Intracranial Atherosclerotic Plaques Research Articles

7T-high resolution MRI-derived radiomic analysis for the identification of symptomatic intracranial atherosclerotic plaques.

High-resolution magnetic resonance imaging (HR-MRI) allows for detailed visualization of intracranial atherosclerotic plaques. Radiomics can be used as a tool for objective quantification of the plaque's characteristics. We analyzed the radiomics features (RFs) obtained from 7 T HR-MRI of patients with intracranial atherosclerotic disease (ICAD) to determine distinct characteristics of culprit and non-culprit plaques. Patients with stroke due to ICAD underwent HR-MRI. Culprit plaques in the vascular territory of the stroke were identified. Degree of stenosis, area degree of stenosis and plaque burden were calculated. A three-dimensional segmentation of the plaque was performed, and RFs were obtained. A machine learning model for prediction and identification of culprit plaques using significantly different RFs was evaluated. The study included 33 patients with ICAD as stroke etiology. Univariate analysis revealed 24 RFs in pre-contrast MRI, 21 in post-contrast MRI, 13 RFs that were different between pre and post contrast MRIs. Additionally, six shape-based RFs significantly differed from culprit and non-culprit plaques. The random forest model achieved an accuracy rate of 81% (88% sensitivity and 75% specificity) in identifying culprit plaques in the independent testing dataset. This model successfully identified the culprit plaques in all patients during the testing phase. Symptomatic plaques had a distinct signature RFs compared to other plaques within the same subject. A machine learning model built with RFs successfully identified the symptomatic atherosclerotic plaques in most cases. Radiomics is a promising tool for stratification of plaques in patients with ICAD.

Dynamic contrast enhancement and wall enhancement index for the quantitative assessment of vascular wall abnormalities in intracranial atherosclerosis: a pilot study

Background: Breakthrough neurotechnologies have allowed for new understanding of some brain disorders; however, identification and differential diagnosis of intracranial stenotic and occlusive lesions remains challenging. Magnetic resonance imaging (MRI) with dynamic contrast enhancement (DCE) is a tool that could be used for the quantitative assessment of endothelial permeability and microvascular volume in atherosclerotic plaques (AP). Aim: To assess quantitative parameters of vascular wall abnormalities in AP area and in obviously unchanged wall of intracranial arteries with MRI DCE and high spatial resolution Т1-weighed images before and after contrast injection, with calculation of the wall enhancement index (WEI) by mathematical modelling. Methods: This was a pilot cross-sectional uncontrolled study with consecutive recruitment of 29 patients with atherosclerotic abnormalities of brachiocephalic arteries, including intracranial. The patients’ median age was 66 [57; 72] years; they were mostly men (75.9%, n = 22). For the assessment of any brain abnormalities, MRI (magnetic induction 3 Tesla, Magnetom Prisma, Siemens) was performed in patients with standard sequence (Т2, T2-FLAIR), as well as MRI DCE for the assessment of intracranial arteries, before and after intravenous contrast injection, with high spatial resolution T1-weighed imaging and suppression of the signal from bloodstream and fat, with the calculation of WEI. Results: There were significant differences in WEI in AP and in unchanged wall (0.962 [0.686; 1.387] vs. 0.111 [0.014; 0.206], p 0.001). No significant differences were found between WEI values in internal carotid arteries APs (0.722 [0.573; 1.580]), middle cerebral arteries (0.921 [0.725; 1.183]), and basilar artery (1.343 [1.002; 1.419]) (p = 0.381). We also found significant difference (p = 0.034) in the extravascular extracellular fraction volumes ve (Tofts) in AP located in the basilar artery (0.171 [0.146; 0.325]), internal carotid arteries (0.579 [0.358; 1.000]), and middle cerebral arteries (0.134 [0.101; 0.269]). Conclusion: This is the first description of quantitative parameters characterizing vascular wall abnormalities in intracranial atherosclerosis. Despite its obviously intact state, vascular walls outside the intracranial AP was shown to be abnormal as well.

The relationship between intracranial atherosclerosis and white matter hyperintensity in ischemic stroke patients: a retrospective cross-sectional study using high-resolution magnetic resonance vessel wall imaging.

