
aFrom the Departments of Neurology (Y.W.K., Y.H.H.)
bRadiology (Y.W.K., D.-H.K., Y.S.K.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for Y.W. Kim
J.M. Hong
dDepartments of Neurology (J.M.H., D.G.P., J.S.L.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for J.M. Hong
D.G. Park
dDepartments of Neurology (J.M.H., D.G.P., J.S.L.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for D.G. Park
J.W. Choi
eRadiology (J.W.C.), Ajou University School of Medicine and Hospital, Suwon, Republic of Korea
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for J.W. Choi
D.-H. Kang
bRadiology (Y.W.K., D.-H.K., Y.S.K.)
cNeurosurgery (D.-H.K.), Kyungpook National University School of Medicine and Hospital, Daegu, Republic of Korea
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for D.-H. Kang
Y.S. Kim
bRadiology (Y.W.K., D.-H.K., Y.S.K.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for Y.S. Kim
O.O. Zaidat
eRadiology (J.W.C.), Ajou University School of Medicine and Hospital, Suwon, Republic of Korea
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for O.O. Zaidat
A.M. Demchuk
eRadiology (J.W.C.), Ajou University School of Medicine and Hospital, Suwon, Republic of Korea
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for A.M. Demchuk
Y.H. Hwang
aFrom the Departments of Neurology (Y.W.K., Y.H.H.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for Y.H. Hwang
J.S. Lee
dDepartments of Neurology (J.M.H., D.G.P., J.S.L.)
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for J.S. Lee
  • Article
  • Figures & Data
  • Info & Metrics
  • References
  • PDF
Loading

Abstract

BACKGROUND AND PURPOSE: Although intracranial atherosclerotic disease is often encountered during endovascular treatment for acute vertebrobasilar occlusions, its clinical implication is not well-known. We aimed to evaluate whether intracranial atherosclerotic disease influences the clinical outcomes following endovascular treatment of acute vertebrobasilar occlusive stroke.

MATERIALS AND METHODS: Fifty-one patients with acute vertebrobasilar occlusive stroke were included. The onset-to-groin puncture time was ≤12 hours, and aspiration- or stent-based thrombectomy was used as the primary treatment method. Following primary endovascular treatment, intracranial atherosclerotic disease (IAD group) was angiographically diagnosed when a fixed focal stenosis was observed at the occlusion site, whereas embolism (embolic group) was diagnosed if no stenosis was observed. Clinical and treatment variables were compared in both groups, and IAD was evaluated as a prognostic factor for clinical outcomes.

RESULTS: The baseline NIHSS score tended to be lower (14 versus 22, P = .097) in the IAD group (n = 19) than in the embolic group (n = 32). The procedural time was longer in the IAD group (96 versus 61 minutes, P = .002), despite similar rates of TICI 2b–3 (89.5% versus 87.5%, P = 1.000). The NIHSS score at 7 days was higher (21 versus 8, P = .060) and poor outcomes (mRS 4–6 at 3 months) were more frequent in the IAD group (73.7% versus 43.8%, P = .038). IAD (odds ratio, 5.469; 95% CI, 1.09–27.58; P = .040) was independently associated with poor outcomes.

CONCLUSIONS: An arterial occlusion related to IAD was associated with a longer procedural time and poorer clinical outcome. Further studies are warranted to elucidate the appropriate endovascular strategy.

ABBREVIATIONS:

FAST
forced arterial suction thrombectomy
IAD
intracranial atherosclerotic disease

Acute vertebrobasilar occlusive stroke is a condition with high morbidity and mortality.1 With the advancement of endovascular treatment, the prognosis of acute ischemic stroke due to intracranial large-artery occlusion has improved.2⇓⇓⇓⇓⇓–8 Recently, successful clinical trials of endovascular treatment have been conducted, but these studies have mostly targeted anterior circulation occlusions.4⇓⇓⇓–8 Evidence of endovascular treatment for posterior circulation occlusions is still lacking, though a few recent studies have shown better clinical outcomes compared with previous results.9,10

Underlying stenosis due to intracranial atherosclerotic disease (IAD) is often encountered during endovascular treatment for acute intracranial large-artery occlusion. Regarding the pathomechanism of stroke, in situ thrombotic occlusions may occur in addition to hemodynamic compromise due to stenosis.11⇓–13 This IAD-related occlusion causes acute ischemic stroke and was reported to be more frequent in the posterior circulation than in the anterior circulation.14 According to previous literature, the prognosis of acute vertebrobasilar occlusions has been associated with various factors, including the initial severity of neurologic deficits, time to treatment, location of the occlusion, degree of collaterals, treatment modalities, and timely reperfusion.1,10,11,15⇓⇓–18 Nevertheless, to our knowledge, IAD has not been evaluated as a prognostic factor, especially in posterior circulation occlusions.

In the present study, we evaluated whether IAD influences the clinical outcome following endovascular treatment of acute ischemic stroke caused by vertebrobasilar occlusion. We compared the interventional factors and clinical outcome between IAD-related and embolic occlusions.

