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. 2026 Jun 22;26:559. doi: 10.1186/s12883-026-05092-0

Short-term outcomes of intracranial angioplasty with the Neuroform EZ stent in patients with hypoperfusion-related symptomatic intracranial atherosclerotic stenosis

Yindan Yao 1,4, Weinv Fan 1, Jin Lv 2, Xiaoxia Liu 1, Yunqin Wu 1, Da Li 1,4, Ou Zhang 1,4, Qiang Li 3,4, Feiyu Chen 3,4,✉
PMCID: PMC13540262  PMID: 42332626

Abstract

Background

This study aimed to evaluate the safety profile and limitations of Neuroform EZ stenting in patients with hypoperfusion-related symptomatic intracranial atherosclerotic stenosis (ICAS), focusing on lesion morphology and risk stratification to identify patient subgroups that require stricter preoperative selection criteria.

Methods

We conducted a retrospective analysis of consecutive patients with hypoperfusion-related symptomatic ICAS who underwent Neuroform EZ stent placement at our institution between January 2020 and October 2023. The primary endpoint was the occurrence of any stroke or death within 30 days post-procedure. Secondary endpoints included technical success rate, incidence of ischemic stroke in the target artery territory from 30 days to 6 months post-procedure, and in-stent restenosis (ISR) rate during follow-up.

Results

A total of 64 patients (64 lesions) were included, all treated with Neuroform EZ stents. The technical success rate was 98.4%. The 30-day stroke or death rate was 6.2% (4/64). The incidence of ischemic stroke in the target artery territory from 30 days to 6 months post-procedure was 1.6% (1/64). During a mean follow-up of 10.4 ± 6.5 months, the ISR rate was 13.7% (7/51). Subgroup analysis revealed that the 30-day perioperative complication rate was significantly higher in patients with Mori type C lesions (25.0%, 4/16) than in those with Mori type A (0%, 0/16) or type B lesions (0%, 0/32) (Fisher’s exact test, P = 0.002). Additionally, the ISR rate was significantly higher in Mori type C lesions (46.2%, 6/13) compared with Mori type A (0%, 0/14) or type B lesions (4.2%, 1/42) (Fisher’s exact test, P < 0.001).

Conclusion

Neuroform EZ stenting may be a reasonable option for carefully selected patients with hypoperfusion-related ICAS and Mori type A/B lesions. However, its use in Mori type C lesions carries substantial periprocedural and restenosis risks and must be approached with extreme caution. These findings provide safety-focused risk stratification but require external validation, and do not prove that Neuroform EZ stenting is superior to standard medical therapy or other stent devices. Further controlled studies are required to validate these observations.

Keywords: Intracranial atherosclerotic stenosis, Endovascular therapy, Neuroform EZ stent, Outcomes, Stroke, Cerebral hypoperfusion

Introduction

Intracranial atherosclerotic stenosis (ICAS) is a leading cause of ischemic stroke worldwide, accounting for 33%–56% of ischemic strokes in Asian populations [1, 2]. Standard first-line management includes dual antiplatelet therapy (DAPT) and risk factor control. However, patients with hemodynamic impairment remain at high risk of recurrence despite optimal medical therapy [3–5].

The SAMMPRIS and VISSIT trials failed to demonstrate superiority of percutaneous transluminal angioplasty and stenting (PTAS) over medical management, largely due to high periprocedural stroke rates (14.7% and 24.1%, respectively) [3, 4]. In recent years, off-label use of aneurysm stents including the Neuroform EZ stent has been increasingly explored for the treatment of ICAS [6–12]. These studies suggested favorable safety profiles, but most included highly selected patients. Du et al. [9] reported a 2.2% 30-day complication rate in 45 patients, but only 15.2% were Mori type C lesions. Li et al. [12] studied 70 MCA patients but excluded lesions > 1 cm, effectively excluding many complex type C lesions. Xu et al. [10] reported 0% 30-day complications in a high-volume center with highly selected patients. Zhou et al. [11] compared Neuroform and Wingspan stents but limited to MCA lesions. None of these prior studies focused strictly on hemodynamically compromised (hypoperfusion) subgroups, nor did they provide detailed quantitative risk stratification for complex Mori type C lesions using the Neuroform EZ platform.

The present study aimed to evaluate the safety profile and limitations of Neuroform EZ stenting in hypoperfusion-related symptomatic ICAS, clarifying which patient subgroups require more stringent selection criteria, rather than a broad assessment of feasibility or efficacy. We analyzed lesion morphological predictors of complications and in-stent restenosis (ISR), providing real-world risk estimates to inform clinical decision-making.

