UNASSIGNED: Vulnerable carotid plaque is closely associated with ischemic stroke. Contrast-enhanced ultrasound (CEUS) and high-resolution magnetic resonance imaging (HR-MRI) are two imaging modalities capable of assessing the vulnerability of carotid plaques. This systematic review aimed to compare the diagnostic performance of CEUS and HR-MRI in the evaluation of histologically defined vulnerable carotid plaques.
UNASSIGNED: A systematic literature search with predefined search terms was performed on PubMed, the Cochrane library, Embase, and Web of Science from January 2001 to December 2023. Studies that evaluated the diagnostic accuracy of vulnerable carotid plaques confirmed by histology with CEUS and/or HR-MRI were included. The pooled values were calculated using a random-effects meta-analysis to determine diagnostic power.
UNASSIGNED: This analysis included a total of 839 patients from 20 studies comprising 1,357 HR-MRI plaques and CEUS 504 plaques. With the reference to histological results, all nine CEUS studies focused on the detection of intraplaque neovascularization (IPN), and three studies also examined morphological changes or ulcerated plaques; meanwhile, among the HR-MRI studies, seven predominantly focused on identifying intraplaque hemorrhage (IPH) and three mainly examined lipid-rich necrotic cores (LRNCs). The pooled sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, diagnostic odds ratio, and the area under the curve (AUC) for CEUS studies were 0.85 [95% confidence interval (CI): 0.81-0.89], 0.76 (95% CI: 0.69-0.83), 3.41 (95% CI: 1.68-6.94), 0.14 (95% CI: 0.05-0.38), 27.68 (95% CI: 5.78-132.62), and 0.89 [standard error (SE) 0.06], respectively; for HR-MRI, these values were 0.88 (95% CI: 0.85-0.90), 0.89 (95% CI: 0.86-0.92), 7.49 (95% CI: 3.28-17.09), 0.17 (95% CI: 0.12-0.24), 49.13 (95% CI: 23.87-101.11), and 0.94 (SE 0.01), respectively. The difference in AUC between the two modalities was not statistically significant (Z=0.82; P=0.68).
UNASSIGNED: CEUS and HR-MRI are valuable noninvasive diagnostic tools for identifying histologically confirmed vulnerable carotid plaques and demonstrate similar diagnostic performance. CEUS is more capable of detecting IPN and morphological changes, while HR-MRI is more suited to classifying IPH and LRNCs.

We present a real-life case of a very young man with multiple risk factors who progressed rapidly from minimally obstructive non-calcified plaque on computed tomography angiography (CCTA) to severe three-vessel coronary disease presenting with STEMI. It questions the reliability of zero coronary calcium in high-risk subgroups like familial hypercholesterolemia, high Lp(a), and the young. While CCTA can accurately visualize non-calcified plaque, its interpretation requires expertise and clinical judgment should consider both imaging and clinical risk factors for management. Advanced plaque quantification, peri-coronary (PCAT), and epicardial (EAT) adipose tissue could help better-stratified patients but the evidence-based clinical application remains unknown.

OBJECTIVE: The primary aim was to systematically assess the available literature on the effect of an essential oils mouthwash without alcohol (EOalc-) compared to an essential oils mouthwash with alcohol (EOalc+) on plaque scores and parameters of gingival health. The secondary aim was to evaluate user appreciation.
METHODS: The MEDLINE-PubMed and Cochrane-CENTRAL databases were searched to identify eligible studies published up to and including March 2024. Papers comparing the effectiveness of EOalc- and EOalc+ were included. The quality was assessed. A descriptive analysis and a meta-analysis were performed.
RESULTS: After screening, seven papers were found to be eligible. The descriptive analysis demonstrates a significant difference in plaque scores in favour of EOalc+. This is confirmed by the meta-analyses of plaque scores in non-brushing and brushing studies (DiffM = 0.40; 95% CI [0.27; 0.53], p < 0.00001 and DiffM = 0.05; 95% CI [0.01; 0.10], p = 0.01, respectively). This finding is also supported by the sub-analysis of brands. The meta-analyses of bleeding and gingival scores in brushing studies did not show significant differences between products. For user appreciation, the difference found was for taste perception in favour of EOalc- (DiffM = 1.63; 95% CI [0.72; 2.55], p = 0.0004).
CONCLUSIONS: When an EO-mouthwash is used in non-brushing or brushing situations, with small to moderate certainty, EOalc- provided less effect regarding plaque control than EOalc+. For bleeding and gingival index there is weak certainty for no difference. In terms of the taste perception EOalc- seems more appreciated.