Materials and Methods

Patients

From consecutive patients with acute ischemic stroke admitted to 2 Korean university hospitals between March 2009 and March 2014, we retrospectively reviewed and enrolled those who met the following criteria: 1) patients who showed acute neurologic symptoms attributable to intracranial vertebral and/or basilar artery occlusion identified by CTA or MRA, 2) time from onset of symptoms to groin puncture of ≤12 hours, and 3) endovascular treatment by using the forced arterial suction thrombectomy (FAST) method with a Penumbra reperfusion catheter (Penumbra, Alameda, California) or stent-based thrombectomy as the primary treatment. Patients were excluded if reperfusion was never observed, because both angiographic etiologies cannot be differentiated; or another etiology of stroke, including vasculitis, arterial dissection, or Moyamoya disease, was diagnosed by transfemoral cerebral angiography. The institutional review board of both hospitals approved this study, and informed consent was obtained from patients and/or their caregivers.

Using transfemoral cerebral angiography, we diagnosed IAD when a significant fixed focal stenosis was observed at the occlusion site during endovascular treatment or final angiography (Fig 1A–D). Significant stenosis was defined according to the following criteria: 1) degree of fixed stenosis of >70%,19 or 2) moderate stenosis with either flow and perfusion impairment on angiography or an evident tendency toward reocclusion,13 even after sufficient primary endovascular treatment was performed. Underlying IAD can be observed from partial recanalization spontaneously or after intravenous thrombolytic treatment, but these cases were excluded in this study because primary thrombectomy devices for intracranial occlusions were allowed. An embolism was diagnosed if no stenosis was observed with sufficient blood flow and without a reocclusion tendency (Fig 1E–H). The steps used to diagnose IAD in an occlusion during endovascular treatment are summarized in Fig 2. Patients were classified into the IAD or embolic group, and the clinical and treatment variables were compared.

Fig 1.
  • Download figure
  • Open in new tab
  • Download powerpoint
Fig 1.

Sequential angiographic images of a patient with an atherosclerotic basilar occlusion (A–D) and a patient with an embolic basilar occlusion (E–H). An occlusion in the basilar artery in a 70-year-old woman (A). Note significant focal stenosis at the occlusion site after the first pass of thrombectomy (B). Follow-up angiography after 10 minutes demonstrates that the vessel is occluding again (C). Significant fixed focal stenosis in the final angiogram after repeat thrombectomy (D). An occlusion in the basilar artery of a 63-year-old man (E). A single forced arterial suction thrombectomy (F), and complete reperfusion of the basilar artery without residual stenosis as shown on the Towne and lateral views, respectively (G and H).

Fig 2.
  • Download figure
  • Open in new tab
  • Download powerpoint
Fig 2.

Steps to angiographically diagnosing intracranial atherosclerotic disease in an occlusion.

Acute Stroke Management Protocol and Endovascular Procedure

The initial neurologic examination, which included the NIHSS, was performed in the emergency department. Nonenhanced brain CT was performed to evaluate brain parenchyma and to exclude intracerebral hemorrhage, while CTA or MRA was used to assess arterial occlusions. In terms of intravenous thrombolysis, recombinant tissue plasminogen activator was administered to patients within a 3-hour (until December 2012) or 4.5-hour window (from January 2013) according to the stroke guidelines.20 Additionally, endovascular treatment was used in the following cases: 1) a baseline NIHSS score of ≥4, 2) baseline modified Rankin Scale score of ≤2, 3) the presence of vertebrobasilar occlusion on CTA or MRA, 4) no intracerebral hemorrhage on brain CT, and 5) groin puncture time of ≤12 hours from the onset of symptoms.

First, a guide catheter was positioned from the femoral artery to the distal V2 segment of the dominant vertebral artery. In most cases, we used a conventional access device such as the Shuttle-SL guide sheath (Cook, Bloomington, Indiana) or Envoy (Codman & Shurtleff, Raynham, Massachusetts), and not a balloon catheter, for posterior circulation treatment. Then, the neurointerventionalists decided to perform a mechanical thrombectomy by using a Penumbra reperfusion catheter (041/4MAX/3MAX; Penumbra) or a stent retriever (Solitaire AB/FR; Covidien, Irvine, California) as the primary strategy. For the FAST method, the Penumbra reperfusion catheter was placed at the proximal end of the clot. After wedging the clot into the catheter tip for several minutes, we withdrew the catheter gently while maintaining a negative pressure by using a 50-mL syringe.21 In case of stent retrieval, a microcatheter was advanced through the occluded segment, and selective angiography was performed distal to the clot to confirm the landing zone of the stent retriever. The microcatheter was placed about 1 cm beyond the distal margin of the clot, and the stent retriever was deployed for several minutes. The stent retriever and microcatheter were drawn back into the guide catheter under remote aspiration through the guide catheter by suction by using a 50-mL syringe.

These procedures were repeated until successful reperfusion. If reperfusion was not achieved or the occlusion was sustained, we applied rescue treatments, including the switching strategy,22 angioplasty,23 stent placement,24 and intra-arterial tirofiban infusion,13 with consensus from the neurointerventionalist and neurologist. Follow-up angiography was performed 10–20 minutes after recanalization. If there were no changes or improvement of flow between the angiographic runs, the endovascular procedure was completed. However, if flow impairment or reocclusion occurred, we performed additional procedures, including repetitive mechanical thrombectomy or rescue treatments.