Methods

Patients

From January 2020 to October 2023, 64 consecutive patients with hypoperfusion-related symptomatic ICAS who underwent PTAS with the Neuroform EZ stent at our institution were enrolled. Baseline characteristics and follow-up data were prospectively collected. Written informed consent, including disclosure of the off-label use of the Neuroform EZ stent, was obtained from all patients or their legally authorized representatives prior to enrollment. The study protocol was approved by the Institutional Review Board of our hospital, and the study was conducted in accordance with the Declaration of Helsinki.

Inclusion criteria were as follows: (1) age between 40 and 80 years; (2) transient ischemic attack (TIA) or ischemic stroke occurring within 90 days prior to intervention, with 70%–99% stenosis in a major intracranial artery—including the intracranial internal carotid artery (ICA), middle cerebral artery (MCA), anterior cerebral artery (ACA), basilar artery (BA), or intracranial vertebral artery (VA)—confirmed by digital subtraction angiography (DSA); (3) the interval between the latest qualifying cerebrovascular event and stent implantation was no less than 7 days; (4) preoperative imaging evidence of hemodynamic impairment in the target artery territory, defined by at least one of the following: (a) watershed infarction on magnetic resonance imaging (MRI), consistent with hemodynamic compromise; (b) hypoperfusion on computed tomography perfusion (CTP) defined as: (1) mean transit time (MTT) > 3 s compared with the contralateral mirror region; (2) reduced cerebral blood flow (CBF) < 30% relative to the contralateral hemisphere, with preserved or increased cerebral blood volume (CBV); (c) collateral circulation graded ≤ 2 according to the American Society of Interventional and Therapeutic Neuroradiology/Society of Interventional Radiology (ASITN/SIR) scale on DSA; (5) presence of at least one established atherosclerotic risk factor (hypertension, diabetes mellitus, hyperlipidemia, or current smoking).

Exclusion criteria included: (1) non-atherosclerotic etiologies (e.g., suspected cerebral vasculitis, arterial dissection, Moyamoya disease); (2) coexisting intracranial aneurysms or arteriovenous malformations; (3) tandem stenosis (≥ 2 stenoses within the same vascular territory); (4) total occlusive lesions.

Perioperative management

All patients received DAPT consisting of aspirin (100 mg daily) and clopidogrel (75 mg daily) for a minimum of 5 days before the procedure. Following the procedure, DAPT was maintained for 6 months, after which patients transitioned to lifelong single antiplatelet therapy (aspirin or clopidogrel). Blood pressure was managed to approximately 80% of baseline levels during the first 72 h post-procedure to mitigate the risk of hyper-perfusion syndrome. Immediate post-procedural non-contrast head CT was performed in all cases to exclude intracranial hemorrhage. Subcutaneous Fragmin® (dalteparin sodium, 2500 IU) was administered every 12 h during hospitalization for 3 days to prevent venous thromboembolism. Management of modifiable cardiovascular risk factors followed the 2021 guidelines of the American Heart Association (AHA)/American Stroke Association (ASA).

Procedures

All procedures were performed under general anesthesia by an experienced interventional neuroradiologist (FY Chen), who had more than 15 years of clinical experience. After general anesthesia and systemic heparinization, an 8 F guiding catheter was placed in the common carotid artery or subclavian artery, and a distal access catheter was advanced to a position proximal to the target lesion. Three-dimensional rotational angiography was performed to accurately measure lesion length, diameter, and reference vessel size. Under fluoroscopic roadmap guidance, a microwire (Synchro® 2, Stryker Neurovascular, USA), with or without a microcatheter (Excelsior® SL-10, Stryker Neurovascular, USA), was navigated across the stenosis into the distal true lumen. Pre-dilation was performed using a non-compliant balloon (Maverick2™, Boston Scientific, USA) selected to match the lesion dimensions (balloon diameter ≥ 80% of the reference vessel diameter). The balloon inflation and deflation pressure was adjusted gradually at a rate of 1 atm per 10 s to minimize vessel wall injury. After successful pre-dilation, a Rebar® 27 microcatheter (Medtronic, USA) was advanced over the exchange microwire to the target site. The Neuroform EZ stent (Stryker Neurovascular, USA) was then delivered through the microcatheter and deployed to fully cover the lesion, with a minimum of 3 mm extension beyond both proximal and distal margins. Post-deployment angiography was performed to evaluate stent apposition, exclude stent thrombosis or distal embolization, and quantify residual stenosis. Post-dilation was performed if residual stenosis ≥ 50% was observed.

