Large Artery Stenosis Research Articles

Expert Perspective: Management of Relapses in Giant Cell Arteritis.

Giant cell arteritis (GCA) is a relapsing large-vessel vasculitis with risk of serious ischemic manifestations including vision loss and vascular damage in the form of large-artery stenosis, aneurysms and dissections. Approximately 50% of patients treated with glucocorticoid (GC) monotherapy and 30% of patients receiving adjunctive therapy with tocilizumab experience disease relapses, often during the first 2 years after diagnosis. Although most relapses in GCA do not involve life- or organ-threatening presentations and can be controlled successfully, frequent relapses may lead to increased use of GC and consequent treatment-related morbidity, in addition to risk of further vascular damage. Emerging data suggests that persistent disease activity may lead to increased vascular morbidity. Additionally, while tocilizumab decreases the frequency of relapses, more than 50% of patients relapse after discontinuation of therapy. Therefore, while interleukin-6 blockade suppresses disease activity, it does not restore tolerance. In this article, we discuss the practical diagnosis and management of GCA relapses from an expert perspective. Current treatment options for GCA relapses, including those recommended by international guidelines, and novel potential therapies are reviewed.

Outcomes of Symptomatic Intracranial Large Artery Stenoses: a Prospective Cohort Study from The Asian Registry of Intracranial Atherosclerosis (ARICAS).

Intracranial large artery atherosclerosis (ICAS) is a common cause of stroke in Asia. Prior epidemiological publications on ICAS have largely been single-country reports. This collaborative study involving several Asian countries aims to investigate the characteristics and outcomes of patients with stroke attributable to ICAS. This is an international, multicentre, observational, prospective cohort study of patients admitted with acute ischemic stroke secondary to ICAS to stroke centres in six Asian countries. Stroke due to ICAS was diagnosed when there was a >50% intracranial large artery stenosis ipslateral to a non-lacunar infarct, without significant ipsilateral extracranial stenosis, cardiac cause or other mechanism found for the stroke. Data was collected on patient demographics, vascular risk factors, stroke location and severity. Outcomes of interest were stroke recurrence and mortality at 12-month follow-up. A total of 356 patients were recruited. Mean age was 62.7  13.8 years, and 39.9% were females. Mean NIHSS on admission was 9 + 8, with majority of patients having mild (39.3%) or moderate (37.9%) strokes. Stroke recurrence was 6.7% (95%CI 4.4 - 9.9%) while mortality rate was 13.2% (95%CI 9.9 - 17.2%) within one year. The risk of stroke recurrence was associated with increasing age (odds ratio OR 1.04, 95% CI 1 - 1.06, p = 0.05) and hypertension (OR 3.23, 95%CI 1.09 - 9.61, p = 0.035). Mortality was associated with age (OR 1.05, 95%CI 1.01 - 1.08, p = 0.006) and NIHSS (OR 1.12, 95%CI 1.07 - 1.17, p <0.001). This multicenter Asian study demonstrates a high risk of stroke recurrence and mortality among patients with acute stroke due to ICAS. They are associated with age (both), as well as hypertension (for recurrence) and NIHSS (for mortality). Better treatment modalities are needed to reduce the frequency of adverse outcomes in symptomatic ICAS.

Endovascular thrombectomy: an effective and safe therapy for perioperative ischemic stroke.

Perioperative ischemic stroke is a rare but devastating complication. Mechanical thrombectomy is a promising therapeutic method, but very little data is available on its efficacy and safety. This study aims to answer this question by comparing the clinical outcomes of perioperative and community-onset stroke patients after endovascular therapy. A retrospective cohort study was conducted on a total of 35 perioperative and 584 community-onset acute ischemic stroke patients who underwent endovascular thrombectomy at our hospital over the past 3.5 years. The recanalization rate, clinical recovery and cerebral hemorrhage within 90 days after therapy were compared between these two patient groups. Endovascular thrombectomy provided perioperative and community-onset ischemic stroke patients with comparable rates of successful reperfusion (mTICI ≥2b grade) (97.1% vs. 97.3%; p = 0. 967) and favorable functional recovery (mRS ≤ 2) (51.4% vs. 43.3%, p = 0.348), with no increase in severe intracranial hemorrhage (0% vs. 2.6 and 1.0%, for hematoma ≥30% of infarcted tissue and intraventricular hemorrhage, respectively) within 90 days. In addition, perioperative stroke patients had higher prevalence of atrial fibrillation (42.9% vs. 26.7%; p = 0.038) and intracranial cerebral artery stenosis without clear embolism (17.1% vs. 3.8%; p < 0.001) than community-onset stroke patients. Endovascular thrombectomy is an effective and safe therapeutic approach for patients with perioperative ischemic stroke, although the results need to be validated by further studies with larger populations. Atrial fibrillation and large artery stenosis may contribute to the pathogenesis of perioperative ischemic stroke.

