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RecruitingNCT06902740PISTIAS-2Updated Jun 12, 2026

PCSK9 Inhibitor With Statin Therapy for Asymptomatic Intracranial Atherosclerosis

A Phase 4 interventional study of Recaticimab and Statin and Statin in Intracranial Atherosclerosis, Intracranial Artery Stenosis and Atherosclerotic Plaque, sponsored by Peking Union Medical College Hospital. Recruiting at 19 sites in China. Open to participants aged 18 Years to 80 Years. Per ClinicalTrials.gov, last updated 2026-06-12.

Sponsored by Peking Union Medical College Hospital · Phase 4, Interventional, and Treatment

Phase
Phase 4
Study type
Interventional
Enrollment
300
Allocation
Randomized
Ages
18 Years to 80 Years
Sex
All
01

Study summary

This is a prospective, multicenter, open-label, blinded-endpoint, randomized controlled trial designed to evaluate the efficacy and safety of PCSK9 inhibitor combined with statin therapy compared to statin monotherapy in reversing asymptomatic intracranial atherosclerosis, assessed using high-resolution magnetic resonance imaging of the intracranial vessel walls.

Read the detailed description

Intracranial atherosclerotic stenosis (ICAS) is a leading cause of ischemic stroke worldwide, accounting for approximately 10-20% of all ischemic strokes in Europe and the United States, and up to 50% in Asian populations. While evidence-based management strategies for symptomatic ICAS have been progressively established over the past decades, asymptomatic ICAS - representing an earlier-stage, broader, high-risk population - has long been under-recognized and under-studied. Asymptomatic ICAS (stenosis > 50%) has a reported prevalence of approximately 6%-13%, and is associated with a substantially increased risk of future cerebrovascular events. Moreover, accumulating evidence has demonstrated that asymptomatic ICAS is independently associated with cognitive decline and incident dementia, likely due to chronic downstream hypo-perfusion and cumulative ischemic injury. Therefore, the development of systematic, evidence-based, and precision prevention strategies for asymptomatic ICAS is essential for reducing the overall disease burden attributable to ICAS-related cerebrovascular and neurodegenerative disorders.

It is well established that dysregulation of lipid metabolism is a fundamental pathophysiological mechanism driving the initiation and progression of ICAS, and low-density lipoprotein cholesterol (LDL-C) has been consistently identified as the primary therapeutic target for atherosclerotic cardiovascular disease and for the prevention of ischemic stroke. Existing evidence has demonstrated that reductions in lipid levels and the regression of atherosclerotic plaques are closely associated with a decreased risk of cardiovascular events. Statin therapy remains the cornerstone of lipid-lowering treatment, capable of stabilizing atherosclerotic plaques and improving clinical outcomes. However, limitations of statins such as the plateau effect of LDL-C reduction, intolerance, and poor adherence in certain patients necessitate alternative or adjunctive lipid-lowering strategies. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, human monoclonal antibodies targeting PCSK9, have shown excellent efficacy in achieving intensive LDL-C reduction and have been extensively validated for safety in large clinical trials. Recently published studies have highlighted the potential of PCSK9 inhibitors in plaque regression and stabilization beyond coronary and carotid arteries. The SLICE-CEA CardioLink-8 trial demonstrated that adding evolocumab to moderate- or high-intensity statin therapy for 6 months significantly reduced the lipid-rich necrotic core in asymptomatic high-risk carotid plaques. Similarly, the ARCHITECT study revealed that alirocumab in combination with high-intensity statin therapy led to significant regression of coronary plaque burden and enhanced plaque stability in asymptomatic patients over a 78-week period. Several observational studies have indicated that intensive lipid-lowering therapy may reverse asymptomatic ICAS. However, to date, no clinical trials have specifically evaluated the efficacy and safety of PCSK9 inhibitors in addition to statin therapy in patients with asymptomatic ICAS. This represents a critical evidence gap, as these patients constitute a broader, earlier, and high-risk population for cerebrovascular events.