Outcome measures

The primary endpoint was the occurrence of any stroke or death within 30 days post-procedure. Secondary endpoints included technical success rate, incidence of ischemic stroke in the target artery territory from 30 days to 6 months post-procedure, and ISR rate during follow-up. Stroke, including both ischemic and hemorrhagic stroke, was defined as a new focal neurological deficit of sudden onset, lasting at least 24 h, with the corresponding lesion confirmed by head CT or MRI. Technical success was defined as successful delivery and deployment of the stent with immediate post-procedural residual stenosis < 50%, as assessed by DSA. ISR was defined as ≥ 70% luminal narrowing within the stent or within 3 mm of either stent edge, confirmed by DSA or computed tomography angiography (CTA).

Clinical and imaging follow-up

Patients were scheduled for clinical follow-up at 1, 3, 6, and 12 months post-procedure via outpatient visits or structured telephone interviews. At 6 months, DSA or CTA was recommended for all patients unless contraindicated; additional imaging was performed if ISR was clinically suspected. Head MRI or CT was obtained in patients presenting with new neurological symptoms. The National Institutes of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS) scores were independently assessed by two blinded stroke neurologists. All endpoint events were adjudicated by an independent, blinded endpoint committee; any disagreements resolved through consensus.

Statistical analysis

Continuous variables with a normal distribution are presented as mean ± standard deviation (SD), while skewed continuous variables are reported as median (interquartile range, IQR). Categorical variables are expressed as frequency (percentage). Group comparisons of perioperative complications and ISR rates across Mori lesion types, lesion locations, and procedural timing categories were performed using the chi-square test or Fisher’s exact test, as appropriate (for expected cell counts < 5). A two-tailed P value < 0.05 was considered statistically significant. All statistical analyses were conducted using SPSS version 25.0 (IBM Corp., Armonk, NY, USA).

Results

Patient and lesion characteristics

Between January 2020 and October 2023, a total of 64 patients with symptomatic intracranial atherosclerotic stenosis (ICAS) (64 lesions) were enrolled and underwent Neuroform EZ stent placement. The mean age was 61.6 ± 9.2 years, and 59.4% of the patients were male. The index ischemic events consisted of ischemic stroke in 70.3% of cases and TIA in 29.7%. The median time from the latest qualifying event to stenting was 19.0 days (IQR: 14.0–36.8 days). Lesion locations included the intracranial ICA (8 lesions, 12.5%), MCA (43 lesions, 67.2%), ACA (3 lesions, 4.7%), BA (8 lesions, 12.5%), and intracranial VA (2 lesions, 3.1%). According to the Mori classification, 25.0% of lesions were type A, 50.0% were type B, and 25.0% were type C. Baseline demographic, clinical, and lesion characteristics are summarized in Table 1.

Table 1.

Demographic and clinical characteristics of the patients

Characteristics Result
Number of patients, n 64
Age, years, mean ± SD 61.6 ± 9.2
Male, n (%) 38 (59.4)
Ischemic events, n (%)
 TIA 19 (29.7)
 Stroke 45 (70.3)
Comorbidities, n (%)
Hypertension 56 (87.5)
Diabetes mellitus 29 (45.3)
Hyperlipidemia (LDL-C ≥ 2.6 mmol/L) 15 (23.4)
Location, n (%)
Anterior circulation
 Intracranial ICA 8 (12.5)
 MCA 43 (67.2)
 ACA 3 (4.7)
Posterior circulation
 BA 8 (12.5)
 Intracranial VA 2 (3.1)
Mori classifications, n (%)
 Mori type A 16 (25.0)
 Mori type B 32 (50.0)
 Mori type C 16 (25.0)
Preoperative stenosis rate (%)
 Mean ± SD 71.2 ± 7.8
 Median (IQR) 74.7 (70.4, 84.3)
Time from symptom onset to procedure (days), median (IQR) 19.0 (14.0, 36.8)
Preoperative NIHSS score, median (IQR) 1.0 (0, 1.0)
Preoperative mRS score, median (IQR) 1.0 (0, 2.0)

TIA transient ischemic attack, ICA internal carotid artery, MCA middle cerebral artery, ACA anterior cerebral artery, BA basilar artery, VA vertebral artery, NIHSS National Institutes of Health Stroke Scale, mRS modified Rankin Scale