Both intracranial atherosclerosis and white matter hyperintensity (WMH) are prevalent among the stroke population. However, the relationship between intracranial atherosclerosis and WMH has not been fully elucidated. Therefore, the aim of this study was to investigate the relationship between the characteristics of intracranial atherosclerotic plaques and the severity of WMH in patients with ischemic stroke using high-resolution magnetic resonance vessel wall imaging. Patients hospitalized with ischemic stroke and concurrent intracranial atherosclerosis at Beijing Tsinghua Changgung Hospital, a tertiary comprehensive stroke center, who underwent high-resolution magnetic resonance vessel wall imaging and conventional brain magnetic resonance imaging were continuously recruited from January 2018 to December 2018. Both intracranial plaque characteristics (plaque number, maximum wall thickness, luminal stenosis, T1 hyperintensity, and plaque length) and WMH severity (Fazekas score and volume) were evaluated. Spearman correlation or point-biserial correlation analysis was used to determine the association between clinical characteristics and WMH volume. The independent association between intracranial plaque characteristics and the severity as well as WMH score was analyzed using logistic regression. The associations of intracranial plaque characteristics with total white matter hyperintensity (TWMH) volume, periventricular white matter hyperintensity (PWMH) volume and deep white matter hyperintensity (DWMH) volume were determined using multilevel mixed-effects linear regression. A total of 159 subjects (mean age: 64.0±12.5 years; 103 males) were included into analysis. Spearman correlation analysis indicated that age was associated with TWMH volume (r=0.529, P<0.001), PWMH volume (r=0.523, P<0.001) and DWMH volume (r=0.515, P<0.001). Point-biserial correlation analysis indicated that smoking (r=-0.183, P=0.021) and hypertension (r=0.159, P=0.045) were associated with DWMH volume. After adjusting for confounding factors, logistic regression analysis showed plaque number was significantly associated with the presence of severe WMH [odds ratio (OR), 1.590; 95% CI, 1.241-2.035, P<0.001], PWMH score of 3 (OR, 1.726; 95% CI, 1.074-2.775, P=0.024), and DWMH score of 2 (OR, 1.561; 95% CI, 1.150-2.118, P=0.004). Intracranial artery luminal stenosis was associated with presence of severe WMH (OR, 1.032; 95% CI, 1.002-1.064, P=0.039) and PWMH score of 2 (OR, 1.057; 95% CI, 1.008-1.109, P=0.023). Multilevel mixed-effects linear regression analysis showed that plaque number was associated with DWMH volume (β=0.128; 95% CI, 0.016-0.240; P=0.026) after adjusted for age and sex. In ischemic stroke patients, intracranial atherosclerotic plaque characteristics as measured by plaque number and luminal stenosis were associated with WMH burden.

Associations between Adipose Tissue-Specific Insulin Resistance and Atherosclerotic Plaques and Burden in Community-Based Population.

We aimed to examine the association between adipose tissue-specific insulin resistance and atherosclerotic burden and plaques in intracranial, extracranial, and coronary arteries in community residents without diabetes. Adipose tissue-specific insulin resistance index (Adipo-IR) was calculated by fasting serum insulin and free fatty acids and categorized into 4 groups according to the quartiles. The 3.0 T magnetic resonance imaging scanner was used to assess intracranial and extracranial atherosclerotic plaques, while computed tomography angiography was used to assess coronary atherosclerotic plaques. Intracranial, extracranial, and coronary atherosclerotic burden was assessed by segmental stenosis segment scores of the corresponding arterial segments, respectively. Binary and ordinal logistic regression models were utilized to investigate the relationship of Adipo-IR with the presence of atherosclerotic plaques and atherosclerotic burden. Of 2,719 participants (mean [standard deviation] age, 60.9 [6.6] years; 1,441 [53.0%] women), the prevalence of intracranial atherosclerotic plaques, extracranial atherosclerotic plaques, and coronary plaques were 432 (15.9%), 975 (35.9%), and 1,160 (42.7%), respectively. Compared with individuals with the lowest quartile, participants with the fourth quartile of the Adipo-IR were associated with intracranial atherosclerotic burden (common odds ratio [cOR]: 1.35; 95% confidence interval [CI]: 0.99-1.82), coronary plaque (odds ratio [OR]: 1.45; 95% CI: 1.15-1.83), and segment stenosis score (cOR: 1.44; 95% CI: 1.15-1.81) after adjustment for age, sex, and current smoking. Adipose tissue-specific insulin resistance is associated with atherosclerotic burden and plaques in intracranial and coronary arteries in Chinese community nondiabetic residents.

Temporal Changes on Postgadolinium MR Vessel Wall Imaging Captures Enhancement Kinetics of Intracranial Atherosclerotic Plaques and Aneurysms.