Current and Emerging Approaches to Imaging Large Vessel Vasculitis.

Large vessel vasculitides (LVV) comprise a group of inflammatory disorders that involve the large arteries, such as the aorta and its primary branches. The cause of LVV is often rheumatologic and includes giant cell arteritis and Takayasu arteritis. Giant cell arteritis is the most common form of LVV affecting people >50 years of age with a slight female predominance. Takayasu arteritis is more frequently seen in younger populations and is significantly more common in women. Prompt identification of LVV is crucial as it can lead to debilitating complications if left untreated, including blindness in the case of giant cell arteritis and large artery stenosis and aneurysms in the case of all forms of LVV. Noninvasive imaging methods have greatly changed the approach to managing LVV. Today, imaging (with ultrasound, magnetic resonance imaging, computed tomography, and positron emission tomography) is routinely used in the diagnosis of LVV. In patients with giant cell arteritis, imaging often spares the use of invasive procedures such as temporal artery biopsy. In addition, vascular imaging is also crucial for longitudinal surveillance of arterial damage. Finally, imaging is currently being studied for its role in assessing treatment response and ongoing disease activity and its potential value in determining the presence of vascular wall remodeling (eg, scarring). This review explores the current uses of noninvasive vascular imaging in LVV.

Takayasu Arteritis Presented with Unilateral Vision Loss : A Case Report

Background: Takayasu Arteritis (TA) is a rare chronic granulomatous inflammation of the aorta or its branches and is prevalent all around the world. It causes stenosis of large arteries and ischaemic damage to target organs. There is usually a delay in recognising TA because of the rarity and unfamiliarity with the disease, unspecific early symptoms and lack of diagnostic equipment for early diagnosis. The purpose of the study to reminding readers of this issue and emphasize the necessity for further research on how to deal with in the best way. Case Report: We report a case of 30 years old male presented on 22nd August 2023 at Institute of Applied Health Sciences (IAHS) Chattogram with gradual loss of vision of left eye over a month accompanied by headache and later on diagnosed as a case of Takayasu’s Arteritis. Conclusion: Visual loss is the most common ocular symptom in Takayasu arteritis. Since a variety of causes may result in reduced vision in Takayasu arteritis. A careful history is very important to ascertain the cause of visual loss in Takayasu arteritis patients to reduce unnessary investigations and referrals. IAHS Medical Journal Volume 6(2) December 2023; 90-92

Aseptic meningitis and Fabry disease.

Fabry disease is caused by enzymatic defects in alpha-galactosidase A that leads to the accumulation of glycosphingolipids throughout the body, resulting in a multisystemic disorder. The most common neurological manifestations are neuropathic pain, autonomic nervous system dysfunction and strokes, but some rarer neurological manifestations exist. Among these, aseptic meningitis is a possible complication. Our objectives were to measure the prevalence of this complication in a cohort of patients with Fabry disease, and to describe its clinical features. We conducted a retrospective review of Fabry disease patients followed at our tertiary referral center between 1995 and September 2023 with at least one episode of meningitis, and performed a systematic review to identify similar published cases. Four patients out of 107 (3.7%) had at least one episode of aseptic meningitis. Our systematic review identified 25 other observations. The median age of these 29 patients was 29.0 years, the median cerebrospinal fluid leukocyte count was 24 cells/mm3 with a predominance of lymphocytes in 64.7% of cases. In 82.8% of the patients, the diagnosis of Fabry disease was unknown before the meningitis. Large artery stenosis was present in 17.2% of patients and 57.1% of patients had a recent stroke concomitant with the meningitis. Several differential diagnoses were evoked, such as multiple sclerosis or central nervous system vasculitis. Our study suggests that Fabry disease should be considered as a cause of aseptic meningitis. The pathophysiological mechanisms underlying meningeal inflammation remain largely unknown but may reflect the dysregulation of pro-inflammatory signaling pathways.

