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j.jstrokecerebrovasdis.2017.09.032

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ARTICLE IN PRESS
Concomitant Asymptomatic Intracranial Atherosclerotic
Stenosis Increase the 30-Day Risk of Stroke in Patients
Undergoing Symptomatic Intracranial Atherosclerotic
Stenosis Stenting
Jin Zhao, MD,*,† Xiaohui Li, MD,†,1 Lu-Xiang Chi, MD,*,1 Bing-Wu Ma,
Yan-Hui Du, MS,‡ Gui-Sheng Chen, MD,‡ Hua-Dong Zhou, MD,§
Jing-Cheng Li, MD,§ Xiao-Jiang Jiang, MD,§ Qing-Wu Yang, MD,‖
Xiong-Fei Zhao,¶ and Xiao-Feng Yao, BM¶
MS,‡
Background: In the Stenting and Aggressive Medical Management for Preventing
Recurrent Stroke in Intracranial Stenosis (SAMMPRIS) trial, 19.1% of ischemic strokes
occurred out of the territory of previously symptomatic stenosis during the mean
follow-up period of 23.4 months. However, it is unknown how many ischemic
strokes were due to a previously asymptomatic intracranial atherosclerotic stenosis (ICAS). The objective of this study was to investigate whether the concomitant
asymptomatic ICAS influences the outcome of patients undergoing symptomatic
ICAS stenting. Methods: We retrospectively reviewed 576 consecutive patients with
nondisabling ischemic stroke (modified Rankin scale score of ≤3) who were treated
with symptomatic ICAS (≥70% stenosis) stenting with or without concomitant asymptomatic ICAS. The baseline characteristics and the 30-day primary end points
(stroke or death after stenting) were compared by bivariate and multivariable logistic analyses. Results: The 30-day rate of primary end points was 5.2%, which
was higher in patients with concomitant asymptomatic ICAS (≥50% stenosis) than
in those without asymptomatic ICAS (no stenosis or <50% stenosis) (8.9% versus
3.8%, P = .014). In patients with concomitant asymptomatic ICAS, 25% of ischemic strokes occurred out of the territory of the stented artery, whereas in patients
without asymptomatic ICAS, no ischemic stroke occurred out of the territory of
the stented artery. Multivariable analysis showed that concomitant asymptomatic ICAS was an independent risk factor for 30-day stroke (odds ratio = 2.37, 95%
From the *Department of Cardiology, Southwest Hospital; †Center of Translational Medicine, College of Pharmacy, Third Military Medical
University, Chongqing, China; ‡Department of Neurology, Affiliated Hospital of Ningxia Medical University, Yinchuan, China; §Department
of Neurology, Daping Hospital; ‖Department of Neurology, Xinqiao Hospital, Third Military Medical University, Chongqing, China; and ¶Department of Neurology, Third Affiliated Hospital of Yanan University, Xianyang, China.
Received July 4, 2017; revision received September 12, 2017; accepted September 20, 2017.
Address correspondence to Xiaohui Li, MD, Center of Translational Medicine, College of Pharmacy, Third Military Medical University, Gaotanyan
35, Shapingba, Chongqing 400038, China. E-mail: lpsh008@aliyun.com.;
Address correspondence to Lu-Xiang Chi, MD, Department of Cardiology, Southwest Hospital, Third Military Medical University, Gaotanyan
30, Shapingba, Chongqing 400038, China. E-mail: chi68754271@126.com.
1
These authors contributed equally to this work.
1052-3057/$ - see front matter
© 2017 Published by Elsevier Inc. on behalf of National Stroke Association.
https://doi.org/10.1016/j.jstrokecerebrovasdis.2017.09.032
Journal of Stroke and Cerebrovascular Diseases, Vol. ■■, No. ■■ (■■), 2017: pp ■■–■■
1
ARTICLE IN PRESS
J. ZHAO ET AL.
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confidence interval, 1.14-5.63; P = .023). Conclusions: Concomitant asymptomatic
ICAS (≥50% stenosis) might increase the 30-day risk of stroke in patients undergoing symptomatic ICAS stenting. Key Words: Atherosclerosis—angioplasty—
stroke—stent.
© 2017 Published by Elsevier Inc. on behalf of National Stroke Association.
