INTRODUCTION

Intracranial atherosclerosis (ICAS) is among the leading causes of ischemic stroke globally and is particularly prevalent in Asian populations [1]. Unlike extracranial atherosclerosis, which often receives more attention due to its accessibility and association with carotid stenosis, ICAS presents distinct clinical and pathophysiological challenges due to its location within the skull and its involvement of smaller caliber cerebral vessels [2].

Intracranial arteries differ from extracranial arteries in several key anatomical and histological aspects, which may contribute to their heightened vulnerability to atherosclerosis and other vascular diseases. Unlike extracranial arteries, intracranial arteries possess a thinner tunica media with fewer elastic fibers and a relatively sparse external elastic lamina. Typically, they lack an adventitial vasa vasorum under normal conditions, which may limit their capacity for repair or remodeling following vascular injury. The combination of a thinner arterial wall and diminished structural support renders intracranial vessels more prone to luminal narrowing and the extension of plaque into the media. Additionally, intracranial arteries are subjected to higher shear stress and more pronounced pulsatile pressures within the rigid cranial vault, factors that can significantly influence endothelial function and atherogenesis [3]. These anatomical features help explain why intracranial atherosclerosis often presents differently from extracranial disease and may require different therapeutic approaches.

Another key anatomical distinction of intracranial arteries is their direct association with perforating branches, a characteristic not commonly seen in extracranial vessels. These small perforators, which arise directly from major intracranial arteries such as the middle cerebral artery (MCA), basilar artery (BA), and vertebral artery, supply deep brain regions including the basal ganglia, thalamus, and brainstem—sites commonly affected by lacunar infarction or intracerebral hemorrhage [4]. Because these perforators originate from atherosclerotic segments, they are especially susceptible to occlusion by mechanisms such as branch atheromatous disease, where plaque extension or microthrombus formation at the branch origin can precipitate lacunar infarctions [5]. This feature contributes to the broader spectrum of stroke mechanisms seen in intracranial atherosclerosis, including not only artery-to-artery embolism, but also perforator infarction, which is a less common pattern in extracranial disease.

Given these anatomical and physiological differences, the development and clinical manifestations of atherosclerosis in intracranial arteries diverge significantly from those in extracranial vessels. These distinctions impact stroke mechanisms—ranging from large-vessel occlusion to perforator infarction—and necessitate tailored approaches for both diagnosis and management. In this review, we discuss how the unique structural characteristics of intracranial arteries contribute to the pathogenesis of ICAS and its varied stroke mechanisms. We also examine how these differences inform modern imaging strategies, particularly high-resolution vessel wall imaging, and influence therapeutic decision-making, including antithrombotic therapy and risk factor management.

DEVELOPMENT OF ICAS

ICAS has traditionally been considered a condition predominantly driven by systemic vascular risk factors such as hypertension, diabetes mellitus, dyslipidemia, and metabolic syndrome. Early studies underscored the significance of metabolic syndrome in the development and progression of ICAS, highlighting how systemic metabolic disturbances can impact intracranial vascular pathology [6]. However, emerging evidence suggests that local hemodynamic forces—particularly wall shear stress (WSS)— play a critical role in determining plaque initiation, distribution, and vulnerability within intracranial arteries. Research increasingly focuses on these biomechanical influences, showing that regions exposed to low and oscillatory WSS are especially prone to plaque accumulation and subsequent ischemic events.

Anatomically, ICAS frequently originates in the mid-segments of intracranial arteries. For example, the curvature of the MCA as viewed from the anterior perspective significantly affects plaque distribution: U-shaped MCAs are more likely to develop atherosclerosis along the superior wall, while inverted U-shaped MCAs tend to accumulate plaque along the inferior wall [7]. Studies comparing vascular geometry reveal that patients with ICAS exhibit greater MCA tortuosity than those with extracranial atherosclerosis [8]. In the BA, atherosclerosis often initiates at the posterior wall near the vertebrobasilar junction, advancing laterally as vessel curvature increases with age [9]. The anatomical and hemodynamic determinants of pontine infarction sites also reflect these patterns. Lower pontine infarctions are frequently linked to atherosclerosis at the vertebrobasilar junction, likely influenced by the angle between the vertebral arteries and the BA, as well as turbulent blood flow at this confluence [10]. In contrast, upper pontine infarctions are more commonly attributed to intrinsic small vessel disease, as the distal BA experiences more stable, laminar flow. Mid-pontine infarctions often result from lateral wall plaques, leading to either short or long circumferential artery infarctions; here, the lateral angulation of the BA plays a role in plaque development along its lateral wall.