Abstract WP255: Association Between Asymptomatic Intracranial Large Artery Stenosis and Neurofilament Light Chain: The Northern Manhattan Study

Introduction: The Neurofilament light chain (NfL) is a neuronal cytoplasmic protein and a reliable biomarker for assessing axonal damage in neurological diseases and traumatic brain injury. Asymptomatic intracranial large artery stenosis (ILAS) has been associated with higher risk of stroke and dementia. Although widely studied in the last few years, the role of NfL concentrations in ILAS is not well understood. Methods: We leveraged data from stroke-free participants in the population-based cohort Northern Manhattan Study (NOMAS) for a pilot study. Arterial stenosis was measured on magnetic resonance angiography in 11 intracranial large arteries and graded as 0 = no stenosis, 1 ≤ 50%, 2 = 50-69%, 3 ≥ 70% stenosis and 4 = flow gap. An asymptomatic Intracranial Large Artery Stenosis (ILAS) score was then developed to reflect the global stenotic burden, with a range of 0 to 44. We also dichotomized the ILAS score into any stenosis &gt; 50% versus none to reflect a more clinically relevant definition of ILAS. NfL concentrations were measured in plasma using Quanterix Simoa™ platform. We conducted generalized linear models adjusting for demographic and vascular risk factors and Wald Chi-Square test to analyze the association between NfL and ILAS score. Results: We included 79 stroke-free NOMAS participants (66% women, 77% Hispanic/Latino, and 75% with hypertension). The mean concentration of NFL was 0.19±0.10 pg/mL with a mean intra-assay coefficient of variation equal to 8.2%. In a model adjusted for age, sex, race/ethnicity, hypertension, diabetes, dyslipidemia and smoking, a higher ILAS score was associated with increased levels of NfL (B=0.01 ± 0.004, p=0.007). In an adjusted model, any stenosis &gt;50% was also associated with increased levels of NfL (B=0.11 ± 0.03, p&lt;0.001). Conclusions: The increased levels of plasma NfL associated with asymptomatic ILAS suggest neuronal injury that may implicate development of neurodegeneration. Confirming these results in a larger sample and longitudinal evaluation of NfL may advance the understanding of the mechanisms by which ILAS may increase the risk of dementia.

Abstract WP239: Apolipoprotein E4 Allele Effect on the Prevalence of Intracranial Large Artery Stenosis

Introduction: Apolipoprotein E4 (ApoE4) allele is linked to increased LDL-Cholesterol, one of the main risk factors for intracranial large artery stenosis (ICAS). Evidence shows that in diabetic men, intima-media thickness is significantly higher in those with ApoE4 than those with ApoE3. While the link between ApoE4 and extracranial atherosclerosis and vascular risk factors is established, the association of these vascular factors with ICAS is unknown. This study investigates the relationship between ApoE4 carrier status and ICAS and whether vascular risk factors influence this relationship. Methods: We rated intracranial large arteries on MR-angiography for their degree of stenosis as 0=no stenosis, 1=&lt;50% stenosis, 2=50-69%, 3=70% or flow gap. We added the score of each of the 11 intracranial arteries to reflect a composite measure of the severity of ICAS. We then related ApoE4 carrier status to the ICAS score using generalized linear models with a Poisson link, adjusting for demographics, vascular risk factors, and cohort. We ran pre-specified interaction models with demographics and vascular risk factors. Results: 4099 individuals from six cohorts were included; 58% were women, the prevalence of hypertension was 76%, diabetes 31%, dyslipidemia 64%, and current smoking 13% (Table). There was no association between ApoE4 carrier and ICAS score (B= 0.08+0.06, p=0.19), but we found statistical interactions between ApoE4 carrier and male sex (p=&lt;0.001), current smoking (p=0.05), and hypertension (p=0.003). ApoE4 carrier status was associated with higher ICAS score among hypertensive men (B=0.52±0.11, P=&lt;0.001) and hypertensive people who smoke (B=0.58±0.20, p=0.01. Conclusion: ApoE4 carrier status was not associated with ICAS overall, but there were associations in subgroups defined by sex, hypertension, and smoking. Whether these interactions influence the risk of stroke and dementia should be further investigated.

Thromboelastographic and Gene Polymorphism Bimodality Detection for Dual Antiplatelet Aggregation Therapy in Individuals with Clopidogrel-resistant Symptomatic Intracranial Artery Stenosis.

