Background and purpose: Intracranial atherosclerotic stenosis (ICAS) is a major cause of ischemic stroke (IS), and high‐resolution vessel wall imaging (HR‐VWI) can be used to assess the plaque characteristics of ICAS. This study aimed to qualitatively and quantitatively assess plaque enhancement of ICAS and to investigate the relationship between plaque enhancement, plaque morphological features, and IS.Methods: Data from adult patients with ICAS from April 2018 to July 2022 were retrospectively collected, and all patients underwent HR‐VWI examination. Plaque enhancement was qualitatively and quantitatively assessed, and the plaque‐to‐pituitary stalk contrast ratio (CR) indicated the degree of plaque enhancement. Plaque characteristics, such as plaque burden and area, were quantitatively measured using HR‐VWI. Furthermore, receiver‐operating characteristic (ROC) analysis was performed to assess the ability of CR to discriminate plaque enhancement. The patients were divided into a symptomatic ICAS group and an asymptomatic ICAS group according to the clinical and imaging characteristics. Univariate and multivariate analyses were performed to investigate which factors were significantly associated with plaque enhancement and symptomatic ICAS. The plaque burden and CR were compared using linear regression.Results: A total of 91 patients with ICAS were enrolled in this study. ICAS plaque burden was significantly associated with plaque enhancement (p = .037), and plaque burden was linearly positively correlated with CR (R = 0.357, p = .001). ROC analysis showed that the cutoff value of CR for plaque enhancement was 0.56 (specificity of 81.8%). Both plaque enhancement and plaque burden were significantly associated with symptomatic ICAS, and only plaque enhancement was an independent risk factor after multivariate analysis.Conclusion: Plaque burden was an independent risk factor for plaque enhancement and showed a linear positive correlation with CR. The cutoff value of CR for plaque enhancement was 0.56, and CR ≥ 0.56 was significantly associated with symptomatic ICAS, which was independently associated with plaque enhancement.

Ischemic stroke is a significant burden on human health worldwide. Carotid Atherosclerosis stenosis plays an important role in the comprehensive assessment and prevention of ischemic stroke patients. High-resolution vessel wall magnetic resonance imaging has emerged as a successful technique for assessing carotid atherosclerosis stenosis. This advanced imaging modality has shown promise in effectively displaying a wide range of characteristics associated with the condition, leading to a comprehensive evaluation. High-resolution vessel wall magnetic resonance imaging not only enables a comprehensive evaluation of the instability of carotid atherosclerosis stenosis plaques but also provides valuable information for understanding the pathogenesis and predicting the prognosis of ischemic stroke patients. The purpose of this article is to review the application of high-resolution magnetic resonance imaging in ischemic stroke and carotid atherosclerotic stenosis.

Background and purpose: Intracranial atherosclerotic stenosis (ICAS) is a major cause of ischemic stroke, and high-resolution vessel wall imaging (HR-VWI) can be used to assess the plaque characteristics of ICAS. This study combined HR-VWI, hemodynamics, and peripheral blood inflammatory indicators to investigate the role of these factors in symptomatic intracranial atherosclerotic stenosis (sICAS) and their inter-relationships. Methods: Patients diagnosed with atherosclerotic middle cerebral artery stenosis were recruited retrospectively from June 2018 to July 2022. Plaque enhancement was qualitatively and quantitatively analyzed, and the degree of plaque enhancement was graded according to the plaque-to-pituitary stalk contrast ratio (CR). Computational fluid dynamics models were constructed, and then hemodynamic parameters, including wall shear stress (WSS) and pressure ratio (PR), were measured and recorded. Univariate and multivariable analyses were performed to identify factors that can predict sICAS. In addition, the correlation analysis between the plaque characteristics on HR-VWI, hemodynamic parameters, and peripheral blood inflammatory indicators was performed to investigate the interrelationships between these factors. Results: Thirty-two patients were included. A higher proportion of plaque enhancement, maximum WSS, and WSS ratio (WSSR) were significantly associated with sICAS. The multiple logistic regression analysis showed that only the WSSR was an independent risk factor for sICAS. The correlation analysis revealed that both the CR and plaque burden showed linear positive correlation with the WSSR (R = 0.411, P = 0.022; R = 0.474, P = 0.007, respectively), and showed linear negative correlation with the lymphocyte to monocyte ratio (R = 0.382, P = 0.031; R = 0.716, P < 0.001, respectively). Conclusions: The plaque enhancement and WSSR were significantly associated with sICAS, WSSR was an independent risk factor for sICAS. Plaque enhancement and plaque burden showed linear correlation with the WSSR and lymphocyte-to-monocyte ratio (LMR). Hemodynamics and inflammation combined to promote plaque progression.