Clinical and Radiographic Evaluation

Data regarding the patient demographics, laboratory findings, imaging findings, and time intervals (ie, the symptom onset-to-door time, door-to-groin puncture, and groin puncture to reperfusion) were collected. The procedural time was defined from the groin puncture to reperfusion. The NIHSS scale was assessed at baseline, on day 7, or at discharge if the patient was discharged earlier than day 7. The clinical outcome was assessed by using the mRS at 3 months, which was classified as favorable (mRS score, 0–3) or poor (mRS score, 4–6). Neurologists and neuroradiologists from each hospital independently reviewed the radiologic data of their own hospital while blinded to the clinical information.

Locations of the occlusions were defined as follows: 1) the intracranial vertebral artery (limited to a single vertebral artery), from the V4 segment of the vertebral artery to below the vertebrobasilar junction; 2) the proximal basilar artery, from the vertebrobasilar junction to the anterior inferior cerebellar artery level; 3) the middle basilar artery, from the anterior inferior cerebellar artery to the superior cerebellar artery level; and 4) the distal basilar artery, from the superior cerebellar artery to the basilar artery top level.15 The presence of any posterior communicating artery was also recorded to assess the collateral flow.

The status of reperfusion was measured by using a TICI score.25 Successful reperfusion was defined as a TICI score of 2b or 3. All patients underwent a follow-up nonenhanced brain CT scan 1 day after endovascular treatment. An intracerebral hemorrhage was classified according to the second European-Australasian Acute Stroke Study classification,26 and symptomatic intracerebral hemorrhage was defined as any hemorrhage associated with an NIHSS score increase of ≥4 within 24 hours.2

Statistical Analysis

Statistical analyses were performed by using SPSS for Windows (Version 20.0; IBM, Armonk, New York). The χ2 test or Fisher exact test was used for frequency comparisons, and the independent t test and Mann-Whitney U test were used for continuous and nonparametric variables, respectively. Binary logistic regression analysis was performed to confirm whether IAD was an independent predictor of poor outcome at 3 months. For this analysis, age, the baseline NIHSS score, the absence of intravenous rtPA, onset-to-reperfusion time, failed revascularization, and the absence of a collateral posterior communicating artery were adjusted. A P value <.05 was considered statistically significant.

Results

Of 55 enrolled patients, 4 were excluded for the following reasons: Three had an undetermined etiology related to no angiographic reperfusion, and one had vertebral artery dissection (Fig 3). Finally, 51 patients were included. IAD accounted for 37.3% (n = 19) of patients, whereas an embolism accounted for 62.7% (n = 32). The baseline demographics were similar between the 2 groups (Table 1). A trend toward lower baseline NIHSS scores was observed in the IAD group compared with the embolic group (median, 14 versus 22; P = .097). Among the stroke risk factors, atrial fibrillation was more prevalent in the embolic group (10.5% versus 40.6%, P = .023). The location of the occlusion on CTA was different between the 2 groups. Occlusions in the middle basilar artery were more frequent in the IAD group (38.5% versus 8.3%), whereas occlusions in the distal basilar artery (15.4% versus 87.5%) were more frequent in the embolic group (overall, P < .001). The incidence of intravenous rtPA administration was higher in the embolic group than in the IAD group (21.1% versus 62.5%, P = .004). The onset-to-groin puncture time did not differ between the IAD and embolic groups (310 ± 137 minutes versus 263 ± 146 minutes, P = .258).

Fig 3.
  • Download figure
  • Open in new tab
  • Download powerpoint
Fig 3.

Flowchart of the present study.

View this table:
  • View inline
  • View popup
Table 1:

Baseline demographics and characteristics

The rate of successful reperfusion did not differ between groups (89.5% versus 87.5%, P = 1.000). The frequency of primary endovascular treatment methods also did not differ; the FAST method with a Penumbra reperfusion catheter was most commonly used (78.9% versus 84.4%, P = .711). The procedural time was significantly longer in the IAD group than in the embolic group (mean, 96.42 ± 46.03 minutes versus 61.16 ± 31.84 minutes; P = .002). During the endovascular procedure, reocclusion after reperfusion of the target vessel occurred more frequently in the IAD group (57.9% versus 15.6%, P = .002), and this group required rescue treatment more frequently (68.4% versus 18.8%, P < .001). Between the IAD and embolic groups, we used the following rescue treatments: conversion to another mechanical thrombectomy device (16.7% versus 6.2%, respectively; P = .348), angioplasty (31.6% versus 12.5%, respectively; P = .146), stent placement (31.6% versus 12.5%, respectively; P = .146), and the administration of intra-arterial tirofiban (31.6% versus 0%, respectively; P = .002). Four patients in the embolic group had extracranial-to-intracranial tandem occlusions, so angioplasty and stent placement were performed for extracranial proximal vertebral artery stenosis. Detailed information on the angiographic and clinical outcomes is presented in Table 2.