Recent research indicates that clopidogrel resistance is connected with a patient's future ischemia risk, hence increasing the likelihood of recurrent ischemic cerebrovascular disease. Thromboelastographic and clopidogrel gene polymorphism testing can be used to see how a person responds to antiplatelet therapy and change the treatment plan accordingly. This may be a good way to make antiplatelet aggregation therapy more effective and safer. The objective of this study was to investigate the efficacy of dual antiplatelet aggregation therapy in patients with symptomatic intracranial large artery stenosis being resistant to clopidogrel tablets. The thromboelastographic and gene polymorphism bimodality detection techniques were used to analyze the clopidogrel resistance influencing factors. 89 patients with symptomatic intracranial large arterial stenosis who were admitted to our hospital from February 2021 to February 2022 were selected, classified as large artery atherosclerotic type by TOAST, and confirmed as having severe intracranial large arterial stenosis (70 % to 99 %) by magnetic resonance angiography (MRA), computed tomographic angiography (CTA), and digital subtraction angiography (DSA). All patients were treated with dual antiplatelet therapy with aspirin and clopidogrel, and thromboelastography and clopidogrel gene polymorphism were monitored 1 week later. 44 of 89 patients were clopidogrel-resistant. Among 44 patients, 20 were ticagrelorresistant and 24 were cilostazol-resistant. Clopidogrel had a resistance rate of 49.4%. The recurrence of ischemic cerebrovascular disease in the three groups was statistically significant (P<0.05) after 3 months of follow-up treatment, but bleeding (intracranial, gastrointestinal, respiratory, urinary, and mucocutaneous) and dyspnea were not. The clopidogrel-resistant group had a higher number of females, as well as higher levels of hypertension, diabetes, and platelet count than the sensitive group (P<0.05), but there was no significant difference in age, smoking, alcohol consumption, previous stroke, glycosylated haemoglobin, creatinine, or low-density cholesterol. Using thromboelastographic and gene polymorphism bimodality detection, we found switching to ticagrelor antiplatelet aggregation therapy as better than switching to cilostazol in patients with symptomatic intracranial large artery stenosis being resistant to clopidogrel tablets. The results may be biased due to the study being a single-centre study and having a limited sample size.

Percutaneous dual intervention in a child with Alagille syndrome –A case report.

Alagille syndrome(ALGS) is a rare autosomal dominant (AD) genetic disorder .ALGS involves multisystem which includes liver ,heart, skeleton, Eyes, kidneys with facial abnormalities. ALGS may involve a particular system like facial dysmorphism, cardiac defect or vertebral defect. Some individual may not have liver anomalies or typical features. We report a case of 9 year old male child with large ostium secundum ASD(16 mm) and branch pulmonary artery stenosis(LPA)diagnosed incidentally at 8 year of age. The child had facial dysmorphism (broad forehead, frontal bossing , triangular facies, hypertelorism, prominent ear and pointed chin, straight nose with bulbous tip. The mental development of the child was borderline. He also had butterfly vertebrae in thoracic and lumber region. He was treated successfully with ASD device closure for ASD and balloon pulmonary valvuloplasty for LPA stensis. Both the procedure was performed simultaneously without any complications. There is no curative management for the disorder so symptomatic management is the only treatment option.

JAK2 V617F Mutation and Large Cerebral Artery Disease in Patients with Myeloproliferative Neoplasms.

The aim of the present study was to clarify the association between the Janus kinase 2 (JAK2) V617F mutation and large cerebral artery disease (LCAD) in patients with myeloproliferative neoplasms (MPNs). We retrospectively analysed patients diagnosed with MPNs between June 1992 and June 2022 who underwent brain magnetic resonance imaging. LCAD was defined as extracranial or intracranial large artery stenosis (≥ 50%) or occlusion on magnetic resonance angiography. A total of 86 patients (47 males; median age, 69 years old) were enrolled in this study. JAK2 V617F mutation was detected in 63 (73.3%) patients and LCAD in 35 (40.7%) patients. Univariate analysis showed that history of ischaemic stroke (LCAD, 62.9% vs. non-LCAD, 11.8%; P＜0.001), JAK2 V617F mutation (91.4% vs. 60.8%, P=0.002), and age ≥ 60 years (85.7% vs. 60.8%, P=0.016) were significantly associated with LCAD. Multiple logistic regression analysis showed that, in addition to ischaemic stroke, age ≥ 60 years and diabetes mellitus, JAK2 V617F mutation (odds ratio 29.2, 95% confidence interval 1.2-709.8, P=0.038) was independently associated with LCAD. LCAD was frequently observed in the intracranial carotid (14/35, 40.0%) and middle cerebral (13/35, 37.1%) arteries. This study revealed a significant association between the JAK2 V617F mutation and LCAD in patients with MPNs. This suggests that the JAK2 V617F mutation may promote cerebrovascular atherosclerosis and could be very important in determining therapeutic strategies for patients with not only JAK2 V617F-mutated MPNs but also LCAD-related stroke.