Whether symptomatic unruptured intracranial aneurysms (UIAs) lead to change in circulating inflammation remains unclear. This study aims to evaluate the role of hematological inflammatory indicators in predicting symptomatic UIA. Adult patients diagnosed with saccular intracranial aneurysm from March 2019 to September 2023 were recruited retrospectively. Clinical and laboratory data, including the white blood cells (WBC), neutral counts (NEUT), lymphocyte counts (LYM), and monocyte counts (MONO) of each patient, were collected. The neutrophil-to-lymphocyte ratio (NLR) and lymphocyte-to-monocyte ratio (LMR) were calculated as NLR = NEUT/LYM, LMR = LYM/MONO, SII = PLT*NEUT/LYM. The hematological inflammatory indicators were compared in symptomatic saccular and asymptomatic UIA patients. Multivariable logistic regression analyses were performed to explore the factors predicting symptomatic UIA. One hundred and fifty UIA patients with a mean age of 58.5 ± 12.4 were included, of which 68% were females. The NLR and LMR were significantly associated with symptomatic UIA, and the association remained in small UIAs (< 7 mm). The multiple logistic regression analysis showed that NLR was independently associated with symptomatic UIA. On ROC curve analysis, the optimal cutoff value of NLR to differentiate symptomatic from asymptomatic was 2.38. In addition, LMR was significantly associated with symptomatic UIA smaller than 7 mm. There was a significant correlation between NLR and symptomatic UIA. The NLR was independently associated with symptomatic UIA.

Background and Purpose: While our previous cross-sectional study linked the lymphocyte-to-monocyte ratio (LMR) to symptomatic ICAS and plaque inflammation, its prospective value for predicting stroke recurrence remained unexplored. This study aimed to validate the association between LMR and plaque instability in a larger cohort and, critically, to determine whether baseline LMR predicts future ischemic events. Methods: We prospectively enrolled adult patients with radiologically confirmed ICAS from April 2018 to July 2024 at our tertiary cerebrovascular center. Comprehensive datasets, including clinical characteristics, laboratory markers (LMR and full inflammatory profiles), and neuroimaging features, were systematically collected and analyzed. Hematologic markers were compared between patients with ICAS with and without plaque enhancement and between those with and without symptoms. Receiver operating characteristic analysis was used to assess the discriminative value of LMR for plaque instability and determine optimal cutoff points. A follow-up was conducted to record stroke recurrence and evaluate the predictive role of baseline LMR. Results: We included 132 patients with confirmed ICAS. LMR emerged as an independent predictor of both plaque enhancement and symptomatic ICAS. An LMR cutoff of 4.0 effectively distinguished symptomatic from asymptomatic plaques. In 120 patients with ICAS with follow-up data, those with LMR of ≤ 4.0 had significantly higher recurrence (32.1% vs 15.6%, P = 0.026) and shorter median recurrence time (P = 0.049) than those with an LMR of > 4.0. Kaplan-Meier analysis showed a significantly lower recurrencefree survival rate in the LMR ≤ 4.0 group than in the LMR > 4.0 group (P = 0.011). Conclusion: A low LMR is associated with plaque instability in ICAS, and an LMR ≤ 4.0 may serve as a practical and accessible hematologic marker that could help identify patients at increased short-term risk of stroke recurrence.

Background and purpose The biological significance of aneurysmal wall enhancement (AWE) on high-resolution vessel wall imaging (HR-VWI) and its relationship with peripheral inflammation in intracranial fusiform aneurysms (IFA) remain incompletely understood. This study aims to investigate the association between circumferential AWE (CAWE) and peripheral immunoinflammatory indices in IFA, and to compare these features in different subtypes of unruptured intracranial aneurysm (UIA). Methods In this retrospective study, 196 patients with UIA (38 fusiform, 158 saccular) were included. Peripheral blood samples collected at admission were used to calculate immunoinflammatory indices, including the neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammation index (SII), and platelet–lymphocyte ratio (PLR). AWE was assessed and categorized by blinded readers. Clinical characteristics and inflammatory markers were compared, and multivariate logistic regression was used to identify variables associated with CAWE in patients with IFA. Results Patients with CAWE in the IFA cohort showed differences in peripheral blood-derived immunoinflammatory indices, with higher monocyte counts and NLR but a lower LMR (all P < 0.05). NLR remained associated with CAWE in a multivariable model (OR: 4.78, 95% CI: 1.21–18.92, P = 0.026). Compared to patients with ISA, the IFA group had a significantly higher rate of CAWE (P = 0.010) and exhibited differences in peripheral inflammatory profiles, characterized by elevated NLR (P = 0.038) and SII (P = 0.035), and decreased LMR (P = 0.028). Conclusion In this single-center retrospective study, CAWE in IFA was associated with differences in peripheral blood immunoinflammatory indices, including NLR. These findings should be interpreted as exploratory and require validation in larger prospective cohorts with longitudinal clinical follow-up.