The PISTIAS-2 is an investigator-initiated, multicentre, prospective, open-label, blinded end-point, randomized controlled trial designed to evaluate the efficacy and safety of PCSK9 inhibitor combined with statin therapy compared to statin monotherapy in patients with asymptomatic ICAS. Patients aged 18 to 80 years with asymptomatic ICAS, defined as 50% to 99% stenosis in at least one major intracranial artery without a prior history of ischemic stroke or transient ischemic attack, will be enrolled for 24-week treatment. Eligible participants will be centrally randomized into two groups: (1) Experimental group [PCSK9 inhibitor combined with statin therapy]: Recaticimab 450 mg every 12 weeks combined with rosuvastatin 10 mg q.n. or atorvastatin 20 mg q.n. (2) Control group [Statin alone]: Rosuvastatin 10 mg q.n. or atorvastatin 20 mg q.n. Considering inter-individual variability in lipid-lowering response, ezetimibe 10 mg once daily is permitted at the discretion of the study physician based on the predefined criteria: (1) patients already receiving statin therapy prior to enrollment whose LDL-C remains above 2.6 mmol/L, and (2) statin-naïve patients whose LDL-C exceeds 2.6 mmol/L at the 12-week lipid profile reassessment. In this trial, we employed a novel PCSK9 inhibitor, Recaticimab, a humanized IgG1 monoclonal antibody engineered with a strategic YTE mutation in its Fc region, which enhances its affinity for the neonatal Fc receptor (FcRn). This modification reduces FcRn-mediated antibody catabolism, thereby extending the half-life of Recaticimab and enabling a prolonged dosing interval of up to 12 weeks.

The primary outcome is the change in intracranial plaque burden from baseline to week 24, measured by high-resolution magnetic resonance imaging (HR-MRI).The key secondary outcomes include: change in stenosis degree from baseline to week 24, time from randomization to the first-ever ischemic stroke or transient ischemic attack, and change in plasma marker glial fibrillary acidic protein(GFAP) and neurofilament light (NfL). Other secondary outcomes include: time from randomization to the occurrence of major adverse cardiovascular events, new-onset silent cerebral infarction, percentage of patients who achieved LDL-C goal at week 24, percentage change in LDL-C relative to baseline, and change in plasma marker Aβ40, Aβ42, Aβ42/Aβ40. In addition, several pre-specified exploratory outcomes have been defined for this study. Details are provided in the "Outcome Measures" section.

After the 24-week treatment period, an extended prospective follow-up (clinical or telephone follow-up) will continue for more than one year to document long-term effects.The sample size is calculated based on the primary outcome and a total of 300 participants are anticipated. An interim analysis will be conducted when 50% of the participants (i.e., 150 subjects) have completed the 24-week follow-up with HR-MRI. An independent Data Safety Monitoring Board will oversee the overall conduct of the trial.

02

Conditions studied

  • Intracranial Atherosclerosis
  • Intracranial Artery Stenosis
  • Atherosclerotic Plaque

Keywords

  • Intracranial Atherosclerosis
  • intracranial artery stenosis
  • atherosclerotic plaque
  • high-resolution magnetic resonance imaging
  • PCSK9 inhibitor
  • statin
  • Recaticimab
03

Who can participate

Ages eligible
18 Years to 80 Years
Sexes eligible
All
Accepts healthy volunteers
No

Inclusion criteria

  1. Age ≥18 and ≤80, male or female;
  2. Asymptomatic intracranial artery stenosis (50%-99%) in the internal carotid artery (C6-7 segments), middle cerebral artery (M1 segment), vertebral artery (V4 segment), or basilar artery, confirmed by angiography (MRA, CTA, or DSA);
  3. Atherosclerosis identified as the cause of intracranial artery stenosis by high-resolution magnetic resonance imaging;
  4. No previous ischemic cerebrovascular events (including ischemic stroke or transient ischemic attack).
  5. Baseline low-density lipoprotein cholesterol ≥ 1.8 mmol/L;
  6. Informed consent signed.

Exclusion criteria

Exclusion Criteria:

  1. Non-atherosclerotic intracranial artery stenosis, including arterial dissection; moya moya disease; systemic vasculitis and primary central nervous system vasculitis; varicella-zoster vasculopathy or other viral vasculopathy; neurosyphilis and other intracranial infections, radiation vasculopathy; fibromuscular dysplasia, sickle cell disease, neurofibromatosis; reversible cerebral vasoconstriction syndrome; postpartum vasculopathy; suspected vasospasm, suspected reperfusion after vessel occlusion.
  2. Upstream tandem extracranial vessel stenosis (≥50%) adjacent to the target intracranial stenotic vessel.
  3. Previous treatment of target intracranial lesion with endovascular intervention or plan to perform endovascular intervention within 6 months, including intracranial stenting, endovascular angioplasty, and thrombectomy.
  4. Any intracranial hemorrhage (parenchymal, subarachnoid, subdural, extradural, intraventricular) within 90 days prior to enrollment.
  5. Presence of intracranial tumors.
  6. Presence of cerebral aneurysms or arteriovenous malformations with indications for interventional therapy.
  7. Major surgery (including open femoral, aortic, or carotid surgery) within previous 30 days or planned in the next 6 months after enrollment.
  8. Presence of any of the following unequivocal cardiac sources of embolism: mitral stenosis, mechanical valve, endocarditis, intracardiac clot or vegetation, myocardial infarction within 3 months, dilated cardiomyopathy, chronic or paroxysmal atrial fibrillation.
  9. New York Heart Association (NYHA) class III or IV, or known left ventricular ejection fraction \< 30%.
  10. Severe liver dysfunction or severe kidney dysfunction: AST and/or ALT > 3 times the ULN; creatinine clearance \< 0.6 mL/s and/or serum creatinine > 265 μmol/L (>3.0 mg/dL); CK >5 times the ULN at screening.
  11. Active bleeding diathesis or coagulopathy (e.g., active peptic ulcer disease, major systemic hemorrhage within 30 days, active bleeding diathesis, platelets count \< 125,000 / uL, hematocrit \< 30%, Hgb \< 10 g/dl, international normalized ratio >1.5, bleeding time > 1 minute beyond normal value upper limit).
  12. Presence of systemic autoimmune diseases: systemic sclerosis, systemic lupus erythematosus, Sjögren's syndrome, Behçet's disease, mixed connective tissue disease, IgG4-related disease.
  13. Dementia or psychiatric problem that hinder their ability to consistently adhere to an outpatient program. Co-morbid conditions that may limit the life expectancy to less than 3 years.
  14. Relative/absolute contraindications to magnetic resonance imaging (MRI) (such as presence of internal metallic objects, claustrophobia, contrast agent allergy, severe renal impairment, epilepsy, hypotension, asthma, and other hypersensitivity respiratory diseases).
  15. Uncontrolled hypertension during the screening period, defined as seated systolic blood pressure (SBP) > 180 mmHg or diastolic blood pressure (DBP) > 110 mmHg.
  16. Prior use of PCSK9 inhibitor before this recruitment.
  17. Known intolerance or allergy to statin.
  18. Pregnancy, lactation, or planning pregnancy.
  19. Currently participating in another study.
04

Study design

Phase
Phase 4
Primary purpose
Treatment
Allocation
Randomized
Intervention model
Parallel assignment
Masking
Single (Outcomes assessor)
Enrollment
300 participants (estimated)

Study arms

  • Experimental
    Recaticimab plus Statin Group

    Recaticimab (450mg every 12 weeks subcutaneously) combined with rosuvastatin 10mg qn or atorvastatin 20mg qn

    Drug: Recaticimab and Statin

  • Active comparator
    Statin Group

    Rosuvastatin 10mg qn or atorvastatin 20mg qn

    Drug: Statin

Interventions

  • DrugRecaticimab and Statin

    Recaticimab (450mg every 12 weeks subcutaneously) combined with rosuvastatin 10mg qn or atorvastatin 20mg qn

  • DrugStatin

    Rosuvastatin 10mg qn or atorvastatin 20mg qn

05

What researchers measure

Primary outcomes

  1. Change in plaque burden from baseline to week 24

    Intracranial plaque burden was assessed at maximum stenosis site by high-resolution magnetic resonance imaging, performed at baseline and the end of the treatment period (24 \[±1\] week) on the same machine. The plaque burden is calculated according to the following formula: plaque burden = \[(vessel wall cross-sectional area - lumen cross-sectional area ) / vessel wall cross-sectional area\] ×100%. The outcome will be centrally assessed by an independent core imaging laboratory blinded to treatment allocation according to a predefined imaging analysis protocol.

    Time frame: From baselie to the end of treatment at 24 weeks

Secondary outcomes

  1. Change in stenosis degree from baseline to week 24

    The degree of stenosis is calculated according to the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) criteria using the formula: \[1-(Dstenosis/Dnormal)\]×100%. Dstenosis represents the vessel diameter at the most stenotic site of the intracranial artery, and Dnormal represents the normal vessel diameter at a reference site.