Population-based differences in vascular anatomy have also been observed. Asian individuals generally display greater intracranial artery tortuosity than White individuals, a feature that intensifies with age and the presence of hypertension [11]. This anatomical trait may partially account for the higher prevalence of ICAS among Asian populations [12]. Further research is needed to clarify the underlying causes of increased intracranial arterial tortuosity seen in Asian populations, with genetic factors likely contributing. These ethnic differences may have implications for both diagnosis and therapy. For instance, increased tortuosity and greater involvement of perforators in Asian patients may enhance the diagnostic value of high-resolution magnetic resonance imaging (HR-MRI) and influence the selection of antiplatelet agents. Cilostazol, which has demonstrated benefits in Asian clinical trials with a lower risk of hemorrhage, may represent a more suitable long-term option in these populations. These findings support a more integrative approach to ICAS—one that combines management of traditional vascular risk factors with imaging-based assessment of cerebral vessel morphology and hemodynamics to improve risk prediction and guide individualized secondary prevention strategies [13,14].

MECHANISM OF STROKE RESULTING FROM ICAS

ICAS can cause ischemic stroke through several distinct pathophysiological mechanisms, reflecting the disease’s complexity beyond simple luminal narrowing (Fig. 1, Table 1). One major mechanism is artery-to-artery embolism, in which unstable atherosclerotic plaques at the stenotic site generate thromboembolic material that migrates distally, leading to infarction. This is supported by imaging findings such as multiple scattered infarcts and microembolic signals on transcranial Doppler. Compared to patients with local branch occlusion, those with artery-to-artery embolism frequently exhibit higher residual platelet reactivity despite aspirin therapy, especially in cases of recurrent stroke [15]. Additionally, high-risk enhancing plaques, considered markers of early recurrence [16], are more frequently observed in these patients. Enhancing plaque has been associated with high WSS in the corresponding area [17]. These findings suggest that more potent antiplatelet therapy may be warranted, particularly during the acute phase of stroke.

A second mechanism is in situ thrombosis, wherein severe stenosis or endothelial injury leads directly to thrombus formation at the lesion site, causing vessel occlusion. This process is analogous to that seen in coronary artery disease during myocardial infarction. Hemodynamic stroke represents another significant contributor, particularly when there is critical stenosis or inadequate collateral circulation. Hypoperfusion distal to the stenosis can result in border zone or watershed zone infarcts, especially under conditions of systemic hypotension. In such scenarios, strategies aimed at enhancing cerebral perfusion, such as induced hypertension in the acute phase, may be beneficial. In selected cases, endovascular revascularization using intracranial stenting may also be considered.

A distinct mechanism in ICAS is the occlusion of perforating arteries, also referred to as local branch occlusive disease. Here, small penetrating arteries originating near an atherosclerotic plaque become blocked, often despite the absence of significant luminal narrowing detectable by conventional imaging. This mechanism typically results in small, deep infarcts and is commonly seen in the territories supplied by the MCA, BA, and vertebral artery. Compared to artery-to-artery embolism, patients with local branch occlusion tend to have longer and more diffuse plaques, which are more likely to encroach on the orifices of perforators [18]. In these patients, antiplatelet agents with antiatherogenic properties, combined with aggressive lowering of low-density lipoprotein (LDL) cholesterol, may help reduce plaque burden and prevent recurrence [19].

Importantly, these mechanisms are not mutually exclusive and may coexist within a single patient. Therefore, a comprehensive assessment—including evaluation of plaque morphology, degree of stenosis, perfusion status, and embolic potential—is essential to tailor effective prevention and treatment strategies.

ADVANCED IMAGING IN ICAS

Two complementary strategies can be employed to determine the underlying mechanism of stroke. First, as previously described, the analysis of brain parenchymal lesions can provide important insights into stroke etiology, analogous to investigating a crime scene for clues about the perpetrator. Lesion patterns identified by diffusion-weighted imaging can help infer whether the underlying mechanism is artery-to-artery embolism, hypoperfusion, or perforator occlusion [20]. The second approach focuses more directly on the affected vessel itself, specifically the intracranial artery. Conventional magnetic resonance angiography (MRA) primarily visualizes the vessel lumen and may fail to capture crucial vessel wall features that contribute to plaque vulnerability and stroke risk.