Introduction
Symptomatic intracranial atherosclerotic stenosis (ICAS)
is one of the most common causes of stroke and is associated with a high risk of recurrent stroke.1 The recently
published Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial
Stenosis (SAMMPRIS) trial2 pointed out that there was
a higher risk of stenting for patients with symptomatic
ICAS than of medical therapy. The occurrences of primary
end points (any stroke or death) in the stent group versus
the medical group was 14.7% versus 5.8% at day 30
(P = .0016), and 23% versus 15% during a median followup of 32.4 months (P = .0252). But even in the medical
treatment group, the risk is high. When the perioperative
strokes were excluded, the rates of subsequent ischemic
strokes were almost the same in the 2 groups. Some registry studies of symptomatic ICAS stenting in China3-5
reported a relative lower 30-day rate of primary end points
(2.0%-7.8%). This discrepancy might be caused by the different selection of patients and the different treatment
methods between them. Further studies are necessary to
define the appropriate patient selection and the best therapeutic approach for various patients.
The SAMMPRIS trial did not exclude stenosis out of
the territory of target intracranial lesion, and 19.1% ischemic strokes occurred out of the territory of the qualifying
artery during the mean follow-up period of 23.4 months.2
The ongoing Registry Study of Stenting for Symptomatic Intracranial Artery Stenosis in China excluded more
than 70% stenosis in other intracranial arteries than the
culprit artery,6 and no ischemic stroke occurred out of
the territory of the stented artery within 30 days after
stenting.3 Although the Warfarin–Aspirin Symptomatic Intracranial Disease (WASID) trial pointed out that the
previously asymptomatic ICAS was the most commonly identified cause of ischemic stroke that occurred out
of the territory of the previously symptomatic ICAS.7
However, in the SAMMPRIS trial, patients with previously asymptomatic ICAS were not reported, so it is
unknown how many ischemic strokes were due to previously asymptomatic ICAS.
In the present study, we retrospectively analyzed 576
consecutive patients with nondisabling ischemic stroke
who were treated with symptomatic ICAS stenting with
or without concomitant asymptomatic ICAS to evaluate
whether the concomitant asymptomatic ICAS influenced
the 30-day outcomes of symptomatic ICAS stenting in a
Chinese population.
Methods
Patients
Under the approval of the institutional review board
of each institution, we retrospectively reviewed the stroke
databases of 5 participating institutions. Each institution had at least 100 intracranial stenting per year. Between
October 2012 and February 2016, 576 consecutive patients with nondisabling ischemic stroke (modified Rankin
scale score of ≤3) who were treated with symptomatic
ICAS (≥70% stenosis) stenting with or without concomitant asymptomatic ICAS were selected. Ischemic stroke
is defined as a new focal neurological deficit of sudden
onset, lasting at least 24 hours, which is not caused by
hemorrhage as shown on computed tomography (CT) or
magnetic resonance imaging (MRI) of the brain. Symptomatic ICAS was defined as ICAS where the current
neurological signs were related to the area of the brain
supplied by it. Asymptomatic ICAS was defined as stenosis that had no relation to the current neurological signs
and had no old visible infarction in neuroimaging in its
respective vascular territory.8 The degree of stenosis was
calculated according to the WASID technique.9
According to the criteria used in the SAMMPRIS trial10,11
we included patients who had a nondisabling ischemic
stroke within the past 30 days, which were attributable
to the 70%-99% atherosclerotic stenosis of 1 major intracranial arteries (intracranial internal carotid artery, middle
cerebral artery [MCA] stem [M1], intracranial vertebral
artery [VA], or basilar artery [BA]) confirmed by catheter angiography. Patients were excluded if they were over
75 years of age and had an acute ischemic stroke within
7 days; other strokes out of the territory of the symptomatic ICAS; a stroke caused by BA or MCA stenosis
at the site of the origin of the perforator; more than 50%
tandem ICAS that was proximal or distal to the target
intracranial lesion; more than 50% bilateral intracranial
VA stenosis; an uncertainty about which artery was symptomatic; an intracranial artery occlusion; more than 50%
stenosis of an extracranial carotid artery or an extracranial VA; severe vessel tortuosity that precluded the
deployment of endovascular devices; a stenosis greater
than 15 mm in length or less than 2 mm in diameter;
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RISK OF 30-DAY STROKE OF SYMPTOMATIC ICAS STENTING
uncontrolled hypertension (systolic >180 mm Hg or diastolic >115 mm Hg); the presence of other potentially
embolic diseases; nonatherosclerotic causes of intracranial stenosis; and a known allergy or contraindication to
heparin, aspirin, clopidogrel, anesthetics, or contrast agents.