View this table:
  • View inline
  • View popup
Table 2:

Angiographic and clinical outcomes

The NIHSS score at 7 days tended to be higher (median, 21 versus 8; P = .060), and a favorable outcome at 3 months was less frequent in the IAD group compared with the embolic group (26.3% versus 56.2%, P = .038; Fig 4). In the IAD group, 50% of patients had an mRS score of 5 compared with 13% in the embolic group; however, the mortality rate did not differ between groups (21.1% versus 21.9%, respectively; P = 1.000). Hemorrhagic complications also did not differ. By multiple logistic regression analysis, IAD (odds ratio, 5.469; 95% confidence interval, 1.085–25.580; P = .040) was an independent predictor of a poor outcome (Table 3).

Fig 4.
  • Download figure
  • Open in new tab
  • Download powerpoint
Fig 4.

Modified Rankin Scale score at 3 months for each group. A favorable outcome is significantly less frequent in the intracranial atherosclerotic disease group compared with the embolism group, despite a similar mortality (mRS, 0–3: 26.3% versus 56.2%; P = .038).

View this table:
  • View inline
  • View popup
Table 3:

Multiple logistic regression analyses for IAD as a poor prognostic factor at 3 months

Discussion

In the current study, we achieved an overall successful reperfusion rate of 83.3%. In addition, 45.1% of the clinical outcomes were favorable, and the mortality rate was 21.6% after endovascular treatment of acute vertebrobasilar occlusions. These outcomes were comparable with those in previous studies.17,27 However, the outcomes were distinctive when occlusions were divided according to angiographically defined classifications (ie, IAD-related and embolic occlusions). In our analysis, IAD was an independent risk factor for poor outcomes.

IAD-related occlusions were frequent in our population. In the current study, IAD accounted for about 40% of the acute vertebrobasilar occlusions. This incidence is much higher than that in the Western population, in which intracranial stenosis was observed in only 5.5% of patients with stent-retriever thrombectomy.28 On the contrary, intracranial stenosis was observed in 22.9% of patients with multimodal endovascular treatment in a Korean study.29 IAD may be more frequent in the posterior circulation than in the anterior circulation. In another study from a Korean hospital, IAD accounted for 37% and 9% of posterior and anterior circulations, respectively.14 Along with a high incidence of IAD in the posterior circulation due to acute ischemic stroke, poor prognosis was a clinical implication in the current study.

Differentiating and defining IAD is of clinical importance because secondary or rescue endovascular treatment would be needed and the proper treatment method is essential. Our definition system was solely based on angiographic findings to determine the endovascular treatment strategy, and it was different from that of the Trial of ORG 10172 in Acute Stroke Treatment classification, which requires a full cardioembolism work-up and a secondary prevention plan.30 As mentioned already, hidden IAD is frequently observed in occlusions, and rescue treatment is often needed and should be urgently determined in the angiography suite.

To differentiate and define IAD, we used several steps based on an intracranial large-artery occlusion, as described in Fig 2. The first step was to exclude other uncommon etiologies such as dissection, Moyamoya disease, and vasculitis.14 Transfemoral cerebral angiography before endovascular treatment can show these uncommon etiologies because it is the criterion standard. The second step is to rule out pure embolism, which can be confirmed by primary thrombectomy endovascular treatment. If full recanalization without remnant stenosis is achieved at the occlusion site, the occlusion is thought to be due to a distant embolism. Because we do not need to consider additional therapy in the angiography suite, whether the embolic mechanism was unclear is irrelevant. If a focal fixed stenosis is sustained, interventionalists should consider whether IAD may be hidden in the occlusion. The third step is to confirm whether the stenosis is significant. If severe stenosis is still observed after a repeat primary thrombectomy, IAD must be present. Usually, a stenotic degree of >70% is considered a significant risk factor for the recurrence of ischemic stroke.19 A stenotic degree of <70% but with a stenotic lesion that has been repeatedly occluded or a flow that is not fluent is also considered a significant stenosis.13 The fourth step is to wait 10–20 minutes after recanalization. We can assess reocclusion and differentiate the iatrogenic vessel injury or vasospasm. By following these steps, we can define the underlying IAD, which should exclude uncommon etiologies and procedural complications. During endovascular treatment, transfemoral cerebral angiography can be performed in real-time to determine whether there is an underlying IAD.

Various factors in IAD-related occlusions seemed to have affected the outcome. First, the location possibly affected it. Baseline CTA findings highlighted differences in the location of the occlusions. In accordance with prior studies,11,15,16 the most common location of occlusions was the proximal and middle basilar artery in the IAD group and the distal basilar artery in the embolic group. Additionally, the location of the occlusion is associated with the prognosis.11,31 For instance, an occlusion of the proximal and middle basilar artery, which serves most of the pons, can be related to extensive ischemia of the pons, leading to a fatal condition such as locked-in syndrome.32 In the Stenting vs Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis study, the basilar artery trunk was associated with poor outcomes because those procedures may disturb the blood flow of basilar perforators.33 In the IAD group of our study, >50% of patients had an mRS score of 5, and the locked-in syndrome can be associated with such disabilities.