HR-MRI, particularly vessel wall MRI (VW-MRI), has emerged as a valuable modality for elucidating the underlying pathology of ICAS and for identifying high-risk plaques associated with stroke. HR-MRI offers detailed visualization of the intracranial arterial wall, enabling the assessment of key plaque characteristics such as eccentricity, contrast enhancement, intraplaque hemorrhage, and positive remodeling [21]. These features are increasingly recognized as markers of plaque instability. For example, contrast enhancement may indicate active inflammation, neovascularization, or increased endothelial permeability, which are factors associated with an elevated risk of plaque rupture. Likewise, intraplaque hemorrhage or the presence of juxtaluminal thrombus suggests recent plaque disruption and thromboembolic potential. VW-MRI can also clarify the relationship between plaque location and the origin of perforating arteries, providing an explanation for the occurrence and size of perforator infarcts based on branching patterns and plaque involvement [22].

Furthermore, HR-MRI is valuable for distinguishing ICAS from other intracranial arteriopathies—such as vasculitis, moyamoya disease, or arterial dissection—based on differences in wall morphology, distribution, and enhancement patterns (Table 2) [23]. This is particularly important in cases of cryptogenic stroke or in patients without conventional vascular risk factors. A key advantage of HR-MRI is its ability to detect nonstenotic atherosclerosis—plaques that do not cause significant luminal narrowing and are often undetectable by standard imaging modalities like MRA or computed tomography angiography. Even in the absence of overt stenosis, such plaques may be clinically significant, especially when unstable or situated near perforator origins.

By providing detailed insights into both the structural and biological features of intracranial plaques, HR-MRI greatly enhances diagnostic precision in ICAS-related stroke, supports risk stratification, and informs individualized treatment strategies. As such, this imaging modality holds considerable promise for guiding more aggressive or targeted secondary prevention in patients at heightened risk of recurrence.

TREATMENT OF SYMPTOMATIC ICAS

Following the SAMMPRIS (Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis) trial, aggressive medical therapy has become the standard first-line approach for symptomatic ICAS [24]. The SAMMPRIS study demonstrated that intensive medical therapy, including dual antiplatelet therapy (aspirin and clopidogrel for 90 days), strict blood pressure and LDL cholesterol control, and comprehensive lifestyle modification, was superior to percutaneous transluminal angioplasty and stenting (PTAS) in preventing recurrent stroke. Notably, the 30-day rate of stroke and death was significantly higher in the PTAS group than in the medical therapy group (14.7% vs. 5.8%), thereby firmly establishing pharmacologic management as the mainstay of treatment.

Regarding antithrombotic therapy, several studies have further refined treatment strategies for ICAS. A subanalysis of the CHANCE (Clopidogrel in High-Risk Patients with Acute Non-disabling Cerebrovascular Events) trial, which originally investigated dual antiplatelet therapy (DAPT) with aspirin and clopidogrel in patients with minor stroke or high-risk transient ischemic attack, revealed that in patients with underlying ICAS, short-term DAPT significantly reduced the risk of recurrent stroke compared to aspirin alone, particularly within the first 21 days [25]. These findings support the early use of DAPT in patients with ICAS-related stroke or transient ischemic attack, consistent with the approach used in the SAMMPRIS trial.

The TOSS (Trial of Cilostazol in Symptomatic Intracranial Arterial Stenosis) series has also provided key insights into long-term antiplatelet management [26]. In TOSS-2, a head-to-head comparison of cilostazol with aspirin versus clopidogrel with aspirin demonstrated that the cilostazol-based regimen was effective in slowing the progression and promoting regression of ICAS, as measured by MRA over a 7-month period in secondary analysis. Additionally, the cilostazol group experienced fewer hemorrhagic complications [27]. These results suggest that cilostazol may be a safer and effective long-term antiplatelet option, particularly in Asian populations, where much of the evidence has been derived and the risk of hemorrhagic stroke is relatively higher than in Western populations. Further studies are needed to determine whether these findings can be generalized to Western populations, where baseline vascular risk and drug response may differ.

Regarding blood pressure targets, the SAMMPRIS trial aimed for a systolic blood pressure of <140 mmHg (or <130 mmHg in patents with diabetes), and achievement of this target was associated with lower stroke recurrence [28]. Observational studies have further supported the benefit of strict blood pressure control—especially maintaining systolic blood pressure below 140 mmHg during subacute and chronic phases—in reducing recurrent ischemic events in ICAS. However, caution is warranted in the hyperacute period after reperfusion, as excessively aggressive blood pressure reduction may compromise perfusion distal to a critical stenosis. Furthermore, the STABLE-ICAS (Strategy for Adequate Blood Pressure Lowering in the Patients With Intracranial Atherosclerosis) study failed to demonstrate noninferiority of intensive blood pressure lowering (<120 mmHg) in ICAS patients with respect to increases in white matter hyperintensity lesions [29].