Background: Depression is the most common mental illness worldwide and generates an enormous health and economic burden. Furthermore, it is known to be associated with an elevated risk of arteriosclerotic cardiovascular diseases (ASCVD), particularly stroke. However, it is not a factor reflected in many ASCVD risk models, including SCORE2. Thus, we analysed the relationship between depression, ASCVD and SCORE2 in our cohort. Methods: We analysed 9350 subjects from the Paracelsus 10,000 cohort, who underwent both a carotid artery ultrasound and completed a Beck Depression Inventory (BDI) screening. Patients were categorised binomially based on the BDI score. Atherosclerotic carotid plaque or absence was dichotomised for logistic regression modelling. Odds ratios and adjusted relative risks were calculated using Stata. Results: Subjects with an elevated BDI (≥14) had higher odds for carotid plaques compared to subjects with normal BDI, especially after adjusting for classical risk factors included in SCORE2 (1.21; 95%CI 1.03-1.43, p = 0.023). The adjusted relative risk for plaques was also increased (1.09; 95%CI 1.01-1.18, p = 0.021). Subgroup analysis showed an increased odds of plaques with increases in depressive symptoms, particularly in women and patients ≤55 yrs. Conclusions: In our cohort, the BDI score is associated with subclinical atherosclerosis beyond classical risk factors. Thus, depression might be an independent risk factor which may improve risk stratification if considered in ASCVD risk prediction models, such as SCORE2. Furthermore, reminding clinicians to take mental health into consideration to identify individuals at increased atherosclerosis risk may provide added opportunities to address measures which can reduce the risk of ASCVD.

BACKGROUND: Although the adverse effects of long-term use of vitamin K oral anticoagulant (OAC), warfarin, on the coronary vasculature are well established, it remains unknown whether non-vitamin K oral anticoagulants play a role in the attenuation of plaque progression and coronary calcification. This study aimed to compare changes in atherosclerotic plaques and calcification of the coronary arteries in patients with atrial fibrillation (AF) treated with edoxaban and warfarin.
METHODS: A total of 150 OAC-naïve patients with AF and atherosclerotic lesions on coronary computed tomography angiography (CCTA) were enrolled and randomly assigned to the edoxaban or warfarin treatment groups. All enrolled patients received rosuvastatin 10mg and 119 patients completed the entire study protocol. Twelve months after the assigned OAC treatment, follow-up CCTA was performed, and changes in plaque and calcium volumes of the coronary arteries were analyzed.
RESULTS: Baseline characteristics of the two groups were well-balanced. The percentage of time in therapeutic range in the warfarin group was 61.1%. Compared with the baseline CCTA, there was a significant reduction in plaque volume after 12 months of OAC and rosuvastatin administration in both groups, and the extent of regression did not differ significantly between the two groups. The increase in calcium volume was greater in the warfarin group than in the edoxaban group, but the difference was not significant.
CONCLUSIONS: In OAC-naïve, moderate-intensity statin treated patients with AF and atherosclerotic coronary lesions, edoxaban use did not have a positive effect on atherosclerotic plaques and coronary calcification compared with warfarin use over a 12-month follow-up period.