Analysis of vessel wall contrast kinetics (ie, wash-in/washout) is a promising method for the diagnosis and risk-stratification of intracranial atherosclerotic disease plaque (ICAD-P) and the intracranial aneurysm walls (IA-W). We used black-blood MR imaging or MR vessel wall imaging to evaluate the temporal relationship of gadolinium contrast uptake kinetics in ICAD-Ps and IA-Ws compared with normal anatomic reference structures. Patients with ICAD-Ps or IAs who underwent MR vessel wall imaging with precontrast, early postcontrast (5-15 minutes), and delayed postcontrast (20-30 minutes) 3D T1-weighted TSE sequences were retrospectively studied. ROIs of a standardized diameter (2 mm) were used to measure the signal intensities of the cavernous sinus, pituitary infundibulum, temporalis muscle, and choroid plexus. Point ROIs were used for ICAD-Ps and IA-Ws. All ROI signal intensities were normalized to white matter signal intensity obtained using ROIs of 10-mm diameter. Measurements were acquired on precontrast, early postcontrast, and delayed postcontrast 3D T1 TSE sequences for each patient.ajnr;45/9/1206/T1T1T1Table 1:MR-VWI parameters for ICAD-Ps and IAsParameterValueSequence3D TSEScan planeAxialFOV (mm)160TR/TE (ms)800/28-32BW (Hx/pixel)370θ120Acceleration2ETL42Matrix acquisition0.5 mm ×0.5 mmMatrix recon0.5 mm ×0.5 mmNo. of slices/thick120/0.5Note:-FOV indicates field of view; TR, the repetition time; TE, the echo time; BW, bandwidth; ETL, echo train length; Matrix recon, matrix reconstruction. Ten patients with 17 symptomatic ICAD-Ps and 30 patients with 34 IA-Ws were included and demonstrated persisting contrast uptake (P < .001) of 7.21% and 10.54% beyond the early phase (5-15 minutes postcontrast) and in the delayed phase (20-30 minutes postcontrast) on postcontrast MR vessel wall imaging. However, normal anatomic reference structures including the pituitary infundibulum and cavernous sinus demonstrated a paradoxical contrast washout in the delayed phase. In both ICAD-Ps and IA-Ws, the greatest percentage of quantitative enhancement (>70%-90%) occurred in the early phase of postcontrast imaging, consistent with the rapid contrast uptake kinetics of neurovascular pathology. Using standard MR vessel wall imaging techniques, our results demonstrate the effects of gadolinium contrast uptake kinetics in ICAD-Ps and IA-Ws with extended accumulating enhancement into the delayed phase (> 15 minutes) as opposed to normal anatomic reference structures that conversely exhibit decreasing enhancement. Because these relative differences are used to assess qualitative patterns of ICAD-P and IA-W enhancement, our findings highlight the importance of standardizing acquisition time points and MR vessel wall imaging protocols to interpret pathologic enhancement for the risk stratification of cerebrovascular pathologies.

Application of high-resolution MRI in evaluating statin efficacy on symptomatic intracranial atherosclerosis.

To investigate the efficacy of statins on symptomatic intracranial atherosclerotic plaques using high-resolution 3.0 T MR vessel wall imaging (HR-MRI). Patients with symptomatic intracranial atherosclerotic plaques (cerebral ischemic events within the last three months) confirmed by HR-MRI from July 2017 to August 2022 were retrospectively included in this study. The enrolled patients started statin therapy at baseline. All the patients underwent the follow-up HR-MRI examination after statin therapy for at least 3 months. A paired sample t-test and Wilcoxon rank sum test were used to evaluate the changes in plaque characteristics after statin therapy. Multivariate linear regression was further used to investigate the clinical factors associated with statin efficacy. A total of 48 patients (37 males; overall mean age = 60.2 ± 11.7 years) were included in this study. The follow-up time was 7.0 (5.6-12.0) months. In patients treated with statins for > 6 months (n = 31), plaque length, wall thickness, plaque burden, luminal stenosis and plaque enhancement were significantly reduced. Similar results were found in patients with good lipid control (n = 21). Younger age, lower BMI and hypertension were associated with decreased plaque burden. Lower BMI, hypertension and longer duration of statin therapy were associated with decreased plaque enhancement. Younger age and hypertension were associated with decreased luminal stenosis (all p < 0.05). HR-MRI can effectively evaluate plaques changes after statin therapy. Statins can reduce plaque burden and stabilize plaques. The effect of statin may have a relationship with age, BMI, hypertension, and duration of statin therapy. High-resolution MRI can be applied to evaluate the efficacy of statins on symptomatic intracranial atherosclerotic plaques. Long-term statin use and well-controlled blood lipid levels can help reduce plaque burden and stabilize plaques. High-resolution MRI provides great help evaluating the changes of plaque characteristics after statin therapy. Efficacy of statins is associated with duration of use, controlled lipid levels, and clinical factors. High-resolution MRI can serve as an effective method for following-up symptomatic intracranial atherosclerosis.

Short-term glycemic variability and intracranial atherosclerotic plaque stability assessed by high-resolution MR vessel wall imaging in type 2 diabetes mellitus

ObjectiveTo investigate the relationship between short-term glycemic variability in patients with T2DM and the vulnerability of intracranial atherosclerotic plaques using HR-MR-VWI. Materials and methodsIn total, 203 patients with acute ischemic stroke (AIS)/transient ischemia (TIA) combined with T2DM were enrolled. All of them underwent HR-MR-VWI during the period between July 2020 and July 2023. 203 patients were divided into groups with higher (1,5-AG≤ 30.7 μmol/L) and lower (1,5-AG> 30.7 μmol/L) short-term glycemic variability. Patients were also divided into the T1WI and non-T1WI hyperintensity groups. Associated factors(FBG, HbA1c, and 1,5-AG)for the T1WI hyperintensity were analyzed by binary logistic regression. We used the area under the curve (AUC), while the sensitivity and specificity were calculated at the optimal threshold. The Delong test was employed to compare the quality of the AUC of the predictors. ResultsThe group with higher short-term glycemic variability had a higher incidence of the hyperintensity on T1WI, higher degree of enhancement, higher degree of stenosis and smaller lumen area (P < 0.05). The T1WI hyperintensity group had higher HbA1c levels, higher hemoglobin levels and lower 1,5-AG levels(P < 0.05). 1,5-AG (OR = 0.971, 95 % CI: 0.954∼0.988, P = 0.001), HbA1c (OR=1.305, 95 % CI: 1.065∼1.598, P = 0.01) and male sex (OR = 2.048, 95 % CI: 1.016∼4.128, P = 0.045)/(OR=2.102, 95 % CI: 1.058∼4.177, P = 0.034) were independent risk factors for the hyperintensity on T1WI. 1,5-AG demonstrated enhanced performance and yielded the highest AUC of the receiver operator characteristic curve (AUC = 0.726), with sensitivity and specificity values of 0.727 and 0.635 respectively. Conclusion1,5-AG, HbA1c and male sex are independent predictors of intracranial plaques with T1WI hyperintensity, the greater short-term glycemic variability, the higher incidence of vulnerable plaques.