For lipid management, the SAMMPRIS protocol recommended an LDL cholesterol target of <70 mg/dL, and achieving this goal correlated with improved outcomes [28]. This is consistent with broader secondary stroke prevention guidelines and is further supported by studies showing that statins not only reduce LDL cholesterol but also promote plaque stabilization and, potentially, regression [19]. Intensive statin therapy has been linked with favorable remodeling of intracranial arteries and decreased inflammatory activity within atherosclerotic plaques, as visualized on vessel wall imaging [30].

PRIMARY PREVENTION IN ASYMPTOMATIC ICAS

ICAS is sometimes detected incidentally during brain imaging performed for routine health screenings, headache evaluation, or other unrelated indications. Although asymptomatic at the time of discovery, such findings require careful evaluation, as they may indicate an increased risk of future cerebrovascular events. Management should begin with a thorough assessment of vascular risk factors, including hypertension, diabetes mellitus, dyslipidemia, and smoking status. Risk factor modification is crucial, with treatment targets aligned with current guidelines—for example, strict blood pressure control, LDL cholesterol reduction (typically to <70 mg/dL in high-risk individuals), and comprehensive lifestyle interventions.

Nevertheless, evidence supporting specific treatment strategies for asymptomatic ICAS remains limited. For comparison, in asymptomatic carotid artery disease, antithrombotic therapy is often recommended when stenosis exceeds 50%. Similarly, in asymptomatic ICAS, antiplatelet therapy—particularly aspirin—may be considered for selected patients who have additional risk factors or imaging evidence of high-risk plaque features. HR-VW-MRI is valuable for detecting nonstenotic but potentially unstable plaques that might otherwise be missed with conventional imaging. Although the optimal management approach for asymptomatic ICAS is still under investigation, a personalized prevention strategy tailored to the individual’s risk profile is advisable to reduce the likelihood of disease progression and future ischemic stroke. The evidence remains primarily observational, and there are no randomized trials specifically evaluating the efficacy of antithrombotic or statin therapy in asymptomatic ICAS. Therefore, preventive treatments such as aspirin or statins should be considered primarily in individuals with high vascular risk profiles or imaging evidence suggestive of plaque vulnerability. Future randomized controlled trials are needed to clarify whether pharmacologic interventions, including antiplatelet or lipid-lowering therapies, can reduce the risk of stroke or slow disease progression in patients with asymptomatic ICAS.

FUTURE DIRECTIONS

Despite advances in the understanding of ICAS, substantial gaps remain in the optimal management of this complex disease. Future research should address several key areas to enhance prevention and treatment strategies. First, improved risk stratification tools are needed to identify patients at the highest risk of stroke. This involves the consideration of stroke mechanisms as well as the development and validation of imaging biomarkers—such as plaque enhancement, positive remodeling, and intraplaque hemorrhage—using HR-VW-MRI. Although these features may help guide treatment decisions, large prospective studies are required to clarify their prognostic value.

Second, randomized controlled trials are essential to establish the efficacy of different antithrombotic and lipid-lowering regimens in patients with ICAS. Determining the optimal duration and combination of dual, or even short-term triple, antiplatelet therapy, assessing the role of novel oral anticoagulants, and evaluating the benefits of intensified lipid-lowering strategies (such as high-dose statins or PCSK9 inhibitors) all warrant further investigation.

Third, the hemodynamic consequences of ICAS, especially in patients with compromised perfusion or inadequate collateral circulation, should be investigated in greater detail. Advanced imaging techniques, such as perfusion MRI or arterial spin labeling, may help to identify patients who could benefit from hemodynamic optimization strategies, including induced hypertension or revascularization procedures. Novel imaging modalities that estimate fractional flow reserve or assess pressure gradients across stenotic segments may also aid in identifying appropriate candidates for endovascular intervention. The role of endovascular therapy should be reevaluated in the context of modern stenting technologies and more rigorous patient selection, particularly for cases of recurrent stroke despite optimal medical therapy.