Second, depending on the angiographic classification, the endovascular procedure differed. The IAD group required a longer procedural time than the embolic group, despite a similar final reperfusion rate. Frequent arterial reocclusions that required repetitive thrombectomy procedures and additional rescue treatments were attributed to the longer procedural duration. Theoretically, endovascular treatment by using mechanical thrombectomy with FAST and a stent retriever can remove a thrombus in the IAD lesion.34 In addition, the IAD lesion must have factors such as plaque disruption, endothelial damage or irritation, or a local platelet activation-prone situation,35 which causes frequent acute arterial reocclusion during endovascular treatment.13 In the current study, 68.4% of the IAD group required rescue treatment for reocclusion.

This study has several potential limitations. First, it was retrospective in nature, though the data were prospectively registered at each hospital. This study was intended for patients who were undergoing endovascular treatment; because the enrolled patients were not randomized and were limited to achieving recanalization, some selection bias may exist. Nonetheless, only 3 patients were excluded due to reperfusion failure, so its effect on the analyses was probably minor. Second, there may be confounding factors, including the choice of rescue treatment and management strategies after endovascular treatment, because the data were collected from 2 different university hospitals. Third, the radiologic definition system differentiating IAD-related and embolic occlusions should be further validated. Although we have focused on the usage of this system for hyperacute treatment and have done our best to gather expert opinions, there are still weaknesses. We do not know what happened in patients whose occluded arteries were never recanalized. In addition, about 10% of patients with atrial fibrillation were still present in the IAD group. Finally, this study did not provide a good strategy for endovascular treatment of IAD-related occlusions in the posterior circulation. Therefore, further studies are warranted to determine a better strategy.

Conclusions

In patients with acute vertebrobasilar stroke who underwent endovascular treatment, IAD-related arterial occlusion was associated with a complicated endovascular procedure and poor clinical outcomes despite successful reperfusion.

Footnotes

  • Disclosures: Osama O. Zaidat—UNRELATED: Consultancy: Stryker, Medtronic; Expert Testimony: payment to both me and my institution; Patents (planned, pending or issued): patent pending. Andrew M. Demchuk—UNRELATED: Grants/Grants Pending: Medtronic,* Comments: unrestricted grant for the Endovascular Treatment for Small Core and Proximal Occlusion Ischemic Stroke trial; Consultancy: Medtronic, Comments: honorarium for Continuing Medical Education events. *Money paid to the institution.

  • This research was partly supported by the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education (NRF-2014R1A1A1008249, J.S.L.).