Procedure
The procedure was performed as we and others described previously.3,12 A combination of aspirin (325 mg/d)
and clopidogrel (75 mg/d) was started 3 days before the
procedure or a loading dose of 300 mg clopidogrel could
be administered at least 4 hours before the procedure.
Patients were heparinized with a target activated clotting time of 225-300 seconds. The procedure was performed
under local anesthesia and conscious sedation, via a
transfemoral approach with a 6F guiding catheter. The
stent diameter was undersized with a stent-to-normal vessel
ratio of .9:1.0. For patients with smooth arterial access,
a Mori A lesion, or mid-BA and distal M1 segment lesions,
a balloon-expandable stent (Apollo stent; Minimally Invasive, Shanghai, China) was selected, and the length of
the stent was chosen just to cover the stenosis. For patients with a tortuous arterial access, a Mori B lesion, a
Mori C lesion, or a lesion with a significant mismatch
in the diameter between the proximal and the distal segments, a self-expanding stent (Gateway balloon plus
Wingspan stent system; Stryker, Maple Grove, MN) was
preferred, and the length of the stent was chosen to cover
at least 2 mm of normal vessel segment on both sides
of the stenosis. Successful revascularization was defined
as the reduction of stenosis to less than 50% with complete enveloping of the lesion after the procedure.
Medical management included aspirin 100 mg/d,
clopidogrel 75 mg/d for 90 days, and atorvastatin 40 mg/d
for at least 6 months after stenting. We targeted a systolic blood pressure lower than 140 mm Hg (<130 mm
Hg if diabetic), a low-density lipoprotein cholesterol level
lower than 1.81 mmol/L, a fasting blood glucose level
lower than 6.1 mmol/L, and a hemoglobin A1c level less
than 7%. Lifestyle modifications such as smoking cessation, weight reduction, and physical exercise were advised.
Follow-Up
The patients were asked to come back for a face-toface interview 30 days after stenting by experienced
neurointerventionalists for clinical assessment and evaluation of neurological symptoms. The primary end points
were stroke (including ischemic or hemorrhagic stroke)
or death. Hemorrhagic stroke was defined as parenchymal hemorrhage, subarachnoid hemorrhage, or
intraventricular hemorrhage detected by CT or MRI, associated with seizures or new neurological symptoms or
signs (headache, change in the level of consciousness, or
focal neurological deficits) lasting 24 hours or longer. Every
patient with a suspected stroke underwent brain MRI or
3
CT. Ischemic strokes were classified as in or out of the
territory of the stented artery.
Medical records, brain CT or MRI, digital subtraction
angiography, and follow-up data of each patient were collected and revalued by 2 experienced neurointerventionalists
who did not participate in the procedure and were unaware
of the research. Consensus from disagreements was reached
through discussion.
Statistical Analysis
The occurrences of 30-day stroke in different groups
were compared by chi-square test or Fisher exact test.
A similar bivariate analysis was performed between the
baseline characteristics and 30-day stroke. Stepwise logistic regression analysis was used to assess the relationship
between 30-day stroke and baseline characteristics. A multivariable model was constructed using the backward
elimination method. Candidate risk factors for multivariable analysis were those with P values of less than .20
in the bivariate analyses described above. A 2-tailed P
value of less than .05 was considered to be statistically
significant. Statistical analyses were performed using IBM
SPSS (version 20; IBM, Armonk, NY).
Results
The baseline characteristics of the 576 patients are summarized in Table 1 . The mean age was 55 years, and
358 patients (62.2%) were male. The prevalence of vascular risk factors was 67.7%, 62.5%, 42.7%, and 42.7% for
hypertension, diabetes mellitus, hyperlipidemia, and
smoking history, respectively. The symptomatic ICAS was
located in the intracranial internal carotid artery in 241
patients (41.8%), in the MCA in 130 patients (22.6%), in
the intracranial VA in 148 patients (25.7%), and in the
BA in 57 patients (9.9%). The patients with a concomitant asymptomatic ICAS of less than 25% stenosis, 25%50% stenosis, 50%-75% stenosis, and 75%-99% stenosis
were 47 (8.2%), 40 (6.9%), 120 (20.8%), and 37 (6.4%), respectively. The median time from the qualifying event
to endovascular treatment was 13 days. Successful
revascularization was achieved in all patients.