Finally, a deeper exploration of the genetic and molecular underpinnings of ICAS, particularly in high-prevalence populations such as Asians, may uncover new therapeutic targets and further illuminate disease pathophysiology. Taken together, a precision medicine approach that integrates imaging, clinical characteristics, and biological data will be critical to advancing the prevention, risk stratification, and treatment of ICAS.

ARTICLE INFORMATION

Author contributions

Conceptualization: all authors; Investigation: SHH; Methodology: all authors; Supervision: BJK; Writing–original draft: all authors; Writing–review & editing: all authors. All authors read and approved the final manuscript.

Conflicts of interest

The authors have no conflicts of interest to declare.

Funding

The authors received no financial support for this study.

Fig. 1.

Stroke mechanisms in intracranial atherosclerosis. (A) Artery-to-artery embolism. (B) In situ thrombosis. (C) Hemodynamic. (D) Local branch occlusion. (E) Nonstenotic atherosclerosis.

REFERENCES

• 1. Banerjee C, Chimowitz MI. Stroke caused by atherosclerosis of the major intracranial arteries. Circ Res 2017;120:502–13. ArticlePubMedPMC
• 2. Kang DW, Kim DY, Kim J, Baik SH, Jung C, Singh N, et al. Emerging concept of intracranial arterial diseases: the role of high resolution vessel wall MRI. J Stroke 2024;26:26–40. ArticlePubMedPMCPDF
• 3. Ha SH, Yoon BH, Koo BG, Shin DH, Lee YB, Kim BJ. Association between impaired brachial flow-mediated dilation and early neurological deterioration in acute ischemic stroke: a retrospective analysis. BMC Neurol 2025;25:47.ArticlePubMedPMCPDF
• 4. Ha SH, Ryu JC, Bae JH, Koo S, Chang JY, Kang DW, et al. Factors associated with two different stroke mechanisms in perforator infarctions regarding the shape of arteries. Sci Rep 2022;12:16752.ArticlePubMedPMCPDF
• 5. Caplan LR. Intracranial branch atheromatous disease: a neglected, understudied, and underused concept. Neurology 1989;39:1246–50. ArticlePubMed
• 6. Kim JS, Nah HW, Park SM, Kim SK, Cho KH, Lee J, et al. Risk factors and stroke mechanisms in atherosclerotic stroke: intracranial compared with extracranial and anterior compared with posterior circulation disease. Stroke 2012;43:3313–8. ArticlePubMed
• 7. Kim BJ, Yoon Y, Lee DH, Kang DW, Kwon SU, Kim JS. The shape of middle cerebral artery and plaque location: high-resolution MRI finding. Int J Stroke 2015;10:856–60. ArticlePubMedPDF
• 8. Kim BJ, Kim SM, Kang DW, Kwon SU, Suh DC, Kim JS. Vascular tortuosity may be related to intracranial artery atherosclerosis. Int J Stroke 2015;10:1081–6. ArticlePubMedPDF
• 9. Kim BJ, Kim HY, Jho W, Kim YS, Koh SH, Heo SH, et al. Asymptomatic basilar artery plaque distribution and vascular geometry. J Atheroscler Thromb 2019;26:1007–14. ArticlePubMedPMC
• 10. Kim BJ, Lee KM, Kim HY, Kim YS, Koh SH, Heo SH, et al. Basilar artery plaque and pontine infarction location and vascular geometry. J Stroke 2018;20:92–8. ArticlePubMedPMCPDF
• 11. Kim BJ, Lee KM, Lee SH, Kim HG, Kim EJ, Heo SH, et al. Ethnic differences in intracranial artery tortuosity: a possible reason for different locations of cerebral atherosclerosis. J Stroke 2018;20:140–1. ArticlePubMedPMCPDF
• 12. Kim JS, Kim YJ, Ahn SH, Kim BJ. Location of cerebral atherosclerosis: why is there a difference between East and West? Int J Stroke 2018;13:35–46. ArticlePubMedPDF
• 13. Ha SH, Jeong S, Park JY, Chang JY, Kang DW, Kwon SU, et al. Association between arterial tortuosity and early neurological deterioration in lenticulostriate artery infarction. Sci Rep 2023;13:19865.ArticlePubMedPMCPDF