Perioperative complications and clinical outcomes

The technical success rate was 98.4% (63/64). One procedure failed due to incomplete stent coverage caused by displacement of the stent delivery guidewire during stent deployment, resulting in suboptimal lesion coverage. The mean degree of stenosis was reduced from 71.2 ± 7.8% preoperatively to 32.3 ± 14.7% immediately post-procedure. In total, four patients experienced disabling strokes within 30 days post-procedure, including three cases of perforator occlusion after BA stenting and one case with intracranial hemorrhage after MCA stenting. No deaths were observed. The rate of any stroke or death within 30 days was 6.2% (4/64). All patients completed at least 6 months of follow-up (mean: 16.2 ± 11.1 months). One patient experienced recurrent ischemic stroke in the target artery territory at 60 days post-procedure. The incidence of ischemic stroke between 30 days and 6 months was 1.6% (1/64), as detailed in Table 2.

Table 2.

Clinical and imaging outcomes

Outcomes Result
Technical success rate (%) 98.4 (63/64)
Postoperative stenosis rate (%)
 Mean ± SD 32.3 ± 14.7
 Median (IQR) 34.5 (20.7, 46.7)
Stroke or death within 30 days after the procedure, n (%) 4 (6.3)
 Symptomatic ischemic stroke 3 (4.7)
 Symptomatic hemorrhage stroke 1 (1.6)
 Death 0 (0)
Ischemic stroke in the target artery territory from 30 days to 6 months post-procedure, n (%) 1 (1.6)
Neurovascular imaging follow-up of lesions, n (%) 51/64 (79.7)
 Follow-up period, months, mean ± SD 10.4 ± 6.5
 In-stent restenosis, n (%) 7/51 (13.7)

IQR interquartile range, SD standard deviation

Univariate analysis revealed that the 30-day perioperative complication rate was significantly higher among patients with Mori type C lesions (25.0%, 4/16) compared with those with type A (0%, 0/16) or type B lesions (0%, 0/32) (Fisher’s exact test, P = 0.002). No statistically significant association was observed between timing of stenting (early vs. delayed) and complication rate (P = 0.583; Table 3).

Table 3.

Incidence rates of complications within 30 days post-procedure

Number of lesions, n 30-day complications, n (%) P
Mori classifications 0.002
 Mori type A 16 0 (0)
 Mori type B 32 0 (0)
 Mori type C 16 4 (25.0)
Operation time 0.583
 Early stage (8–14 days) 20 2 (10.0)
 Late stage (> 14 days) 44 2 (4.5)

ISR analysis

Among the 64 patients, 51 (79.7%) underwent vascular imaging follow-up (DSA or CTA), with a median follow-up duration of 10.4 ± 6.5 months. In this subgroup, 7 patients (13.7%) developed in-stent restenosis (n = 4) or in-stent occlusion (n = 3); only one occlusion was symptomatic. By lesion location, ISR rates were as follows: MCA (5/38, 13.1%), BA (1/4, 25.0%), ACA (1/3, 33.3%); no cases of ISR were observed in intracranial ICA (0/8) or intracranial VA (0/2) lesions (Table 4).

Table 4.

ISR incidence rate during the follow-up period

Number of lesions, n ISR, n (%) P
Mori classifications, n (%) <0.001
 Mori A 14 0 (0)
 Mori B 24 1 (4.2)
 Mori C 13 6 (46.2)
Operation time 0.186
 Early stage (8–14 days) 16 4 (25.0)
 Late stage (> 14 days) 35 3 (8.6)

ISR in-stent restenosis

Univariate analysis demonstrated a significantly higher ISR rate in Mori type C lesions (46.2%, 6/13) compared with type A (0%, 0/14) or type B lesions (4.2%, 1/42) (Fisher’s exact test, P < 0.001). There was no significant association between timing of stenting (early vs. delayed) and ISR risk (P = 0.186; Table 4).

Discussion

This study reports the single-center clinical experience and short-term outcomes of intracranial angioplasty with the Neuroform EZ stent in patients with hypoperfusion-related symptomatic ICAS. The key findings include a technical success rate of 98.4%, a 30-day stroke or death rate of 6.2%, an ischemic stroke rate of 1.6% in the target artery territory between 30 days and 6 months post-procedure, and an ISR rate of 13.7% during follow-up. Collectively, these results suggest that Neuroform EZ stenting may serve as an acceptable treatment for symptomatic ICAS due to hypoperfusion in selected patients.