Association between intracranial aneurysm wall enhancement and intracranial atherosclerotic plaque: a cross-sectional study using high-resolution vessel wall imaging.

Intracranial aneurysms and intracranial atherosclerosis are prevalent cerebrovascular diseases, and individuals with atherosclerosis have a higher incidence of aneurysms than those without atherosclerosis. However, few studies have conducted combined analyses to investigate the potential association between intracranial aneurysms and intracranial atherosclerosis. This retrospective cross-sectional study aimed to investigate the association between the characteristics of the aneurysm wall and intracranial large arterial plaque using high-resolution vessel wall imaging (HR-VWI). Hospitalized patients diagnosed with anterior circulation unruptured intracranial aneurysms (UIAs), who were diagnosed at Huashan Hospital of Fudan University in Shanghai, China, between March 2016 to February 2018, were consecutively recruited for this study. The patients' pre-treatment HR-VWI images and 3D time-of-flight magnetic resonance angiography (3D-TOF-MRA) images were collected. The patients and UIAs were divided into two groups according to the presence or absence of plaque in the M1 segment of the middle cerebral artery (MCA). Clinical information and aneurysm characteristics were compared between the two groups. Aneurysm wall enhancement (AWE) and M1 plaque were graded on scales of 0 to 2 on HR-VWI. Based on the gradings, the correlation between AWE and the M1 plaques was analyzed. A total of 109 patients with 128 saccular UIAs in the anterior circulation were enrolled in the study. Of the patients, there were 56 patients (with 65 UIAs) in the group with M1 plaque and 53 patients (with 63 UIAs) in the group without plaque. There were significant differences between the two groups in terms of both their clinical information (age and hypertension) and aneurysm characteristics (AWE pattern and AWE degree). The grades of the AWE patterns and the AWE degrees of the UIAs were higher in the group with M1 plaque than in the group without plaque. In the M1 plaque group, the grade of M1 plaque was positively correlated with the grade of AWE pattern (correlation coefficient R=0.41, P=0.001) and the grade of AWE degree (correlation coefficient R=0.50, P<0.001). MCA atherosclerosis plaque was associated with the AWE of saccular aneurysms. When evaluating UIAs, attention should also be paid to the large arterial wall, which may assist in assessing the stability of the aneurysm and enable better decision making.

Investigating the relationship between intracranial atherosclerotic plaque remodelling and diabetes using high-resolution vessel wall imaging.

Intracranial atherosclerosis, a leading cause of stroke, involves arterial plaque formation. This study explores the link between plaque remodelling patterns and diabetes using high-resolution vessel wall imaging (HR-VWI). To investigate the factors of intracranial atherosclerotic remodelling patterns and the relationship between intracranial atherosclerotic remodelling and diabetes mellitus using HR-VWI. Ninety-four patients diagnosed with middle cerebral artery or basilar artery atherosclerosis were enrolled. Their basic clinical data were collected, and HR-VWI was performed. The vascular area at the plaque (VAMLN) and normal reference vessel (VAreference) were delineated and measured using image postprocessing software, and the Remodelling index (RI) was calculated. According to the value of the RI, the patients were divided into a positive remodelling (PR) group, intermediate remodelling (IR) group, negative remodelling (NR) group, PR group and non-PR (N-PR) group. The PR group exhibited a higher prevalence of diabetes and serum cholesterol levels than the IR and NR groups [45.2%, 4.54 (4.16, 5.93) vs 25%, 4.80 ± 1.22 and 16.4%, 4.14 (3.53, 4.75), respectively, P < 0.05]. The diabetes incidence was also significantly greater in the PR group than in the N-PR group (45.2% vs 17.5%, P < 0.05). Furthermore, the PR group displayed elevated serum triglyceride and cholesterol levels compared to the N-PR group [1.64 (1.23, 2.33) and 4.54 (4.16, 5.93) vs 4.54 (4.16, 5.93) and 4.24 (3.53, 4.89), P < 0.05]. Logistic regression analysis revealed diabetes mellitus as an independent influencing factor in plaque-PR [odds ratio (95% confidence interval): 3.718 (1.207-11.454), P < 0.05]. HR-VWI can clearly show the morphology and signal characteristics of intracranial vascular walls and plaques. Intracranial atherosclerotic plaques in diabetic patients are more likely to show PR, suggesting poor plaque stability and a greater risk of stroke.