• 14. Woo HG, Kim HG, Lee KM, Ha SH, Jo H, Heo SH, et al. Blood viscosity associated with stroke mechanism and early neurological deterioration in middle cerebral artery atherosclerosis. Sci Rep 2023;13:9384.ArticlePubMedPMCPDF
• 15. Noh KC, Choi HY, Woo HG, Chang JY, Heo SH, Chang DI, et al. High-on-aspirin platelet reactivity differs between recurrent ischemic stroke associated with extracranial and intracranial atherosclerosis. J Clin Neurol 2022;18:421–7. ArticlePubMedPMCPDF
• 16. Kim JM, Jung KH, Sohn CH, Moon J, Shin JH, Park J, et al. Intracranial plaque enhancement from high resolution vessel wall magnetic resonance imaging predicts stroke recurrence. Int J Stroke 2016;11:171–9. ArticlePubMedPDF
• 17. Woo HG, Kim HG, Lee KM, Ha SH, Jo H, Heo SH, et al. Wall shear stress associated with stroke occurrence and mechanisms in middle cerebral artery atherosclerosis. J Stroke 2023;25:132–40. ArticlePubMedPMCPDF
• 18. Ha SH, Chang JY, Lee SH, Lee KM, Heo SH, Chang DI, et al. Mechanism of stroke according to the severity and location of atherosclerotic middle cerebral artery disease. J Stroke Cerebrovasc Dis 2021;30:105503.ArticlePubMed
• 19. Ha SH, Kim BJ. Dyslipidemia treatment and cerebrovascular disease: evidence regarding the mechanism of stroke. J Lipid Atheroscler 2024;13:139–54. ArticlePubMedPMCPDF
• 20. Kim BJ, Kang HG, Kim HJ, Ahn SH, Kim NY, Warach S, et al. Magnetic resonance imaging in acute ischemic stroke treatment. J Stroke 2014;16:131–45. ArticlePubMedPMC
• 21. Lee SH, Jung JM, Kim KY, Kim BJ. Intramural hematoma shape and acute cerebral infarction in intracranial artery dissection: a high-resolution magnetic resonance imaging study. Cerebrovasc Dis 2020;49:269–76. ArticlePubMedPDF
• 22. Kim BJ, Lee DH, Kang DW, Kwon SU, Kim JS. Branching patterns determine the size of single subcortical infarctions. Stroke 2014;45:1485–7. ArticlePubMed
• 23. Kim SM, Ha SH, Kwon H, Kim YJ, Ahn SH, Kim BJ. Targeting the culprit: vessel wall magnetic resonance imaging for evaluating stroke. Ann Clin Neurophysiol 2021;23:17–28. ArticlePDF
• 24. Derdeyn CP, Chimowitz MI, Lynn MJ, Fiorella D, Turan TN, Janis LS, et al. Aggressive medical treatment with or without stenting in high-risk patients with intracranial artery stenosis (SAMMPRIS): the final results of a randomised trial. Lancet 2014;383:333–41. ArticlePubMed
• 25. Liu L, Wong KS, Leng X, Pu Y, Wang Y, Jing J, et al. Dual antiplatelet therapy in stroke and ICAS: subgroup analysis of CHANCE. Neurology 2015;85:1154–62. ArticlePubMedPMC
• 26. Kwon SU, Cho YJ, Koo JS, Bae HJ, Lee YS, Hong KS, et al. Cilostazol prevents the progression of the symptomatic intracranial arterial stenosis: the multicenter double-blind placebo-controlled trial of cilostazol in symptomatic intracranial arterial stenosis. Stroke 2005;36:782–6. ArticlePubMed
• 27. Kwon SU, Hong KS, Kang DW, Park JM, Lee JH, Cho YJ, et al. Efficacy and safety of combination antiplatelet therapies in patients with symptomatic intracranial atherosclerotic stenosis. Stroke 2011;42:2883–90. ArticlePubMed
• 28. Turan TN, Nizam A, Lynn MJ, Egan BM, Le NA, Lopes-Virella MF, et al. Relationship between risk factor control and vascular events in the SAMMPRIS trial. Neurology 2017;88:379–85. ArticlePubMedPMC
• 29. Park JM, Kim BJ, Kwon SU, Hwang YH, Heo SH, Rha JH, et al. Intensive blood pressure control may not be safe in subacute ischemic stroke by intracranial atherosclerosis: a result of randomized trial. J Hypertens 2018;36:1936–41. ArticlePubMed
• 30. Ha SH, Ryu JC, Bae JH, Koo S, Kwon B, Song Y, et al. High serum total cholesterol associated with good outcome in endovascular thrombectomy for acute large artery occlusion. Neurol Sci 2022;43:5985–91. ArticlePDF

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References

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