Immune Markers Are Associated With Asymptomatic Intracranial Large Artery Stenosis and Future Vascular Events in NOMAS.

Inflammation contributes to atherosclerosis but is incompletely characterized in intracranial large artery stenosis (ICAS). We hypothesized that immune markers would be associated with ICAS and modify the risk ICAS confers on future vascular events. This study included a subsample of stroke-free participants in the prospective NOMAS (Northern Manhattan Study), who had blood samples analyzed with a 60-plex immunoassay (collected from 1993 to 2001) and ICAS assessment with time-of-flight magnetic resonance angiography (obtained from 2003 to 2008). We dichotomized ICAS as either ≥50% stenosis or not (including no ICAS). We ascertained post-magnetic resonance imaging vascular events. We used least absolute shrinkage and selection operator procedures to select immune markers independently associated with ICAS. Then, we grouped selected immune markers into a derived composite Z score. Using proportional odds regression, we quantified the association of the composite immune marker Z score, ICAS, and risk of vascular events. Among 1211 participants (mean age, 71±9 years; 59% women; 65% Hispanic participants), 8% had ≥50% ICAS. Using least absolute shrinkage and selection operator regression, we identified CXCL9 (C-X-C motif chemokine ligand 9), HGF (hepatocyte growth factor), resistin, SCF (stem cell factor), and VEGF-A(vascular endothelial growth factor A) to have the strongest positive relationships with ≥50% ICAS in fully adjusted models. Selected markers were used to derive a composite immune marker Z score. Over an average follow-up of 12 years, we found that each unit increase in immune marker Z scores was associated with an 8% (95% CI, 1.05-1.11), 11% (95% CI, 1.06-1.16), and 5% (95% CI, 1.01-1.09) increased hazard of death, vascular death, and any vascular event, respectively, in adjusted models. We did not find a significant interaction between immune marker Z scores and ICAS in their relationship with any longitudinal outcome. Among a diverse stroke-free population, selected serum immune markers were associated with ICAS and future vascular events. Further study is needed to better understand their role in the pathogenesis of ICAS and as a potential therapeutic target in stroke prevention.

Early detection of stroke at the sudden sensorineural hearing loss stage.

Sudden sensorineural hearing loss (SSNHL) can be a prodromal symptom of ischemic stroke, especially posterior circulation strokes in the anterior inferior cerebellar artery (AICA) area. Early diagnosis and optimal treatment for vascular SSNHL provide an opportunity to prevent more extensive area infarction. The objective of our research was to find clues that suggest stroke at the stage of isolated sudden hearing loss. We retrospectively investigated the medical records of patients who received an initial diagnosis of sudden sensorineural hearing loss upon admission from January 2017 to December 2022 at Capital Medical University Affiliated Beijing Tiantan Hospital. Among these patients, 30 individuals who developed acute ischemic stroke during their hospital stay were enrolled as the case group. To create a control group, we matched individuals from the nonstroke idiopathic SSNHL patients to the case group in terms of age (±3 years old) at a ratio of 1:4. We collected the clinical characteristics, pure tone hearing threshold test results, and imaging information for all patients included in the study. Three models were constructed to simulate different clinical situations and to identify vascular sudden sensorineural hearing loss (SSNHL). The results revealed that patients with SSNHL who had three or more stroke risk factors, bilateral hearing loss, moderately severe to total hearing loss, and any intracranial large artery stenosis and occlusion (≥50%) were at a higher risk of developing ischemic stroke during hospitalization. Consistent with previous studies, the presence of vertigo at onset also played a significant role in the early detection of upcoming stroke. Clinicians should be alert to SSNHL patients with bilateral hearing loss, moderately severe to total hearing loss and other aforementioned features. Early pure tone audiometric hearing assessment and vascular assessment are necessary for high-risk patients with SSNHL.

Transradial intra-aortic catheter looping in the angioplasty of severe intracranial symptomatic arteriosclerotic diseases.