    Time frame: From baseline to the end of treatment at 24 weeks

  2. Time from randomization to the first-ever ischemic stroke or transient ischemic attack

    Ischemic Stroke: Defined as an acute cerebral infarction with clinical signs or imaging evidence of a new acute focal neurological injury persisting for more than 24 hours, excluding other non-ischemic causes. Transient Ischemic Attack (TIA): Defined as a sudden onset of focal neurological deficit due to cerebral or retinal ischemia, which completely resolves within 24 hours. Imaging (CT or MRI) must show no evidence of a new cerebral infarction. Other non-ischemic causes, such as brain infection, trauma, tumor, epilepsy, severe metabolic disorders, or progressive neurological diseases, must be excluded.

    Time frame: From baseline to the end of treatment at 24 weeks

  3. Change in plasma marker glial fibrillary acidic protein(GFAP)

    Change in plasma marker glial fibrillary acidic protein(GFAP) quantified using the Single Molecule Array platform from baseline to the end of treatment at 24 weeks

    Time frame: From baseline to the end of treatment at 24 weeks

  4. Change in plasma marker neurofilament light(NfL)

    Change in plasma marker Neurofilament light(NfL) quantified using the Single Molecule Array platform from baseline to the end of treatment at 24 weeks

    Time frame: From baseline to the end of treatment at 24 weeks

  5. Time from randomization to the occurrence of major adverse cardiovascular events

    Composite major adverse cardiovascular endpoints includes ischemic stroke, myocardial infarction, and cardiovascular mortality as a cluster

    Time frame: From baseline to the end of treatment at 24 weeks

  6. Silent cerebral infarction

    New-onset silent cerebral infarction is defined as an imaging-detected infarct without acute clinical symptoms

    Time frame: at 24 weeks of treatment

  7. Percentage of patients who achieved LDL-C goal at week 24

    Percentage of patients achieving the LDL-C target at week 24 of treatment, defined as LDL-C \< 1.8 mmol/L or LDL-C \< 2.6 mmol/L based on ASCVD risk assessment.

    Time frame: at 24 weeks of treatment

  8. Percentage change in LDL-C relative to baseline

    Percentage change in LDL-C level at 24 weeks of treatment relative to baseline

    Time frame: From baseline to the end of treatment at 24 weeks

  9. Change in Plasma marker Aβ42/Aβ40

    Change in plasma markers Aβ42/Aβ40 from baseline to the end of treatment at 24 weeks

    Time frame: From baseline to the end of treatment at 24 weeks

Other outcomes

  1. Time from randomization to the time of the first occurrence of transient ischemic attack

    Transient Ischemic Attack (TIA): Defined as a sudden onset of focal neurological deficit due to cerebral or retinal ischemia, which completely resolves within 24 hours. Imaging (CT or MRI) must show no evidence of a new cerebral infarction. Other non-ischemic causes, such as brain infection, trauma, tumor, epilepsy, severe metabolic disorders, or progressive neurological diseases, must be excluded.

    Time frame: From baseline to the end of treatment at 24 weeks

  2. Time from randomization to the time of the first occurrence of ischemic stroke

    Ischemic Stroke: Defined as an acute cerebral infarction with clinical signs or imaging evidence of a new acute focal neurological injury persisting for more than 24 hours, excluding other non-ischemic causes.

    Time frame: From baseline to the end of treatment at 24 weeks

  3. Time from randomization to the time of the occurrence of any stroke

    Any stroke includes ischemic and hemorrhagic stroke

    Time frame: From baseline to the end of treatment at 24 weeks

  4. Time from randomization to the time of the occurrence of myocardial infarction

    Time from randomization to the time of the occurrence of myocardial infarction

    Time frame: From baseline to the end of treatment at 24 weeks

  5. Time from randomization to the time of the occurrence of vascular death

    Time from randomization to the time of the occurrence of vascular death

    Time frame: From baseline to the end of treatment at 24 weeks

  6. Time from randomization to the time of the occurrence of any death

    All-cause mortality will be calculated between two arms

    Time frame: From baseline to the end of treatment at 24 weeks

  7. Changes in cognitive scale scores

    Cognitive function will be evaluated via MMSE and MOCA at baseline and week 24

    Time frame: From baseline to the end of treatment at 24 weeks

  8. Changes in traditional lipid parameters

    Changes in traditional lipid profiles, especially total cholesterol (TC), triglycerides (TG) and HDL-C.