HDL subfractions determined by microfluidic chip electrophoresis predict the vulnerability of intracranial plaque: A HRMRI study

AimHigh-density lipoprotein (HDL) can be divided into several subfractions based on density, size and composition. Accumulative evidence strongly suggests that the subfractions of HDL have very different roles in the pathogenesis of atherosclerosis. The purpose of this study was to further delineate the relationship between HDL subfractions extracted by microfluidic chip electrophoresis and the vulnerability of plaques in patients with intracranial atherosclerosis with a high-resolution magnetic resonance imaging (HRMRI) study. MethodsWe prospectively enrolled patients with single atherosclerotic plaque in the middle cerebral artery (MCA) or basilar artery (BA) between July 2020 and Dec 2022 and performed 3-tesla HRMRI on the relevant artery. The HDL cholesterol concentration and HDL subfractions (HDL-2a, HDL-2b and HDL-3) percentage were analyzed in serum samples from the same patients by electrophoresis on a microfluidics system. ResultsA total of 81 MCA or BA plaques [38 (46.9%) symptomatic and 43 (53.1%) asymptomatic] in 81 patients were identified on HRMRI. Patients with symptomatic plaques had a significantly lower HDL-2b level than asymptomatic plaques [symptomatic vs. asymptomatic: 0.16 (0.10–0.18) vs. 0.27(0.21–0.34), p = 0.001]. After adjusting for demographics and vascular risk factors, logistic regression showed that HDL-2b was inversely associated with asymptomatic plaques (B = −0.04, P = 0.017). According to receiver operating characteristic (ROC) curve model analysis, the cutoff point of HDL-2b in predicting asymptomatic plaques was 0.21 mmol/L (Area under curve: 0.719, specificity: 73.7%, sensitivity: 72.1%). Furthermore, plaque enhancement on HRMRI (P < 0.001), positive remodeling (P < 0.001), plaque load (P < 0.001) and luminal stenosis (P < 0.001) were superior among patients with HDL-2b < 0.21 mmol/L. ConclusionsOur data showed that serum HDL-2b levels may serve as a biomarker for predicting vulnerability in intracranial atherosclerotic plaques.

Morning blood pressure surge and intracranial atherosclerotic plaque characteristics: a high-resolution magnetic resonance vessel wall imaging study.

To investigate the relationship between morning blood pressure surge (MBPS) and intracranial atherosclerotic plaque burden and vulnerability. A total of 267 ischaemic stroke patients were retrospectively analysed. Sleep-trough and prewaking MBPS were calculated from ambulatory blood pressure monitoring (ABPM). Plaque characteristics, including intraplaque haemorrhage (IPH), maximum wall thickness (max WT), and stenosis degree, were obtained from high-resolution MR vessel wall imaging (HR-vwMRI). Linear and logistic regression were used to detect the association. Subjects with the top tertile of sleep-trough MBPS (≥15.1 mmHg) had a lower prevalence (9.1% vs. 19.6%, P = .029) of severe stenosis (≥70%) than others. Subjects within the top tertile of prewaking MBPS (≥7.6 mmHg) had a lower percentage of IPH (27.3% vs. 40.4%, P = .035) than others. After adjusting for stroke risk factors (age, sex, diabetes, hyperlipidaemia, hyperhomocysteinaemia, smoking, and family stroke history) and 24-h mean systolic blood pressure, 10 mmHg sleep-trough MBPS increment was associated with 0.07mm max WT reduction, and the top tertile MBPS group was associated with a lower chance of severe stenosis (odd ratio = 0.407, 95% CI, 0.175-0.950). Additionally, an increased prewaking MBPS is associated with a lower incidence of IPH, with OR = 0.531 (95% CI, 0.296-0.952). Subgroup analysis demonstrated that the positive findings could only be seen in non-diabetic subjects. Increment of MBPS is negatively associated with intracranial atherosclerotic plaque burden and vulnerability, and this relationship remains significant in the non-diabetic subgroup. This study provided evidence that MBPS was associated with the intracranial atherosclerotic plaque burden and vulnerability on HR-vwMRI.

Association between the fetal-type posterior cerebral artery and intracranial anterior and posterior circulating atherosclerotic plaques using multi-contrast magnetic resonance vessel wall imaging.