This study aims to investigate the effect and feasibility of intra-aortic catheter looping via transradial access in angioplasty for symptomatic intracranial severe (>70%) atherosclerotic stenosis or occlusion of large arteries (SISOLAs). Patients with SISOLAs who underwent transradial endovascular angioplasty using the catheter looping technique in the ascending aorta were retrospectively enrolled. The clinical data and treatment outcomes were analyzed. Fifteen patients aged 48-71 years were enrolled in this study. Left vertebrobasilar artery occlusion was present in 1 (6.7%) patient, severe left middle cerebral artery stenosis in 7 (46.7%) patients, severe left internal carotid artery (ICA) stenosis of the ophthalmic segment in 4 (26.7%) patients, severe left ICA stenosis of the cavernous segment in 2 (13.3%) patients, and severe right middle cerebral artery stenosis in 2 (13.3%) patients. The arterial stenosis ranged from 70 to 92% (mean 86%) before stenting. The looping of a guiding catheter in the ascending aorta via transradial access for angioplasty was successful in all patients (100%). The vertebral artery intracranial segment occlusion was successfully recanalized, while severe stenosis in the remaining 14 patients was successfully eliminated. After endovascular recanalization, the residual stenosis was reduced by 12-26% (median 18%). No puncture-related complications or surgical-related neurological complications occurred in these patients. In the follow-up angiography conducted on 10 (66.7%) patients after 6-25 months, no in-stent restenosis was detected. Intra-aortic guiding catheter looping via transradial access for endovascular angioplasty of SISOLAs is technically safe, feasible, and effective, especially when the transfemoral artery approach is difficult or impossible to undertake.

Prominent veins sign is associated with malignant cerebral edema after acute ischemic stroke

Malignant cerebral edema (MCE) is often associated with severe physical disability and a high mortality rate. The current prediction of MCE is focused on infarct volume, and tools are relatively lacking. The prominent veins sign (PVS-SWI) is considered a marker of severely impaired tissue perfusion. This study aimed to determine whether PVS-SWI is associated with early-onset MCE. Patients with acute ischemic stroke (AIS) due to severe large arterial stenosis or occlusion (SLASO) from June 2018 to June 2020 were included. The ASPECTS score assessed the extent of PVS-SWI, and 4–10 was defined as a positive group. The primary outcome was MCE, defined as the deterioration of neurological function and midline structural excursions of >5 mm during hospitalization. The secondary outcomes included worsening of the NIHSS by ≥ 2 points, in-hospital death, and death within 1 year after stroke. Logistic regression was used to assess the correlation between PVS-SWI and outcomes. The study included 157 patients， 40 (25.5%) of whom developed MCE. PVS-SWI was more prevalent in patients who developed MCE (75.0% vs 45.3%; P = 0.001). In multivariate regression analysis, PVS-SWI was an independent predictor of MCE development in patients with larger infarct sizes (OR: 4.00， 95%CI: 1.54–10.35，p = 0.004). In patients with small infarct sizes, PVS-SWI was an independent predictor of a worsening NIHSS of ≥2(OR: 11.13， 95%CI: 2.26–54.89， p = 0.003）. However, PVS-SWI was not associated with death. The main finding of our study was that in patients with larger infarct sizes, a positive PVS-SWI increased the risk of developing MCE. In these patients, more interventions may be needed.

Mediterranean-style diet and intracranial large artery stenosis in the Northern Manhattan Study

ObjectivesGiven Mediterranean-style diet (MeDi) reduces risk of cardiovascular events, we hypothesized MeDi may also be protective against intracranial large artery stenosis (ICAS), a common cause of stroke worldwide. MethodsThis cross-sectional study included stroke-free participants of the Northern Manhattan Study, a diverse population-based study of stroke risk factors. We represented MeDi continuously (range 0-8) based on enrollment food frequency questionnaires, excluding alcohol consumption. We evaluated ICAS both dichotomously at clinically relevant stenosis severities and continuously as a score (possible range 0-44), summated from stenosis severity scores of major intracranial arteries from time-of-flight magnetic resonance angiography. We used logistic or zero-inflated Poisson regression, adjusting for key confounders. ResultsAmong 912 included participants (mean age 64±8 years, 59% female, 65% Hispanic, mean MeDi score 4±1.5), 5% and 8% of participants had ≥50% or ≥70% ICAS, respectively (score median [interquartile range]: 0 [0-2]). Increased MeDi score was inversely associated with ICAS, but did not reach statistical significance (≥50% stenosis odds ratio (OR) [95% confidence interval (CI)]: 0.89 [0.79-1.06]; ≥70% stenosis OR [95% CI]: 0.91 [0.74-1.13]; stenosis score β-estimate [95% CI]: -0.02 [-0.06-0.01]). ConclusionIn this stroke-free subsample, we did not find a significant association between MeDi and ICAS. We may have been limited by statistical power.