All patients had a 30-day follow-up. The occurrences
of 30-day primary end points in different groups are shown
in Table 2 . In patients without asymptomatic ICAS or
with a concomitant asymptomatic ICAS of less than 50%
stenosis, no ischemic stroke occurred out of the territory of the stented artery. In patients with a concomitant
asymptomatic ICAS of 50% stenosis or higher, 9 patients (5.7%) had an ischemic stroke in the territory of
the stented artery, 3 patients (1.9%) had an ischemic stroke
in the territory of a previously asymptomatic ICAS (i.e.,
25% ischemic strokes occurred out of the territory of the
stented artery). All hemorrhage strokes occurred in the
territory of the stented artery. No death was found.
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J. ZHAO ET AL.
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Table 1. Baseline characteristics
Patients
(N = 576)
Characteristic
Age (y)
Male
Hypertension
Hyperlipidemia
Diabetes mellitus
Coronary artery disease
Smoking history
Absence of statin use before stroke
Days from stroke to stenting
Symptomatic ICAS location
Intracranial ICA
MCA
Intracranial VA
BA
Mori classification of symptomatic ICAS
Mori A
Mori B
Mori C
Type of stent
Balloon-expandable stent
Self-expanding stent
Concomitant asymptomatic ICAS
Patients with concomitant asymptomatic
ICAS of less than 25% stenosis
Patients with concomitant asymptomatic
ICAS of 25%-50% stenosis
Patients with concomitant asymptomatic
ICAS of 50%-75% stenosis
Patients with concomitant asymptomatic
ICAS of 75%-99% stenosis
55.1 (10.4)
358 (62.2)
390 (67.7)
360 (62.5)
246 (42.7)
69 (12.0)
246 (42.7)
342 (59.4)
13 (9-15)
241 (41.8)
130 (22.6)
148 (25.7)
57 (9.9)
178 (30.9)
289 (50.2)
109 (18.9)
379 (65.8)
197 (34.2)
244 (42.4)
47 (8.2)
40 (6.9)
120 (20.8)
37 (6.4)
Abbreviations: BA, basilar artery; ICA, internal carotid artery;
ICAS, intracranial atherosclerotic stenosis; MCA, middle cerebral
artery; VA, vertebral artery.
Values are mean ± standard deviation, n (%), or median
(interquartile range).
Table 3 shows that patients with a concomitant asymptomatic ICAS of 50%-75% stenosis had more 30day strokes than those without asymptomatic ICAS (8.3%
versus 3.6%, P = .040). Due to the trends shown in Table 3
and the criteria used in the post hoc analyses of the WASID
trial,13,14 we then divided the patients into 2 groups: patients without asymptomatic ICAS (no stenosis or <50%
stenosis) and patients with concomitant asymptomatic ICAS
(≥50% stenosis).
Bivariate analysis (Table 4 ) revealed that diabetes mellitus (7.3% versus 3.6%, P = .049) and concomitant
asymptomatic ICAS (≥50% stenosis) (8.9% versus 3.8%,
P = .014) were related to a higher rate of 30-day stroke.
These factors were included in a multivariable analysis,
as well as coronary artery disease (P = .075) and absence
of statin use before stroke (P = .110). The statistically significant factors identified for the final model were diabetes
mellitus (odds ratio [OR] = 2.13, 95% confidence interval [CI], 1.06-4.62; P = .037), the absence of statin use during
stroke (OR = 1.97, 95% CI, 1.03-4.58; P = .043), and a concomitant asymptomatic ICAS (OR = 2.35, 95% CI, 1.135.48; P = .019) (Table 5 ). After adjusting for diabetes mellitus
and the absence of statin use before stroke, concomitant
asymptomatic ICAS was independently associated with
30-day stroke (OR = 2.37, 95% CI, 1.14-5.63; P = .023).