Intracranial atherosclerotic disease (ICAD) is one of the most common causes of ischemic stroke. The fetal-type posterior cerebral artery (FTP) affects intracranial collateral circulation, which is closely related to the occurrence and development of ICAD. Knowledge of the relationship between FTP and ICAD is important for developing treatment strategies for FTP patients diagnosed with atherosclerotic diseases. This study aims to quantitatively analyze the association between the FTP and intracranial atherosclerotic plaques using magnetic resonance vessel wall imaging (VW-MRI). This retrospective study enrolled patients with recent cerebrovascular symptoms (stroke or transient ischemic attack <2 weeks) who were diagnosed with atherosclerotic plaque(s) by VW-MRI in one hospital from October 2018 to March 2022. They were classified into the FTP group and the non-FTP group. Plaque characteristics and vascular-related parameters in intracranial arteries were compared between the two groups. Univariate and multivariate logistic regressions were performed to determine the odds ratios (ORs) and corresponding 95% confidence intervals (CIs) of the plaque characteristics between the two groups. A total of 104 patients (mean age: 61.8±9.8 years, 57 males) were included for VW-MRI scan analysis. 40 (38.46%) and 64 (61.54%) were classified into the FTP and the non-FTP groups, respectively. The plaques of middle cerebral artery (MCA) in the FTP group were more likely to occur on the dorsal and superior walls of the lumen compared with the non-FTP group (37.50% vs. 17.19%, P=0.001). The remodeling index (RI) of MCA was statistically different between the two groups (1.071±0.267 vs. 0.886±0.235, P=0.007). No significant differences were found in vertebrobasilar artery (VBA) plaque distributions (17.50% vs. 9.38%, 10.00% vs. 12.50%, 20.00% vs. 17.19%, P>0.05) and characteristics between the two groups (RI: 1.095±0.355 vs. 0.978±0.251; eccentricity index: 0.539±1.622 vs. 0.550±0.171, P>0.05). The plaques in the FTP group were more likely to occur on the dorsal and superior walls of the MCA, and the presentence of FTP was found to be significantly correlated with vascular remodeling of MCA atherosclerotic plaques. The relationship between the severity of intracranial atherosclerosis and the presence of FTP can provide valuable information for clinicians to intervene early and prevent the occurrence of stroke.

Association between Urine Albumin-to-creatinine Ratio and Intracranial Atherosclerotic Plaque in Chinese Adults - Results from the PRECISE Study.

Intracranial plaque may cause stroke in the absence of luminal stenosis. Although urine albumin-to-creatinine ratio (ACR) has been proved an established risk factor for cardiovascular disease, stroke and carotid atherosclerosis, little is known on the relationship between urine ACR and intracranial plaque. Subjects with history of stroke or coronary heart disease (CHD) were excluded in the PRECISE study. The intracranial plaque was assessed by vessel wall magnetic resonance imaging (MRI). Subjects were stratified according to ACR tertiles. Logistic regression and ordinal regression were performed to analyze the association between ACR and the presence of intracranial plaque or sum of the stenosis score for each artery. 2962 individuals were included with the mean age of 61.0±6.6 years. The median ACR was 11.7mg/g (interquartile range 7.0-22.0 mg/g), and the mean estimated glomerular filtration rate (eGFR) based on combination of creatinine and cystatin C was 88.5±14.8 ml/min·1.73m2. 495 (16.7%) participants had intracranial plaque. The highest ACR tertile with ACR ＞16.00mg/g was independently associated with the presence of intracranial plaque (OR 1.38, 95% CI: 1.05-1.82, p=0.02) and the odds of higher intracranial plaque burden (common OR 1.39, 95% CI: 1.05-1.83, p=0.02) after adjustment of confounding factors. No significant association was observed between eGFR and intracranial plaque presence or intracranial plaque burden. Among a low-risk community-dwelling population without prior stroke or CHD in China, ACR was independently associated with intracranial plaque presence and plaque burden measured by vessel wall MRI.

Age-dependent sex differences in non-stenotic intracranial plaque of embolic stroke of undetermined source

Age and sex have effect on atherosclerosis. This study aimed to investigate their effect on non-stenotic intracranial atherosclerotic plaque (NIAP) in embolic stroke of undetermined source (ESUS) using high-resolution magnetic resonance imaging (HR-MRI). We retrospectively recruited consecutive ESUS patients who underwent intracranial HR-MRI to assess the plaque characteristics (remodeling index [RI], plaque burden [PB], fibrous cap [FC], discontinuity of plaque surface [DPS], intraplaque hemorrhage [IPH] and complicated plaque [CP]). We divided patients into three groups (< 60 years, 60–74 years, ≥ 75 years). 155 patients with ipsilateral NIAP were found from 243 ESUS patients, with 106 men (68.39%) and 49 women (31.61%). In total population or age group under 60 years, there were no significant differences in plaque characteristics between men and women (all p > 0.05). In age group of 60–74 years, men were associated with higher PB (66.27 ± 9.17% vs 60.91 ± 8.86%, p = 0.017) and RI (1.174 vs 1.156, p = 0.019), higher prevalence of DPS (82.50% vs 60.00%, p = 0.036) and complicated plaque (85.00% vs 63.33%, p = 0.036). For subjects ≥ 75 years old, PB were significantly higher in twomen vs men (68.85 ± 6.14% vs 62.62 ± 7.36%, p = 0.040). In addition, the probability for PBupper (≥ median PB), RIupper (≥ median RI) and vulnerable plaque increased as age increased, and its predictive power for index ESUS was higher in men than women. This study identified age-dependent sex differences in NIAP characteristics of ESUS patients, which will help us clarify their etiology.