    Time frame: From baseline to the end of treatment at 24 weeks

  9. Change in Lipoprotein (a) level

    Non-traditional lipid parameters such as Lipoprotein (a) level will be detected at baseline and week 24

    Time frame: From baseline to the end of treatment at 24 weeks

  10. Visit-to-visit lipid variability of LDL-C

    Lipid variability during the treatment period, which can be evaluated by the following indicators: coefficient of variation (CV), standard deviation (SD), variability independent of the mean (VIM), average real variability (ARV).

    Time frame: From baseline to the end of treatment at 24 weeks

  11. Change in high-sensitivity C-reactive protein

    Inflammatory markers such as high-sensitivity C-reactive protein (hs-CRP) will be detected at baseline and week 24

    Time frame: From baseline to the end of treatment at 24 weeks

  12. Change in plasma marker pTau217

    Markers of neurological disorders such asplasma marker pTau217 will be detected at baseline and week 24

    Time frame: From baseline to the end of treatment at 24 weeks

  13. Changes in DNA methylation status of peripheral blood cells

    DNA methylation, particularly RNF213, an important epigenetic factor, may play a role in the progression of ICAS.

    Time frame: From baseline to the end of treatment at 24 weeks

  14. Changes in Senescence-Associated Secretory Phenotype

    Previous studies have shown that lipid-lowering has an obvious scavenging effect on senescent cells. Senescence associated β-galactosidase, SA-β-gal, is thought to be a sign of aging

    Time frame: From baseline to the end of treatment at 24 weeks

  15. Change in length of plaque

    length of plaque was evaluated by high-resolution MRI at baseline and week 24

    Time frame: From baseline to the end of treatment at 24 weeks

  16. Change in plaque maximum thickness

    the maximum thickness of plaque was evaluated by high-resolution MRI at baseline and week 24

    Time frame: From baseline to the end of treatment at 24 weeks

  17. Change in the outer-wall boundary area at the maximal stenotic site

    the outer-wall boundary area at the maximal stenotic site was evaluated by high-resolution MRI at baseline and week 24

    Time frame: From baseline to the end of treatment at 24 weeks

  18. Change in remodeling index of the plaque

    Remodeling index of the plaque is calculated by the ratio of the diameter of the lumen at the most severe lesion to the diameter of the proximal reference lumen, positive remodeling defined as remodeling index \> 1.1

    Time frame: From baseline to the end of treatment at 24 weeks

  19. Change in plaque enhancement

    plaque enhancement will be detected via contrast enhanced high- resolution MRI

    Time frame: From baseline to the end of treatment at 24 weeks

  20. Change in brain volume

    Total brain volume will be evaluated by MRI 3D-T1WI at baseline and week 24

    Time frame: From baseline to the end of treatment at 24 weeks

  21. Change in cortical thickness

    The thickness and surface area of cerebral cortex in all and different brain regions were quantitatively determined based on MRI

    Time frame: From baseline to the end of treatment at 24 weeks

  22. Change in cerebral small vessel disease burden

    cerebral small vessel disease burden were quantitatively determined based on MRI at baseline and week 24

    Time frame: From baseline to the end of treatment at 24 weeks

  23. Change in white matter hyperintensity

    White matter hyperintensity (WMH) in all and different brain regions were quantitatively determined based on MRI

    Time frame: From baseline to the end of treatment at 24 weeks

  24. Change in collateral circulation status

    Collateral circulation status will be assessed using standardized imaging-based grading scales to evaluate the extent and quality of collateral blood flow.

    Time frame: From baseline to the end of treatment at 24 weeks

  25. Adverse events

    An Adverse Event (AE) is any untoward medical occurrence in clinical trial subject administered a pharmaceutical product and which does not necessarily have a causal relationship with the treatment.

    Time frame: From baseline to the end of treatment at 24 weeks

  26. Serious Adverse Events

    A Serious Adverse Event (SAE) is any untoward medical occurrence that, at any dose: (1) results in death; (2) is life-threatening; (3) requires inpatient hospitalization or prolongation of existing hospitalization; (4)results in persistent or significant disability/incapacity; (5) is a congenital anomaly/birth defect; (6) is otherwise considered medically significant by the investigator.