Discussion
In the present study, the 30-day rate of primary end
points was 5.2% (3.8% in patients without asymptomatic ICAS [no stenosis or <50% stenosis] versus 8.9% in
patients with concomitant asymptomatic ICAS [≥50% stenosis]), which was lower than that reported in the stent
group of the SAMMPRIS trial (14.7%), but was similar
to some ongoing registry studies of symptomatic ICAS
stenting in China (2.0%-7.8%).3-5 Concomitant asymptomatic ICAS (≥50% stenosis) was an independent risk factor
for 30-day stroke (OR = 2.37, 95% CI, 1.14-5.63; P = .023).
Table 2. Primary end points within 30 days after stenting
Patients with concomitant asymptomatic ICAS
30-d primary end points
Ischemic stroke in the territory of
previously symptomatic ICAS
Ischemic stroke in other territory
Hemorrhage stroke
Death
Patients without
asymptomatic ICAS
(n = 332)
Less than 25%
stenosis
(n = 47)
25%-50%
Stenosis
(n = 40)
50%-75%
Stenosis
(n = 120)
75%-99%
Stenosis
(n = 37)
12
12
2
1
2
2
10
7
4
2
0
0
0
0
1
0
0
0
0
2
1
0
1
1
0
Abbreviation: ICAS, intracranial atherosclerotic stenosis.
Values are n (%).
ARTICLE IN PRESS
RISK OF 30-DAY STROKE OF SYMPTOMATIC ICAS STENTING
5
Table 3. The occurrences of 30-day stroke in different groups
Patients without asymptomatic ICAS
Patients with concomitant asymptomatic ICAS of less than 25% stenosis
Patients with concomitant asymptomatic ICAS of 25-50% stenosis
Patients with concomitant asymptomatic ICAS of 50-75% stenosis
Patients with concomitant asymptomatic ICAS of 75-99% stenosis
Patients without
30-d stroke
Patients with
30-d stroke
P Value
320 (96.4)
45 (95.7)
38 (95)
110 (91.7)
33 (89.2)
12 (3.6)
2 (4.3)
2 (5.0)
10 (8.3)
4 (10.8)
Ref
.688
.654
.040
.065
Abbreviations: ICAS, intracranial atherosclerotic stenosis; Ref, reference.
Values are n (%).
Several reasons might contribute to the relatively low
primary end point rates in the present study. First, the
median time from the qualifying event to the stent treatment was 13 days in our study, which was different from
the SAMMPRIS trial (7 days) and the ongoing Registry
Study of Stenting for Symptomatic Intracranial Artery Stenosis in China (21 days). Exclusion of patients with a recent
ischemic stroke may exclude those patients with a high
risk of ischemic event recurrence, and therefore, the benefit
of stent placement to reduce the stroke recurrence may
also be diminished. Second, we excluded patients whose
stroke was caused by BA or MCA stenosis at the site of
origin of the perforator. Crushing the atherosclerotic plaque
by balloon or stent may send debris or thrombus into
these perforators or may cause a mechanical obstruction of these perforators, and excessively twisting or tearing
perforators by balloon may cause intracranial hemorrhage.15
Third, both balloon-mounted stents and self-expanding
stents were used in our study. A self-expanding stent has
lower radial force and is less apt at achieving good
revascularization in calcified lesions, whereas a balloonmounted stent is more rigid and is difficult to navigate
along tortuous vessels. Selection of the suitable stent might
get the most advantages.
In our study, 25% ischemic stroke occurred out of the
territory of the stented artery in patients with concomitant asymptomatic ICAS (≥50% stenosis), and no ischemic
stroke occurred out of the territory of the stented artery
in patients without asymptomatic ICAS (no stenosis or
<50% stenosis) within 30 days after symptomatic ICAS
stenting. The China Interventional Stroke Registry (CISR)
reported that 23.5% ischemic strokes occurred out of the
territory of the stented artery within 30 days after symptomatic ICAS stenting.5 In a review of 2196 patients treated
with ICAS stenting for 2314 lesions, the median rates of
ischemic events in any territory and ipsilateral ischemic
events were 9.4% (range 0%-25%) and 5.4% (range 0%13.7%), respectively, over a median or mean follow-up
period ranging from 1 to 67 months.16 The variations in
ischemic stroke that occurred out of the territory of the
stented artery might be due to the different characteristics of the patients and the different follow-up period.