Indicates open access to non-subscribers at www.ajnr.org

References

  1. 1.↵
    1. Smith WS
    . Intra-arterial thrombolytic therapy for acute basilar occlusion: pro. Stroke 2007;38:701–03 doi:10.1161/01.STR.0000247897.33267.42 pmid:17261720
    Abstract/FREE Full Text
  2. 2.↵
    1. Saver JL,
    2. Jahan R,
    3. Levy EI, et al
    ; SWIFT Trialists. Solitaire flow restoration device versus the Merci retriever in patients with acute ischaemic stroke (SWIFT): a randomised, parallel-group, non-inferiority trial. Lancet 2012;380:1241–49 doi:10.1016/S0140-6736(12)61384-1 pmid:22932715
    CrossRefPubMed
  3. 3.↵
    1. Nogueira RG,
    2. Lutsep HL,
    3. Gupta R, et al
    ; TREVO 2 Trialists. Trevo versus Merci retrievers for thrombectomy revascularisation of large vessel occlusions in acute ischaemic stroke (TREVO 2): a randomised trial. Lancet 2012;380:1231–40 doi:10.1016/S0140-6736(12)61299-9 pmid:22932714
    CrossRefPubMed
  4. 4.↵
    1. Berkhemer OA,
    2. Fransen PSS,
    3. Beumer D, et al
    . A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med 2015;372:11–20 doi:10.1056/NEJMoa1411587 pmid:25517348
    CrossRefPubMed
  5. 5.↵
    1. Campbell BC,
    2. Mitchell PJ,
    3. Kleinig TJ, et al
    ; EXTEND-IA Investigators. Endovascular therapy for ischemic stroke with perfusion-imaging selection. N Engl J Med 2015;372:1009–18 doi:10.1056/NEJMoa1414792 pmid:25671797
    CrossRefPubMed
  6. 6.↵
    1. Goyal M,
    2. Demchuk AM,
    3. Menon BK, et al
    ; ESCAPE Trial Investigators. Randomized assessment of rapid endovascular treatment of ischemic stroke. N Engl J Med 2015;372:1019–30 doi:10.1056/NEJMoa1414905 pmid:25671798
    CrossRefPubMed
  7. 7.↵
    1. Jovin TG,
    2. Chamorro A,
    3. Cobo E, et al
    ; REVASCAT Trial Investigators. Thrombectomy within 8 hours after symptom onset in ischemic stroke. N Engl J Med 2015;372:2296–306 doi:10.1056/NEJMoa1503780 pmid:25882510
    CrossRefPubMed
  8. 8.↵
    1. Saver JL,
    2. Goyal M,
    3. Bonafé A, et al
    ; SWIFT PRIME Investigators. Stent-retriever thrombectomy after intravenous t-PA vs. t-PA alone in stroke. N Engl J Med 2015;372:2285–95 doi:10.1056/NEJMoa1415061 pmid:25882376
    CrossRefPubMed
  9. 9.↵
    1. Eom YI,
    2. Hwang YH,
    3. Hong JM, et al
    . Forced arterial suction thrombectomy with the Penumbra reperfusion catheter in acute basilar artery occlusion: a retrospective comparison study in 2 Korean university hospitals. AJNR Am J Neuroradiol 2014;35:2354–59 doi:10.3174/ajnr.A4045 pmid:25034774
    Abstract/FREE Full Text
  10. 10.↵
    1. Singer OC,
    2. Berkefeld J,
    3. Nolte CH, et al
    ; ENDOSTROKE Study Group. Mechanical recanalization in basilar artery occlusion: the ENDOSTROKE study. Ann Neurol 2015;77:415–24 doi:10.1002/ana.24336 pmid:25516154
    CrossRefPubMed
  11. 11.↵
    1. Eckert B,
    2. Kucinski T,
    3. Pfeiffer G, et al
    . Endovascular therapy of acute vertebrobasilar occlusion: early treatment onset as the most important factor. Cerebrovasc Dis 2002;14:42–50 doi:10.1159/000063722 pmid:12097850
    CrossRefPubMed
  12. 12.↵
    1. Schulte-Altedorneburg G,
    2. Hamann GF,
    3. Mull M, et al
    . Outcome of acute vertebrobasilar occlusions treated with intra-arterial fibrinolysis in 180 patients. AJNR Am J Neuroradiol 2006;27:2042–47 pmid:17110663
    Abstract/FREE Full Text
  13. 13.↵
    1. Kang DH,
    2. Kim YW,
    3. Hwang YH, et al
    . Instant reocclusion following mechanical thrombectomy of in situ thromboocclusion and the role of low-dose intra-arterial tirofiban. Cerebrovasc Dis 2014;37:350–55 doi:10.1159/000362435 pmid:24941966
    CrossRefPubMed
  14. 14.↵
    1. Lee JS,
    2. Hong JM,
    3. Lee KS, et al
    . Endovascular therapy of cerebral arterial occlusions: intracranial atherosclerosis versus embolism. J Stroke Cerebrovasc Dis 2015;24:2074–80 doi:10.1016/j.jstrokecerebrovasdis.2015.05.003 pmid:26163890
    CrossRefPubMed
  15. 15.↵
    1. Cross DT 3rd.,
    2. Moran CJ,
    3. Akins PT, et al
    . Relationship between clot location and outcome after basilar artery thrombolysis. AJNR Am J Neuroradiol 1997;18:1221–28 pmid:9282845
    Abstract
  16. 16.↵
    1. Voetsch B,
    2. DeWitt LD,
    3. Pessin MS, et al
    . Basilar artery occlusive disease in the New England Medical Center Posterior Circulation Registry. Arch Neurol 2004;61:496–504 doi:10.1001/archneur.61.4.496 pmid:15096396
    CrossRefPubMed
  17. 17.↵
    1. Miteff F,
    2. Faulder KC,
    3. Goh AC, et al
    . Mechanical thrombectomy with a self-expanding retrievable intracranial stent (Solitaire AB): experience in 26 patients with acute cerebral artery occlusion. AJNR Am J Neuroradiol 2011;32:1078–81 doi:10.3174/ajnr.A2447 pmid:21493763
    Abstract/FREE Full Text
  18. 18.↵
    1. Pfefferkorn T,
    2. Holtmannspötter M,
    3. Schmidt C, et al
    . Drip, ship, and retrieve: cooperative recanalization therapy in acute basilar artery occlusion. Stroke 2010;41:722–26 doi:10.1161/STROKEAHA.109.567552 pmid:20150550
    Abstract/FREE Full Text
  19. 19.↵
    1. Kasner SE,
    2. Chimowitz MI,
    3. Lynn MJ, et al
    ; Warfarin Aspirin Symptomatic Intracranial Disease Trial Investigators. Predictors of ischemic stroke in the territory of a symptomatic intracranial arterial stenosis. Circulation 2006;113:555–63 doi:10.1161/CIRCULATIONAHA.105.578229 pmid:16432056