    Time frame: From baseline to the end of treatment at 24 weeks

06

Study locations

2 of 19 sites recruiting
  • Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College
    Beijing, Beijing Municipality 100730, China
    • Weihai Xu, MD · Contact · xuwh@pumch.cn · 86+13651147766
    • Weihai Xu, MD · Principal investigator
    Recruiting
  • Chinese PLA General Hospital
    Beijing, Beijing Municipality 100853, China
    • Shiwen Wu, MD · Contact · wu_shiwen@outlook.com · 86+13910238117
    • Shiwen Wu, MD · Principal investigator
    Not yet recruiting
  • The Third Affiliated Hospital of Sun Yat-sen University, Yuedong Hospital
    Meizhou, Guangdong, China
    • Ying Bian, MD · Contact · bianying1001@126.com · 86+13692279949
    • Ying Bian, MD · Principal investigator
    Not yet recruiting
  • Cangzhou Hospital of Integrated Traditional Chinese and Western Medicine
    Cangzhou, Hebei, China
    Not yet recruiting
  • Peking University Third Hospital Qinhuangdao Hospital
    Qinhuangdao, Hebei, China
    • Yaqun Liu, MD · Contact · bysyqhdyyyxll@163.com · 86+18533550025
    • Yaqun Liu, MD · Principal investigator
    Not yet recruiting
  • Hebei Provincial People's Hospital
    Shijiazhuang, Hebei 050051, China
    Recruiting
  • Tangshan Worker's Hospital
    Tangshan, Hebei 063000, China
    • Baoquan Lu, MD · Contact · balcom@163.com · 86+13930565557
    • Baoquan Lu, MD · Principal investigator
    Not yet recruiting
  • First Affiliated Hospital of Harbin Medical University
    Harbin, Heilongjiang, China
    • Hongquan Jiang, MD · Contact · quan@hrbmu.edu.cn · 86+13796707995
    • Hongquan Jiang, MD · Principal investigator
    Not yet recruiting
  • The first affiliated hospital of zhengzhou university
    Zhengzhou, Henan, China
    • Bo Song, MD · Contact · fccsongb@zzu.edu.cn · 86+13603983297
    • Bo Song, MD · Principal investigator
    Not yet recruiting
  • Taihe Hospital
    Shiyan, Hubei 442000, China
    • Zhibing Ai, MD · Contact · aizhibing1@126.com · 86+13997833207
    • Zhibing Ai, MD · Principal investigator
    Not yet recruiting
  • Zhongnan Hospital of Wuhan University
    Wuhan, Hubei, China
    • Bin Mei, MD · Contact · neuromei20@163.com · 86+13037196699
    • Bin Mei, MD · Principal investigator
    Not yet recruiting
  • Baotou Central Hospital
    Baotou, Inner Mongolia 014000, China
    • Jingfen Zhang, MD · Contact · 1846224761@qq.com · 86+13947253466
    • Jingfen Zhang, MD · Principal investigator
    Not yet recruiting
  • Nanjing First Hospital
    Nanjing, Jiangsu 210000, China
    • Qiwen Deng, MD · Contact · qiw_deng@njmu.edu.cn · 86+15366110212
    • Qiwen Deng, MD · Principal investigator
    Not yet recruiting
  • Jining First People's Hospital
    Jining, Shandong 272000, China
    • Zhongrui Yan, MD · Contact · zhongruiy@163.com · 86+15910000699
    • Zhongrui Yan, MD · Principal investigator
    Not yet recruiting
  • Liaocheng People's Hospital
    Liaocheng, Shandong 252000, China
    • Guanzeng Li, MD · Contact · 13396350996@163.com · 86+13396350996
    • Guanzeng Li, MD · Principal investigator
    Not yet recruiting
  • The Affiliated Hospital of Qingdao University
    Qingdao, Shandong, China
    • Naidong Wang, MD · Contact · wangnaidong163@163.com · 86+18661809550
    • Naidong Wang, MD · Principal investigator
    Not yet recruiting
  • Weifang People's Hospital
    Weifang, Shandong 261000, China
    Not yet recruiting
  • Chongqing General Hospital
    Chongqing, China
    • Jingxi Ma, MD · Contact · majingxi@ucas.ac.cn · 86+15765059385
    • Jingxi Ma, MD · Principal investigator
    Not yet recruiting
  • Huashan Hospital, Fudan University
    Shanghai, China
    • Jianhui Fu, MD · Contact · jianhuifu@126.com · 86+13701818645
    • Jianhui Fu, MD · Principal investigator
    Not yet recruiting
07

