A three-dimensional (3D) cardiovascular magnetic resonance (CMR) vessel wall imaging (VWI) technique based on 3D T1 weighted (T1w) Sampling Perfection with Application-optimized Contrast using different flip angle Evolutions (SPACE) has recently been used as a promising CMR imaging modality for evaluating extra-cranial and intra-cranial vessel walls. However, this technique is yet to be validated against the current diagnostic imaging standard. We therefore aimed to evaluate the diagnostic performance of 3D CMR VWI in characterizing carotid disease using intra-arterial digital subtraction angiography (DSA) as a reference. Consecutive patients with at least unilateral > 50% carotid stenosis on ultrasound were scheduled to undergo interventional therapy were invited to participate. The following metrics were measured using 3D CMR VWI and DSA: lumen diameter of the common carotid artery (CCA) and segments C1–C7, stenosis diameter, reference diameter, lesion length, stenosis degree, and ulceration. We assessed the diagnostic sensitivity, specificity, accuracy, and receiver operating characteristic (ROC) curve of 3D CMR VWI, and used Cohen’s kappa, the intraclass correlation coefficient (ICC), and Bland-Altman analyses to assess the diagnostic agreement between 3D CMR VWI and DSA. The ICC (all ICCs ≥0.96) and Bland-Altman plots indicated excellent inter-reader agreement in all individual morphologic measurements by 3D CMR VWI. Excellent agreement in all individual morphologic measurements were also found between 3D CMR VWI and DSA. In addition, 3D CMR VWI had high sensitivity (98.4, 97.4, 80.0, 100.0%), specificity (100.0, 94.5, 99.1, 98.0%), and Cohen’s kappa (0.99, 0.89, 0.84, 0.96) for detecting stenosis > 50%, stenosis > 70%, ulceration, and total occlusion, respectively, using DSA as the standard. The AUC of 3D CMR VWI for predicting stenosis > 50 and > 70% were 0.998 and 0.999, respectively. The 3D CMR VWI technique enables accurate diagnosis and luminal feature assessment of carotid artery atherosclerosis, suggesting that this imaging modality may be useful for routine imaging workups and provide comprehensive information for both the vessel wall and lumen.

The application of voxel-mirrored homotopic connectivity (VMHC) analysis to study the central mechanism of migraine has been limited. Furthermore, little is known about inter-hemispheric functional connectivity (FC) alterations during resting state in female patients with migraine. This study aimed to investigate potential interictal VMHC impairments in migraine without aura (MwoA) patients and the relationship between connectivity alterations and clinical parameters. Resting-state functional magnetic resonance imaging data and clinical information were acquired from 43 female MwoA patients and 43 matched healthy controls. VMHC analysis was used to compare differences between these two groups, and brain regions showing significant differences were chosen as a mask to perform a seed-based FC group comparison. Subsequent correlation analysis was conducted to explore the relationship between abnormal inter-hemispheric FC and clinical data. Compared with healthy controls, female MwoA patients revealed significantly decreased VMHC in the bilateral cerebellum; cuneus; and lingual, middle occipital, precentral and postcentral gyri. Seed-based FC analysis indicated disrupted intrinsic connectivity in the cerebellum, and default mode, visual and sensorimotor network. These VMHC and FC abnormalities were negatively correlated with clinical indexes including duration of disease, migraine days and visual analogue scale. These inter-hemispheric FC impairments and correlations between abnormal VMHC and FC and clinical scores may improve our understanding of the central mechanism of female-specific migraine.

(1) Aim: We aim to evaluate the association between arousals during sleep and subclinical coronary atherosclerosis detected by coronary computed tomography angiography (CTA) in patients with obstructive sleep apnea (OSA). (2) Methods: This was a cross-sectional study. Consecutive newly diagnosed OSA patients, who underwent coronary CTA examinations within 3 months of the sleep study, were eligible. We used the arousal index (ArI) derived from polysomnography to assess arousals during sleep and a semi-automated plaque quantification software to characterize and quantify the subclinical coronary atherosclerosis. Multiple regression models were used to evaluate the associations of the ArI with the coronary atherosclerotic plaque presence, volume, and composition. (3) Results: A total of 99 patients with OSA were included in the study. In the multivariable models, patients with a high ArI (ArI > 32.2 events/h) were more likely to have coronary plaques compared to those with a low ArI (ArI ≤ 32.2 events/h) (OR: 3.29 [95% CI: 1.284 to 8.427], p = 0.013). Furthermore, the ArI exhibited significant associations with total (β = 0.015), noncalcified (β = 0.015), and low-attenuation (β = 0.012) coronary plaque volume after accounting for established risk factors (p = 0.008, 0.004, and 0.002, respectively). However, no association between the ArI and calcified plaque volume was found. (4) Conclusion: Repetitive arousals during sleep are associated with an increased coronary plaque burden in patients with OSA, which remained robust after adjusting for multiple established cardiovascular risk factors.