Intraluminal arterial transit artifact as a predictor of intracranial large artery stenosis on 3D time of flight MR angiography: Expanding the application of arterial spin labeling MRI in ischemic stroke.

The objective of this study was to evaluate the diagnostic value of "intraluminal arterial transit artifact" in the prediction of intracranial large artery stenosis and to determine if this finding is predictive of ischemic stroke in the territory of the involved artery. The presence of arterial transit artifact (ATA) within the lumen of an intracranial large vessel was noted on three-dimensional time of flight (3D-TOF) magnetic resonance angiography (MRA) (ATA group). The patients with stenosis but with no ATA (no-ATA group), patients with total occlusion (total occlusion group), and patients with no stenosis/occlusion (normal group) were included in the analysis. There were four groups of patients included in the final analysis, the ATA group (n = 22), the no-ATA group (n = 23), the normal group (n = 25), and the total occlusion group (n = 9). Among patients with any demonstrable stenosis (n = 45), the presence of ATA within the stenotic segment was predictive of stenosis of ≥56% (Sensitivity of 100% [85.2-100, 95% CI], specificity of 100% [86.4-100, 95% CI]), with area under curve of 1.0 (0.92-.0, 95% CI). The presence of intra-arterial ATA signal was significantly associated with ischemic stroke as compared with the no-ATA group (86.36% vs. 26.08%, P = 0.0003). Intraluminal ATA was found to be an independent predictor of infarction in the territory of the involved artery. Intraluminal ATA is predictive of stenosis of at least 56% in the involved artery on 3D-TOF MRA. Intraluminal ATA sign may be an independent predictor of infarction in the territory of the involved artery.

The role of intracranial artery calcification (IAC) in stroke subtype and risk of vascular events

ObjectiveTo test the hypothesis that intracranial arterial calcification (IAC) is associated with intracranial large artery stenosis (ILAS) and a higher risk of vascular events and mortality. MethodWe leveraged data from two cohorts, the New York-Presbyterian Hospital/Columbia University Irving Medical Center Stroke Registry Study (NYP/CUIMC-SRS) and the Northern Manhattan Study (NOMAS) to test our hypotheses. We measured IAC using CT scans of participants in both cohorts and expressed IAC as present (vs not) and in tertiles. For the CUIMC-SRS, demographic, clinical and ILAS status was collected retrospectively. In NOMAS, we used research brain MRI and MRA to define asymptomatic ILAS and covert brain infarcts(CBI). We built models adjusted for demographics and vascular risk factors for cross-sectional and longitudinal analyses. ResultsCross-sectionally, IAC was associated with ILAS in both cohorts (OR 1.78, 95% CI: 1.16-2.73 for ILAS-related stroke in the NYP/CUIMC-SRS and OR 3.07, 95%CI 1.13-8.35 for ILAS-related covert brain infarcts in NOMAS). In a meta-analysis of both cohorts, IAC in the upper (HR 1.25, 95%CI 1.01-1.55) and middle tertile (HR 1.27, 95%CI 1.01-1.59) was associated with higher mortality compared with participants with no IAC. There were no longitudinal associations between IAC and risk of stroke or other vascular events. ConclusionIn these multiethnic populations, IAC is associated with symptomatic and asymptomatic ILAS as well as higher mortality. IAC may be a useful marker of higher mortality, the role of IAC as an imaging marker of risk of stroke is less certain.