References and documents

Publications

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  • Zhu J, Wang Y, Li J, Deng J, Zhou H. Intracranial artery stenosis and progression from mild cognitive impairment to Alzheimer disease. Neurology. 2014 Mar 11;82(10):842-9. doi: 10.1212/WNL.0000000000000185. Epub 2014 Jan 31. PubMed 24489130 ↗
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  • Gao P, Wang T, Wang D, Liebeskind DS, Shi H, Li T, Zhao Z, Cai Y, Wu W, He W, Yu J, Zheng B, Wang H, Wu Y, Dmytriw AA, Krings T, Derdeyn CP, Jiao L; CASSISS Trial Investigators. Effect of Stenting Plus Medical Therapy vs Medical Therapy Alone on Risk of Stroke and Death in Patients With Symptomatic Intracranial Stenosis: The CASSISS Randomized Clinical Trial. JAMA. 2022 Aug 9;328(6):534-542. doi: 10.1001/jama.2022.12000. PubMed 35943472 ↗
  • Chimowitz MI, Lynn MJ, Derdeyn CP, Turan TN, Fiorella D, Lane BF, Janis LS, Lutsep HL, Barnwell SL, Waters MF, Hoh BL, Hourihane JM, Levy EI, Alexandrov AV, Harrigan MR, Chiu D, Klucznik RP, Clark JM, McDougall CG, Johnson MD, Pride GL Jr, Torbey MT, Zaidat OO, Rumboldt Z, Cloft HJ; SAMMPRIS Trial Investigators. Stenting versus aggressive medical therapy for intracranial arterial stenosis. N Engl J Med. 2011 Sep 15;365(11):993-1003. doi: 10.1056/NEJMoa1105335. Epub 2011 Sep 7. PubMed 21899409 ↗
  • Li S, Tang M, Zhang D, Han F, Zhou L, Yao M, Li M, Cui L, Zhang S, Peng B, Jin Z, Zhu Y, Ni J. The prevalence and prognosis of asymptomatic intracranial atherosclerosis in a community-based population: Results based on high-resolution magnetic resonance imaging. Eur J Neurol. 2023 Dec;30(12):3761-3771. doi: 10.1111/ene.16057. Epub 2023 Sep 22. PubMed 37738517 ↗
  • Gutierrez J, Khasiyev F, Liu M, DeRosa JT, Tom SE, Rundek T, Cheung K, Wright CB, Sacco RL, Elkind MSV. Determinants and Outcomes of Asymptomatic Intracranial Atherosclerotic Stenosis. J Am Coll Cardiol. 2021 Aug 10;78(6):562-571. doi: 10.1016/j.jacc.2021.05.041. PubMed 34353533 ↗
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Individual participant data

Plan to share: Undecided

08

Registry details

Key details

Study ID
NCT06902740
Lead sponsor
Peking Union Medical College Hospital
Collaborators
Chinese PLA General Hospital, Hebei General Hospital, Taihe Hospital, Weifang People's Hospital, Nanjing First Hospital, Nanjing Medical University, Baotou Central Hospital, Jining First People's Hospital, Liaocheng People's Hospital, Tangshan Worker's Hospital, Chongqing General Hospital, First Affiliated Hospital of Harbin Medical University, Cangzhou Hospital of Integrated Traditional Chinese and Western Medicine, The First Affiliated Hospital of Zhengzhou University, The Affiliated Hospital of Qingdao University, Zhongnan Hospital, Huashan Hospital
Responsible party
Wei-Hai Xu (MD & PhD, Peking Union Medical College Hospital) — Principal investigator
First posted
Mar 30, 2025
Start date
Nov 7, 2025
Primary completion
Dec 31, 2027 (estimated)
Completion
Dec 31, 2028 (estimated)
Last update
Jun 12, 2026

Study contacts

Weihai Xu, MD
Contact
xuwh@pumch.cn
86+13651147766
Yiyang Liu, PhD
Contact
liuyydoct@163.com
86+13938912070

Oversight

Data monitoring committee
Yes
FDA-regulated drug
No
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

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