Background: Left ventricular hemodynamic forces (LV HDFs) are altered in myocardial dysfunction. While infarct location and size influence post-ST-segment elevation myocardial infarction (STEMI) remodeling, their specific effects on HDFs remain unclear. This study investigated how infarct location and size impact left ventricular HDFs and assessed HDFs’ prognostic value for predicting subsequent heart failure (HF) in STEMI patients. Methods: In this retrospective study, 275 STEMI patients underwent cardiac magnetic resonance (CMR) 3–7 days after primary percutaneous coronary intervention. HDFs were derived from routine CMR cine images. Patients were stratified by infarct location (anterior vs. non-anterior) and median infarct size (IS). Key parameters—apical–basal (A-B) and lateral-septal (L-S) forces, their ratio, force direction angle (φ), and force reversal during systolic–diastolic transition—were compared. The primary endpoint was new-onset congestive HF during follow-up. Results: Compared to non-anterior STEMI, anterior STEMI showed significantly impaired A-B and L-S HDFs throughout the cardiac cycle (all p < 0.05) and was independently associated with force reversal (OR 2.31, 95% CI: 1.05–5.07). Larger IS correlated with reduced A-B HDFs and altered force distribution (increased L-S/A-B ratio, decreased φ). Force reversal predicted HF (HR: 2.10, 95% CI: 1.22–3.62) and provided incremental prognostic value beyond left ventricular ejection fraction (LVEF) alone (C-statistic: LVEF 0.680 vs. LVEF + force reversal 0.770, p = 0.034). Conclusions: Anterior infarction causes global HDF impairment and force reversal, while larger IS primarily reduces longitudinal forces and disrupts force distribution. Force reversal predicts subsequent HF and enhances prognostic value beyond LVEF.

Background/Objectives: This study aimed to investigate the associations between preoperative carotid high-resolution magnetic resonance imaging (HR-MRI) plaque features and coronary atherosclerotic burden, and to compare the cross-vascular association patterns of plaque burden-related measures and individual vulnerable plaque features. Methods: This retrospective study included consecutive patients who underwent carotid revascularization and had both preoperative carotid HR-MRI and coronary computed tomography angiography (CTA) between April 2017 and December 2024. Carotid plaque characteristics included calcification, lipid-rich necrotic core (LRNC), intraplaque hemorrhage (IPH), loose matrix (LM), ulceration, maximum wall thickness (MWT), maximum wall area (MWA), and normalized wall index (NWI). Coronary atherosclerotic burden was characterized using coronary artery calcium score (CACS), maximum luminal stenosis, and the number of diseased coronary arteries; the number of coronary arteries with ≥50% stenosis was additionally recorded. Associations between carotid plaque characteristics and coronary atherosclerotic burden were evaluated using correlation analyses and multivariable logistic regression. Results: A total of 162 patients were included (mean age, 66.11 ± 7.54 years; 138 [85.2%] men). CACS ≥ 400 was present in 76 patients (46.9%), obstructive coronary disease (≥50% stenosis in at least one coronary artery) in 96 patients (59.3%), and involvement of ≥3 diseased coronary arteries in 128 patients (79.0%). Greater coronary atherosclerotic burden was consistently associated with higher carotid calcification volume and MWT and NWI (all p < 0.05). After adjustment for clinical risk factors and correction for multiple testing, calcification volume, MWT and NWI remained associated with CACS ≥ 400, obstructive coronary disease, and involvement of ≥3 diseased coronary arteries. In contrast, individual vulnerable plaque features, including LRNC, IPH, LM, and ulceration, showed weaker and less consistent associations. Conclusions: In patients undergoing carotid revascularization, preoperative carotid HR-MRI-derived plaque burden-related features showed more consistent associations with coronary atherosclerotic burden than individual vulnerable plaque features. These findings suggest that plaque burden-related and vulnerable plaque features may reflect different aspects of atherosclerosis, with plaque burden-related measures more closely reflecting cumulative systemic atherosclerotic involvement and vulnerable plaque features primarily characterizing local plaque composition and instability.