Abstract 045: A Radiomics Based Pipeline for Paired Risk‐Stratification of Intracranial Atherosclerotic Plaques

Introduction High resolution vessel wall imaging (HR‐VWI) enables accurate visualization of intracranial atherosclerotic plaques. Radiomics can be utilized as an objective quantification method of plaque appearance and shape. We aimed to analyze the radiomics features (RFs) obtained from 7T‐HR‐VWI to differentiate between culprit and non‐culprit plaques in patients with intracranial atherosclerotic disease (ICAD). Methods Patients with ICAD as stroke etiology undergoing HR‐VWI were included in the study. Culprit plaques in the vascular territory of the stroke were identified. The degree of stenosis, area degree of stenosis and plaque burden were calculated. Three‐dimensional segmentation of the plaque was performed, and RFs were extracted. We then evaluated multiple machine learning models to predict and identify culprit plaques using significantly different RFs. The dataset was then randomly divided into training and testing datasets, and the trained model was evaluated on the independent testing dataset. Results The study included 33 patients with ICAD as the cause of stroke. Univariate analysis revealed 38 significantly different RFs between culprit and non‐culprit plaques in pre‐contrast MRI, 39 in post‐contrast MRI and 25 RFs that were different between pre and post contrast MRIs. Additionally, seven shape‐based RFs exhibited significant distinctions between the two plaque types. The random forest model achieved an accuracy rate of 81% (88% sensitivity and 75% specificity) in identifying culprit plaques in the independent testing dataset. This model successfully identified the culprit plaque in 7 out of 8 cases during the testing phase. Conclusion In this study symptomatic culprit plaques had a different signature RFs compared to other plaque within the same subject. A machine learning model built with RFs successfully identified the symptomatic atherosclerotic plaques in most cases. Radiomics is a promising tool for stratification of plaques in patients with ICAD.

Characteristics and evaluation of atherosclerotic plaques: an overview of state-of-the-art techniques.

Atherosclerosis is an important cause of cerebrovascular and cardiovascular disease (CVD). Lipid infiltration, inflammation, and altered vascular stress are the critical mechanisms that cause atherosclerotic plaque formation. The hallmarks of the progression of atherosclerosis include plaque ulceration, rupture, neovascularization, and intraplaque hemorrhage, all of which are closely associated with the occurrence of CVD. Assessing the severity of atherosclerosis and plaque vulnerability is crucial for the prevention and treatment of CVD. Integrating imaging techniques for evaluating the characteristics of atherosclerotic plaques with computer simulations yields insights into plaque inflammation levels, spatial morphology, and intravascular stress distribution, resulting in a more realistic and accurate estimation of plaque state. Here, we review the characteristics and advancing techniques used to analyze intracranial and extracranial atherosclerotic plaques to provide a comprehensive understanding of atheroma.

The association of intracranial atherosclerosis with cerebral small vessel disease imaging markers: a high-resolution magnetic resonance imaging study

To evaluate the association of intracranial non-stenotic atherosclerotic plaque with cerebral small vessel disease (CSVD) imaging markers in a CSVD population using 3.0 T high-resolution magnetic resonance imaging (HRMRI), which was validated in embolic stroke of undetermined source (ESUS) cohort. We retrospectively recruited consecutive patients who were diagnosed with CSVD or ESUS from January 2015 to December 2019. All patients underwent intracranial HRMRI to assess intracranial non-stenotic atherosclerotic plaques. Baseline and imaging data were collected and were measured among all patients. Among 153 patients with CSVD, there were 59 with intracranial atherosclerotic plaque (IAP) and 94 with non-IAP, including 36 with intracranial atherosclerotic complicated plaque (IACP). Among 227 ESUS patients, there were 155 with IAP and 72 with non-IAP, including 127 with IACP. In the CSVD population, we found that: (1) CSVD burden was associated with IAP (p = 0.036) and IACP (p = 0.008); (2) IAP was associated with white matter hyperintensity (51% vs. 34%; P = 0.039), and IACP was associated with lacunes (69% vs. 35%; P = 0.009) and enlarge perivascular space (69% vs. 39%; P = 0.022). A similar association of CSVD imaging markers with IAP or IACP was found in the ESUS population. Furthermore, the association of unilateral IAP or IACP with CSVD imaging markers of ipsilateral hemisphere was identified in the two cohorts. This is the first report that intracranial non-stenotic atherosclerotic plaque, especially complicated plaque, is closely associated with CSVD imaging markers, which provide further evidence for the association of large artery atherosclerosis with CSVD.

A Non-Linear Role of Hyperlipidemia on Progression of Intracranial Atherosclerotic Plaques and Acute Downstream Ischemic Events.