The 30-day stroke or death rate in our cohort (6.2%) was significantly lower than those reported in the SAMMPRIS (14.7%) and VISSIT (24.1%) trials [3, 4], but slightly higher than the 5.1% observed in the stent arm of the CASSISS trial [13]. Previous studies on Neuroform EZ stenting for symptomatic ICAS have reported 30-day stroke or death rates ranging from 0% to 5.2% [9–12]. The relatively higher rate in our study may be attributed to differences in patient selection—specifically, a greater proportion of complex lesions (e.g., Mori type C)—and potentially less procedural volume at our center compared with high-volume institutions in prior reports. Additionally, variations in perioperative management protocols, including blood pressure control targets and antiplatelet regimens, may contribute to outcome heterogeneity across studies.

Consistent with the seminal work by Mori et al. [14], we found that Mori type C lesions were associated with a significantly higher 30-day perioperative complication rate (25.0%, 4/16) compared with Mori type A (0%, 0/16) or type B lesions (0%, 0/32) (P = 0.002), reinforcing the established association between lesion complexity and procedural risk. Subgroup analysis revealed an elevated complication rate in patients with basilar artery (BA) lesions, which aligns with findings from the SAMMPRIS trial indicating that perforator occlusion is a major mechanism of periprocedural stroke in posterior circulation stenosis [15]. However, this contrasts with the CASSISS trial’s post hoc analysis, which showed no significant difference in 30-day outcomes between anterior and posterior circulation lesions [16]. This discrepancy may stem from differences in sample size—our BA subgroup included only eight patients—and procedural nuances such as balloon sizing, dilation pressure, and stent positioning. Notably, patients who underwent early stenting (≤ 14 days from symptom onset) exhibited a numerically higher risk of perioperative complications compared with those treated later. Potential mechanisms include: (1) mechanical disruption of unstable atherosclerotic plaques during stenting—the so-called “snowplow effect”—leading to distal embolization or perforator occlusion; and (2) impaired cerebrovascular autoregulation and incomplete blood-brain barrier recovery in the acute phase, increasing susceptibility to hyperperfusion injury or hemorrhagic transformation [17]. These considerations support deferring intervention until plaque stabilization occurs, typically beyond the first two weeks after index event.

Our technical success rate of 98.4% is consistent with previously published series reporting rates between 97.6% and 100% for Neuroform EZ stenting [6, 9–12, 18]. The single failure resulted from guidewire displacement during stent deployment, preventing adequate lesion coverage. This highlights a well-recognized limitation of open-cell stents: once deployed, they cannot be retrieved or repositioned. Therefore, meticulous preoperative planning—including accurate lesion measurement via 3D rotational angiography—and stable guidewire positioning are critical to ensure successful delivery.

Our study showed that the incidence of ischemic stroke beyond 30 days through 6 months postoperatively was 1.6% (1/64) and the overall incidence of stroke or death within 6 months was 7.8% (5/64), which was similar to the stent group in the CASSISS trial (7.4%, 13/176) [13]. It suggested that the short-term results of Neuroform EZ stenting for symptomatic ICAS were acceptable. Du et al. showed that the incidence of stroke or death was 2.2% (1/45) during a mean follow-up of 8.8 months after Neuroform EZ stenting [9]. Li et al. showed that the rate of stroke or death within 1 year postoperatively was 1.4% (1/70) [12]. These studies suggest that Neuroform EZ stenting may be effective for symptomatic ICAS, with a lower risk of stroke recurrence.

ISR was significantly associated with an increased risk of recurrent ischemic events in the territory of the stented intracranial artery [19]. The ISR rate in our cohort (13.7%) closely mirrors the pooled incidence of 13.6% reported in a meta-analysis of ICAS stenting among Asian populations [20], although it is marginally lower than the range observed in previous Neuroform EZ studies (0%–19.0%) [9, 11, 12]. These discrepancies may reflect differences in ISR definition thresholds (e.g., ≥ 70% vs. ≥50% stenosis), imaging modality utilization (DSA vs. CTA), follow-up completeness (79.7% vs. near-complete in some studies), and duration of surveillance.

Several studies have shown that ISR was associated with younger age [20], diabetes [21], longer length of lesion [22], stenosis location [20, 23, 24], calcification [24], residual stenosis [20, 24], local anesthesia [23], rapid balloon inflation [22], balloon-expanded stent [23], longer stent length [23], balloon inflation pressure and intraprocedural arterial dissection [24]. The present study identified Mori type C lesions as a strong independent predictor of ISR, with a striking rate of 46.2% (6/13), compared with 0% in type A and 4.2% in type B lesions (P < 0.001). This is likely attributable to the longer segment involvement typical of Mori type C lesions, resulting in greater endothelial injury and increased neointimal hyperplasia—a known driver of restenosis [21, 22, 25]. Furthermore, early stenting (≤ 14 days) was associated with a trend toward higher ISR incidence, possibly due to interference with early endothelial healing processes. Delayed intervention may allow partial plaque stabilization and re-endothelialization, thereby mitigating excessive tissue proliferation [17].