Correlation Analysis of Middle Cerebral Artery Stenosis and Enlarged Perivascular Space in Patients with Moyamoya Disease (S45.007)

<h3>Objective:</h3> To explore the correlation between the MCA stenosis and the CSO-EPVS in patients with MMD and whether brain atrophy plays a mediating role. <h3>Background:</h3> Moyamoya disease (MMD) is a nonatherosclerotic cerebrovascular structural abnormality. Previous studies have found that central semiovale Enlarged enlarged perivascular spaces (CSO-EPVS) are associated with decreased regional cerebral blood flow in MMD patients, but the specific mechanism remains unclear. <h3>Design/Methods:</h3> 177 patients from 2017 to 2022 were consecutively enrolled in this single-center Moyamoya disease cohort. All 354 MCAs were divided into three groups according to the severity of MCA on the MRA: no stenosis, mild or moderate stenosis, and severe stenosis or occlusion. The correlation between cerebral hemisphere volume, MCA stenosis and CSO-EPVS was analyzed, and the confounding factors including age, gender and hypertension were adjusted. <h3>Results:</h3> MCA stenosis was significantly associated with CSO-EPVS (no stenosis vs mild or moderate stenosis: 95%CI [0.954, 4.473], P=0.000; no stenosis vs severe stenosis or occlusion: 95%CI [4.419, 9.586], P=0.000). Cerebral hemisphere volume was correlated with CSO-EPVS (no stenosis vs mild or moderate stenosis: 95%CI [−0.824, 0.414], P=0.047; no stenosis vs severe stenosis or occlusion: 95%CI [−1.051, 4.431], P=0.018), but there was no significant correlation between MCA stenosis and the hemisphere volume (no stenosis vs mild or moderate stenosis: 95%CI [−0.097, 0.123], P=0.434; no stenosis vs. severe stenosis or occlusion: 95%CI [−1.012, 1.210], P=0.403). Mediating variable analysis showed that hemisphere volume had no mediating effect in the correlation between the MCA stenosis and CSO-EPVS (no stenosis vs mild or moderate stenosis: 95%CI [−0.039, 0.329], P=0.910; no stenosis vs severe stenosis or occlusion: 95%CI [−0.118, 0.106], P=0.350). <h3>Conclusions:</h3> Our study shows the association between the MCA stenosis and CSO-EPVS without brain atrophy as a mediator, highlighting the potential correlation between large artery stenosis and small cerebral vessel. <b>Disclosure:</b> Mr. Han has nothing to disclose. Ms. Hong has nothing to disclose. Ding-Ding Zhang has nothing to disclose. Xiaoyuan Fan has nothing to disclose. Ming Yao has nothing to disclose. Jun Ni has nothing to disclose.

Culprit Plaques of Large Parent Arteries, Rather than Cerebral Small Vessel Disease, Contribute to Early Neurological Deterioration in Stroke Patients with Intracranial Branch Atheromatous Disease

Introduction: Intracranial branch atheromatous disease (BAD) has been applied to occlusions that occur at the origin of large caliber penetrating arteries due to the microatheromas or large parent artery plaques. This study aimed to explore the association between culprit plaques of large parent arteries, neuroimaging markers of cerebral small vessel disease (CSVD), and the risk of early neurological deterioration (END) in stroke patients with BAD. Methods: A total of 97 stroke patients with BAD in the vascular territories of the lenticulostriate arteries or paramedian pontine arteries, diagnosed using high-resolution magnetic resonance imaging, were prospectively recruited in this observational study. A culprit plaque in the middle cerebral artery was defined as the only arterial plaque on the ipsilateral side of an infarction visible on diffusion-weighted imaging. A culprit plaque in the basilar artery (BA) was identified when it was observed within the same axial slices of an infarction or on the adjacent upper or lower slice, whereas a plaque within the BA located in the ventral region was considered non-culprit. If more than one plaque was present in the same vascular territory, the most stenotic plaque was chosen for the analysis. Four CSVD neuroimaging markers, including white matter hyperintensity, lacunes, microbleeds, and enlarged perivascular spaces, were evaluated in accordance with the total CSVD score. The associations between neuroimaging features of lesions within large parent arteries, neuroimaging markers of CSVD, and the risk of END in stroke patients with BAD were investigated using logistic regression analysis. Results: END occurred in 41 stroke patients (42.27%) with BAD. The degree of large parent artery stenosis (p < 0.001), culprit plaques of large parent arteries (p < 0.001), and plaque burden (p < 0.001) were significantly different between the END and non-END groups in stroke patients with BAD. In logistic regression analysis, culprit plaques of large parent arteries (odds ratio, 32.258; 95% confidence interval, 4.140–251.346) were independently associated with the risk of END in stroke patients with BAD. Conclusions: Culprit plaques of large parent arteries could predict the risk of END in stroke patients with BAD. These results suggest that lesions in the large parent arteries, rather than damage to the cerebral small vessels, contribute to END in stroke patients with BAD.