    Abstract/FREE Full Text
  20. 20.↵
    1. Jauch EC,
    2. Saver JL,
    3. Adams HP, et al
    ; American Heart Association Stroke Council, Council on Cardiovascular Nursing, Council on Peripheral Vascular Disease, Council on Clinical Cardiology. Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2013;44:870–947 doi:10.1161/STR.0b013e318284056a pmid:23370205
    Abstract/FREE Full Text
  21. 21.↵
    1. Kang DH,
    2. Hwang YH,
    3. Kim YS, et al
    . Direct thrombus retrieval using the reperfusion catheter of the Penumbra system: forced-suction thrombectomy in acute ischemic stroke. AJNR Am J Neuroradiol 2011;32:283–87 doi:10.3174/ajnr.A2299 pmid:21087940
    Abstract/FREE Full Text
  22. 22.↵
    1. Kang DH,
    2. Kim YW,
    3. Hwang YH, et al
    . Switching strategy for mechanical thrombectomy of acute large vessel occlusion in the anterior circulation. Stroke 2013;44:3577–79 doi:10.1161/STROKEAHA.113.002673 pmid:24021683
    Abstract/FREE Full Text
  23. 23.↵
    1. Kashiwagi J,
    2. Kiyosue H,
    3. Hori Y, et al
    . Endovascular recanalization of acute intracranial vertebrobasilar artery occlusion using local fibrinolysis and additional balloon angioplasty. Neuroradiology 2010;52:361–70 doi:10.1007/s00234-010-0658-9 pmid:20119683
    CrossRefPubMed
  24. 24.↵
    1. Eckert B,
    2. Koch C,
    3. Thomalla G, et al
    . Aggressive therapy with intravenous abciximab and intra-arterial rtPA and additional PTA/stenting improves clinical outcome in acute vertebrobasilar occlusion: combined local fibrinolysis and intravenous abciximab in acute vertebrobasilar stroke treatment (FAST)—results of a multicenter study. Stroke 2005;36:1160–65 doi:10.1161/01.STR.0000165918.80812.1e pmid:15890988
    Abstract/FREE Full Text
  25. 25.↵
    1. Higashida RT,
    2. Furlan AJ,
    3. Roberts H, et al
    ; Technology Assessment Committee of the Society of Interventional Radiology. Trial design and reporting standards for intra-arterial cerebral thrombolysis for acute ischemic stroke. Stroke 2003;34:e109–37 doi:10.1161/01.STR.0000082721.62796.09 pmid:12869717
    Abstract/FREE Full Text
  26. 26.↵
    1. Hacke W,
    2. Kaste M,
    3. Fieschi C, et al
    . Randomised double-blind placebo-controlled trial of thrombolytic therapy with intravenous alteplase in acute ischaemic stroke (ECASS II): Second European-Australasian Acute Stroke Study Investigators. Lancet 1998;352:1245–51 doi:10.1016/S0140-6736(98)08020-9 pmid:9788453
    CrossRefPubMed
  27. 27.↵
    1. Lutsep HL,
    2. Rymer MM,
    3. Nesbit GM
    . Vertebrobasilar revascularization rates and outcomes in the MERCI and multi-MERCI trials. J Stroke Cerebrovasc Dis 2008;17:55–57 doi:10.1016/j.jstrokecerebrovasdis.2007.11.003 pmid:18346645
    CrossRefPubMed
  28. 28.↵
    1. Gascou G,
    2. Lobotesis K,
    3. Machi P, et al
    . Stent retrievers in acute ischemic stroke: complications and failures during the perioperative period. AJNR Am J Neuroradiol 2014;35:734–40 doi:10.3174/ajnr.A3746 pmid:24157734
    Abstract/FREE Full Text
  29. 29.↵
    1. Yoon W,
    2. Kim SK,
    3. Park MS, et al
    . Endovascular treatment and the outcomes of atherosclerotic intracranial stenosis in patients with hyperacute stroke. Neurosurgery 2015;76:680–86; discussion 686 doi:10.1227/NEU.0000000000000694 pmid:25988927
    CrossRefPubMed
  30. 30.↵
    1. Adams HP Jr.,
    2. Bendixen BH,
    3. Kappelle LJ, et al
    . Classification of subtype of acute ischemic stroke: definitions for use in a multicenter clinical trial—TOAST. Trial of Org 10172 in Acute Stroke Treatment. Stroke 1993;24:35–41 doi:10.1161/01.STR.24.1.35 pmid:7678184
    Abstract/FREE Full Text
  31. 31.↵
    1. Brandt T,
    2. von Kummer R,
    3. Müller-Küppers M, et al
    . Thrombolytic therapy of acute basilar artery occlusion: variables affecting recanalization and outcome. Stroke 1996;27:875–81 doi:10.1161/01.STR.27.5.875 pmid:8623107
    Abstract/FREE Full Text
  32. 32.↵
    1. Nordgren RE,
    2. Markesbery WR,
    3. Fukuda K, et al
    . Seven cases of cerebromedullospinal disconnection: the “locked-in” syndrome. Neurology 1971;21:1140–48 doi:10.1212/WNL.21.11.1140 pmid:5166219
    FREE Full Text
  33. 33.↵
    1. Fiorella D,
    2. Derdeyn CP,
    3. Lynn MJ, et al
    ; SAMMPRIS Trial Investigators. Detailed analysis of periprocedural strokes in patients undergoing intracranial stenting in Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis (SAMMPRIS). Stroke 2012;43:2682–88 doi:10.1161/STROKEAHA.112.661173 pmid:22984008
    Abstract/FREE Full Text
  34. 34.↵
    1. Lee JS,
    2. Hong JM,
    3. Lee KS, et al
    . Primary stent retrieval for acute intracranial large artery occlusion due to atherosclerotic disease. J Stroke 2016;18:96–101 doi:10.5853/jos.2015.01347 pmid:26467196
    CrossRefPubMed
  35. 35.↵
    1. Bang OY
    . Intracranial atherosclerosis: current understanding and perspectives. J Stroke 2014;16:27–35 doi:10.5853/jos.2014.16.1.27 pmid:24741562
    CrossRefPubMed
  • Received November 7, 2015.
  • Accepted after revision April 24, 2016.
  • © 2016 by American Journal of Neuroradiology
View Abstract
PreviousNext
Back to top