Importantly, the 25.0% perioperative complication rate and 46.2% ISR rate observed in Mori type C lesions are preliminary single-center findings derived from small subgroups (n = 13–16). These exact percentages are highly susceptible to small-sample bias and should not be generalized as definitive epidemiological rates. They provide preliminary hypothesis-generating risk estimates but require larger validation cohorts to confirm their precision.

Our results provide clear, safety-focused clinical guidance: Neuroform EZ stenting may be a reasonable option for carefully selected patients with Mori type A/B lesions. However, its use in Mori type C lesions carries substantial periprocedural and restenosis risks and must be approached with extreme caution. This is a direct, actionable recommendation for clinical practice. We acknowledge that the small sample sizes for ACA (n = 3), BA (n = 8), and VA (n = 2).

subgroups are far too small to draw generalizable or reliable safety conclusions across all major intracranial arteries.

Several limitations should be acknowledged. First, this was a retrospective, single-center study with a relatively small sample size (n = 64), which limits statistical power and increases the risk of selection bias. There was no medical therapy-only control group or direct comparison with alternative stent systems (e.g., Wingspan). Therefore, no claims of superiority or non-inferiority can be made relative to standard treatments. Second, the association between Mori type C lesions and adverse outcomes is a well-established principle in neuro-intervention. Our study confirms but does not revise or address this problem, and no new technical solutions to reduce complications or restenosis were tested or proposed. Third, the uneven distribution of lesion locations—particularly the small number of intracranial VA and ACA cases—may affect the generalizability of our findings. Fourth, several procedural variables—including balloon type, residual stenosis, and intraoperative dissection—were not systematically analyzed, potentially confounding outcome assessments. Fifth, the mean follow-up duration of 10.4 months is insufficient to evaluate long-term stent durability, including risks of late ISR, stent thrombosis, or delayed clinical deterioration. Finally, all data were derived from a single center; thus, external validation in independent, multicenter cohorts is essential to confirm whether the Mori-based risk stratification can be generalized to other populations and practice settings.

Conclusion

Neuroform EZ stenting may be a reasonable option for carefully selected patients with hypoperfusion-related ICAS and Mori type A/B lesions. However, its use in Mori type C lesions is associated with substantial periprocedural and restenosis risks and must be approached with extreme caution. These preliminary single-center safety-focused findings require larger, multicenter validation to confirm their generalizability.

Acknowledgements

We would like to express our gratitude to all the participants in the study.

Abbreviations

ACA

Anterior cerebral artery

ASITN/SIR

Interventional and Therapeutic Neuroradiology/Society of Interventional Radiology

BA

Basilar artery

CT

Computer tomography

DAPT

Dual antiplatelet therapy

ICA

Intracranial internal carotid artery

IQR

Interquartile range

ICAS

Intracranial atherosclerotic stenosis

ISR

In-stent restenosis

MCA

Middle cerebral artery

MRI

Magnetic resonance imaging

mRS

Modified Rankin scale

NIHSS

National Institutes of Health Stroke Scale

PTAS

Percutaneous transluminal angioplasty and stenting

TIA

Transient ischemic attack

VA

Vertebral artery

Authors’ contributions

All authors contributed to the study conception and design. Material preparation, data collection and analysis were performed by YY, WF, JL, XL, YW, DL, OZ, QL, and FC. The first draft of the manuscript was written by YY and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

Funding

This study was supported by the Project of Ningbo Key Medical Discipline (2026-A24), the Key Department at Ningbo NO.2 Hospital (2023-Y03), and the Research Project on Integrated Traditional Chinese and Western Medicine for Chronic Disease Management, sponsored by the China National Center for the Development of Traditional Chinese Medicine Science and Technology (CXZH2024036-3, 2025036), and the Zhejiang Clinovation Pride.

Data availability

The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.

Declarations

Ethics approval and consent to participate

All procedures performed in the study involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. The study was approved by the institutional ethics committee of the Ningbo No.2 Hospital (NBEY-KY-2020-058-01). Written informed consent were obtained from all patients.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.

Footnotes

Publisher’s note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.


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