Our study pointed out that the concomitant asymptomatic ICAS (≥50% stenosis) was an independent risk
factor for 30-day stroke. This finding could be explained by asymptomatic ICAS activation or progression.
Stresses such as physical trauma and inflammation may
trigger platelet aggregation, plaque erosion, or rupture
in patients with severe atherosclerosis in the cervical and
cranial vessels.17 Chronic cerebral hypoperfusion secondary to asymptomatic ICAS progression may confer risk
of stroke14 because of a potential disruption of the cerebral autoregulation or of a decreased washout of small
emboli.18 Histopathological studies also demonstrated that
the fibrous cap of plaques within the intracranial artery
was thicker than that of plaques within the coronary and
carotid arteries,19-22 combined with the reduced expression of inhibitors of inflammation, 23 the prominent
expression of proinflammatory proteasomes,24 and the
absence of an external elastic lamina,25 which make it more
susceptible to inflammatory changes and plaque instability.
Our study concluded that concomitant asymptomatic
ICAS (≥50% stenosis) is a risk factor for 30-day stroke
in patients undergoing symptomatic ICAS stenting.
However, in patients undergoing symptomatic ICAS
stenting, there is not enough evidence to stent for the
concomitant asymptomatic ICAS. Should these patients
not be offered stenting, should the asymptomatic lesions
be treated with stent concurrently, or is this just a risk
factor for symptomatic ICAS stenting? Further studies
should be done to answer these questions.
Our study has several limitations. First, our study was
a retrospective study and only the 30-day primary end
points were examined. Prospective trials with a large population and long follow-up should be done to test the
conclusion. Second, patients with transient ischemic attack
were not taken into consideration because sometimes it
is difficult to distinguish which ICAS was symptomatic.
Conclusions
In the present study, we retrospectively reviewed 576
consecutive patients with nondisabling ischemic stroke
who were treated with symptomatic ICAS stenting with
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J. ZHAO ET AL.
6
Table 4. Bivariate analyses of baseline characteristics versus
the occurrences of 30-day stroke
Overall
Age
≥55 y
<55 y
Sex
Male
Female
Hypertension
Yes
No
Hyperlipidemia
Yes
No
Diabetes mellitus
Yes
No
Coronary artery
disease
Yes
No
Smoking history
Yes
No
Absence of statin use
before stroke
Yes
No
Days from stroke to
stenting
13 d or more
Less than 13 d
Symptomatic artery
location
Anterior artery
Posterior artery
Mori type of
symptomatic ICAS
Mori C type
Other types
Stent type
Self-expanding stent
Balloon-expandable
stent
Concomitant
asymptomatic ICAS
(≥50% stenosis)
With
Without
Patients
with events
Table 5. Multivariate logistic regression results for the risk
factors associated with 30-day stroke
OR (95% CI)
P Value
2.13 (1.06-4.62)
1.97 (1.03-4.58)
.037
.043
2.35 (1.13-5.48)
.019
P Value
311
265
17 (5.5)
13 (4.9)
.763
358
218
20 (5.6)
10 (4.6)
.601
390
186
23 (5.9)
7 (3.8)
.281
360
216
21 (5.8)
9 (4.2)
.383
246
330
18 (7.3)
12 (3.6)
.049
Diabetes mellitus
Absence of statin use
before stroke
Concomitant asymptomatic
ICAS (≥50% stenosis)
Abbreviations: CI, confidence interval; ICAS, intracranial atherosclerotic stenosis; OR, odds ratio.
69
507
7 (10.1)
23 (4.5)
.075
246
330
16 (6.5)
14 (4.2)
.227
342
234
22 (6.4)
8 (3.4)
.110
291
285
14 (4.8)
16 (5.6)
.665
371
205
18 (4.8)
12 (5.9)
.604
109
467
7 (6.4)
23 (4.9)
.527
197
379
11 (5.6)
19 (5.0)
.770
157
419
14 (8.9)
16 (3.8)
.014
Abbreviation: ICAS, intracranial atherosclerotic stenosis.
Values are n (%).
or without concomitant asymptomatic ICAS. The current
results indicate that concomitant asymptomatic ICAS (≥50%
stenosis) is a risk factor for 30-day stroke in patients undergoing symptomatic ICAS stenting. Concomitant
asymptomatic ICAS should be taken into consideration
when evaluating the effect of symptomatic ICAS stenting.
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