In this issue

American Journal of Neuroradiology: 37 (11)
American Journal of Neuroradiology
Vol. 37, Issue 11
1 Nov 2016
  • Table of Contents
  • Index by author
  • Complete Issue (PDF)
Advertisement
Print
Download PDF
Email Article

Thank you for your interest in spreading the word on American Journal of Neuroradiology.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Effect of Intracranial Atherosclerotic Disease on Endovascular Treatment for Patients with Acute Vertebrobasilar Occlusion
(Your Name) has sent you a message from American Journal of Neuroradiology
(Your Name) thought you would like to see the American Journal of Neuroradiology web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Effect of Intracranial Atherosclerotic Disease on Endovascular Treatment for Patients with Acute Vertebrobasilar Occlusion
Y.W. Kim, J.M. Hong, D.G. Park, J.W. Choi, D.-H. Kang, Y.S. Kim, O.O. Zaidat, A.M. Demchuk, Y.H. Hwang, J.S. Lee
American Journal of Neuroradiology Nov 2016, 37 (11) 2072-2078; DOI: 10.3174/ajnr.A4844

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Share
Effect of Intracranial Atherosclerotic Disease on Endovascular Treatment for Patients with Acute Vertebrobasilar Occlusion
Y.W. Kim, J.M. Hong, D.G. Park, J.W. Choi, D.-H. Kang, Y.S. Kim, O.O. Zaidat, A.M. Demchuk, Y.H. Hwang, J.S. Lee
American Journal of Neuroradiology Nov 2016, 37 (11) 2072-2078; DOI: 10.3174/ajnr.A4844
del.icio.us logo Digg logo Reddit logo Twitter logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One
Purchase

Jump to section

  • Article
    • Abstract
    • ABBREVIATIONS:
    • Materials and Methods
    • Results
    • Discussion
    • Conclusions
    • Footnotes
    • References
  • Figures & Data
  • Info & Metrics
  • References
  • PDF

Related Articles

  • No related articles found.
  • PubMed
  • Google Scholar

Cited By...

  • Clot Meniscus Sign: An Angiographic Clue for Choosing between Stent Retriever and Contact Aspiration in Acute Basilar Artery Occlusion
  • Choice of ANaesthesia for EndoVAScular treatment of acute ischaemic stroke at posterior circulation (CANVAS II): protocol for an exploratory randomised controlled study
  • Significance of angiographic clot meniscus sign in mechanical thrombectomy of basilar artery stroke
  • Endovascular treatment of tandem occlusions in vertebrobasilar stroke: technical aspects and outcome compared with isolated basilar artery occlusion
  • Stroke mechanisms and outcomes of isolated symptomatic basilar artery stenosis
  • Mechanical thrombectomy for basilar artery occlusion: efficacy, outcomes, and futile recanalization in comparison with the anterior circulation
  • First attempt recanalization with ADAPT: rate, predictors, and outcome
  • Single-center experience with the Tigertriever device for the recanalization of large vessel occlusions in acute ischemic stroke
  • Mechanical thrombectomy and rescue therapy for intracranial large artery occlusion with underlying atherosclerosis
  • First Pass Effect: A New Measure for Stroke Thrombectomy Devices
  • Acute Basilar Artery Occlusion: Differences in Characteristics and Outcomes after Endovascular Therapy between Patients with and without Underlying Severe Atherosclerotic Stenosis
  • Crossref
  • Google Scholar

This article has not yet been cited by articles in journals that are participating in Crossref Cited-by Linking.

More in this TOC Section

  • Causes of Death in Endovascularly Treated Patients with Acute Stroke
  • Treatment of Proximal Posterior Inferior Cerebellar Artery Aneurysms by Intrasaccular Flow Disruption: A Multicenter Experience
  • Emergency Department Visits for Chronic Subdural Hematomas within 30 Days after Surgical Evacuation with and without Middle Meningeal Artery Embolization
Show more INTERVENTIONAL

Similar Articles

Advertisement

News and Updates

  • Lucien Levy Best Research Article Award
  • Thanks to our 2021 Distinguished Reviewers
  • Press Releases

Resources

  • Evidence-Based Medicine Level Guide
  • How to Participate in a Tweet Chat
  • AJNR Podcast Archive
  • Ideas for Publicizing Your Research
  • Librarian Resources
  • Terms and Conditions

Opportunities

  • Share Your Art in Perspectives
  • Get Peer Review Credit from Publons
  • Moderate a Tweet Chat

American Society of Neuroradiology

  • Neurographics
  • ASNR Annual Meeting
  • Fellowship Portal
  • Position Statements

© 2022 by the American Society of Neuroradiology | Print ISSN: 0195-6108 Online ISSN: 1936-959X

Powered by HighWire