Intracranial atherosclerotic stenosis (ICAS) is the leading cause of ischemic stroke worldwide. Hyperlipidemia is a major contributor to atherosclerosis. However, the effect of hyperlipidemia on the evolution of intracranial atherosclerotic plaques and downstream ischemic episodes remains unclear. In this study, we aimed to assess the radiological features of ICAS plaques and to explore the relationship between hyperlipidemia and plaque progression. We included people with ICAS (≥50% stenosis) undergoing high-resolution magnetic resonance imaging. The culprit plaque was defined as the sole, or in case of multiple stenosis, the narrowest plaque on the intracranial artery responsible for acute ischemic stroke. Demographic, clinical data, plaque features on MRI, and lipid parameters were compared between culprit and non-culprit plaques. Plaque enhancement was graded as Grade 0, 1 and 2 by comparing to the adjacent normal vessel wall and pituitary funnel after contrast enhancement on T1-weighted sequences. 162 patients were included (mean age 57.7±12.1 years, male 61.6%), 110 of whom were identified as culprit plaque with an ipsilateral acute stroke. High-grade enhancement was the most prominent MRI feature of the culpable plaque (Grade-2: OR 6.539, 95%CI 1.706-23.707, p=0.006). LDL cholesterol was significantly associated with overall acute ischemic stroke caused by culprit plaque. After stratification by enhancement grading LDL was independently associated with ischemic events in Grade-1 enhancement plaques (OR 6.778, 95%CI 2.122-21.649, p=0.001). In patients with Grade-2 enhancement plaques, however, LDL was not associated with ischemic event; in contrast, Neutrophil/Lymphocyte ratio was independently associated with ischemic events caused by Grade-2 enhancement plaques (OR 2.188, 95%CI 1.209-3.961, p=0.010). LDL was related with ischemia events in intermediate stage of intracranial atherosclerotic plaque progression, an excellent period for intensive lipid-lowering treatment. In advanced stage, inflammatory agents maybe the main contributor to ischemic events.

Discordantly high Apo B with LDL-C or non-HDL-C in relation to presence and burden of cerebral atherosclerotic plaques

Data are limited on associations between apolipoprotein B (Apo B) and cerebral atherosclerosis. Our study aimed to estimate associations between discordant Apo B with low-density lipoprotein cholesterol (LDL-C) or non-high-density lipoprotein cholesterol (Non-HDL-C) and the odds of the presence and burden of intra-/extra-cranial atherosclerotic plaques. This cross-sectional study was based on the baseline survey from the PolyvasculaR Evaluation for Cognitive Impairment and vaScular Events (PRECISE) study, a population-based prospective cohort study. Participants with complete baseline data but without taking lipid-lowering medication were included in this analysis. Discordant Apo B with LDL-C or Non-HDL-C were defined by residuals and cut-off values (LDL-C: 3.4 mmol/L, Non-HDL-C: 4.1 mmol/L). We used binary and ordinal logistic regression models to explore associations between discordant Apo B with LDL-C or Non-HDL-C and the presence and burden of intra-/extra-cranial atherosclerotic plaques. A total of 2,943 participants were enrolled in this study. Discordantly high Apo B with LDL-C was associated with an increased odds of the presence of intracranial atherosclerotic plaque [odds ratio (OR),1.28; 95% CI,1.01-1.61], intracranial atherosclerotic burden [common odds ratio (cOR), 1.31; 95%CI,1.04-1.64], the presence of extracranial atherosclerotic plaque (OR, 1.37; 95%CI,1.14-1.66), and extracranial atherosclerotic burden (cOR, 1.32; 95%CI,1.10-1.58) compared with the concordant group. Discordantly low Apo B with Non-HDL-C was associated with decreased odds of the presence and burden of intra-/extra-cranial atherosclerotic plaques. Discordantly high Apo B with LDL-C or Non-HDL-C were associated with an increased odds of the presence and burden of intra-/extra-cranial atherosclerotic plaques. This demonstrated that discordantly high Apo B might be important for early assessment of risk of cerebral atherosclerotic plaques in addition to LDL-C and Non-HDL-C.

Incremental value of enhanced plaque length for identifying intracranial atherosclerotic culprit plaques: a high-resolution magnetic resonance imaging study

ObjectivesBesides plaque enhancement grade, the incremental value of enhancement-related high-resolution MRI features in defining culprit plaques needs further evaluation. This study was focused on assessing whether plaque enhancement features contribute to culprit plaque identification and further risk stratification.MethodsWe retrospectively studied patients who experienced an acute ischaemic stroke and transient ischaemic attack due to intracranial atherosclerosis from 2016 to 2022. The enhancement features included enhancement grade, enhanced length, and enhancement quadrant. Associations between plaque enhancement features and culprit plaques, as well as diagnostic value, were investigated using logistic regression and receiver operating characteristic analyses.ResultsOverall, 287 plaques were identified, of which 231 (80.5%) and 56 (19.5%) were classified as culprit and non-culprit plaques, respectively. Comparison of the pre- and post-enhancement images revealed enhanced length longer than the plaque length in 46.32% of the culprit plaques. Multivariate logistic regression showed that enhanced length longer than plaque length (OR 6.77; 95% CI 2.47–18.51) and grade II enhancement (OR 7.00; 95% CI 1.69–28.93) were independently associated with culprit plaques. The area under the curve value for the combination of stenosis and plaque enhancement grade for the diagnosis of culprit plaques was 0.787, which increased significantly to 0.825 on the addition of enhanced length longer than the plaque length (p = 0.026 for DeLong’s test).ConclusionsEnhanced length longer than the plaque length and grade II enhancement were independently associated with culprit plaques. The combination of the enhanced plaque features resulted in better culprit plaque identification.