BACKGROUND: To investigate the relationship between pericarotid fat density measured in carotid CTA and vulnerable carotid plaque.
METHODS: This retrospective study included 374 participants who underwent carotid CTA between June 1, 2021, and December 1, 2021 (234 males, median age 68 years [interquartile range: 61-75]). Two groups, symptomatic and asymptomatic, were defined based on either diffusion-weighted MRI or a clinical history of acute ischemia or TIA within 6 months before or after CTA. The relationship between pericarotid fat density and cerebrovascular ischemic events was assessed using receiver operating characteristic analysis and binary logistic regression analysis.
RESULTS: In the symptomatic group (n = 135), mean pericarotid fat density (-63.3 ± 21.7 vs. -81.7 ± 16.9 HU, respectively; p < 0.001) and median maximum plaque thickness (4 [interquartile range: 3-6] vs. 3.7 [interquartile range: 2.6-4.7] mm, respectively; p = 0.002) were higher, while plaque density (42.1 ± 19.6 vs. 50.6 ± 20.4 HU, respectively; p = 0.001) was lower compared to the asymptomatic group. Pericarotid fat density (OR: 1.038, 95% CI: 1.023-1.053, p < 0.001) was identified as an independent predictor for symptomatic patients. The optimal cut-off value for pericarotid fat density predicting symptomatic patients was estimated as -74 HU (area under the curve: 0.753, 95% CI:0.699-0.808, p < 0.001). Inter-reader agreement for pericarotid fat density was found to be almost perfect (intraclass correlation coefficient: 0.818, 95% CI: 0.770-0.856, p < 0.001).
CONCLUSIONS: Pericarotid fat density may serve as an imaging biomarker in predicting acute cerebrovascular ischemic events.

OBJECTIVE: The aim of this study was to determine the prognostic value of coronary computed tomography angiography (CCTA)-derived atherosclerotic plaque analysis in ISCHEMIA.
METHODS: Atherosclerosis imaging quantitative computed tomography (AI-QCT) was performed on all available baseline CCTAs to quantify plaque volume, composition, and distribution. Multivariable Cox regression was used to examine the association between baseline risk factors (age, sex, smoking, diabetes, hypertension, ejection fraction, prior coronary disease, estimated glomerular filtration rate, and statin use), number of diseased vessels, atherosclerotic plaque characteristics determined by AI-QCT, and a composite primary outcome of cardiovascular death or myocardial infarction over a median follow-up of 3.3 (interquartile range 2.2-4.4) years. The predictive value of plaque quantification over risk factors was compared in an area under the curve (AUC) analysis.
RESULTS: Analysable CCTA data were available from 3711 participants (mean age 64 years, 21% female, 79% multivessel coronary artery disease). Amongst the AI-QCT variables, total plaque volume was most strongly associated with the primary outcome (adjusted hazard ratio 1.56, 95% confidence interval 1.25-1.97 per interquartile range increase [559 mm3]; P = .001). The addition of AI-QCT plaque quantification and characterization to baseline risk factors improved the model\'s predictive value for the primary outcome at 6 months (AUC 0.688 vs. 0.637; P = .006), at 2 years (AUC 0.660 vs. 0.617; P = .003), and at 4 years of follow-up (AUC 0.654 vs. 0.608; P = .002). The findings were similar for the other reported outcomes.
CONCLUSIONS: In ISCHEMIA, total plaque volume was associated with cardiovascular death or myocardial infarction. In this highly diseased, high-risk population, enhanced assessment of atherosclerotic burden using AI-QCT-derived measures of plaque volume and composition modestly improved event prediction.

UNASSIGNED: Studies of the neurovascular contribution to dementia have largely focused on cerebral small vessel disease (CSVD), but the role of intracranial atherosclerotic disease (ICAD) remains unknown in the general population. The objective of this study was to determine the risk of incident dementia from ICAD after adjusting for CSVD and cardiovascular risk factors in a US community-based cohort.
UNASSIGNED: We acquired brain magnetic resonance imaging examinations from 2011 through 2013 in 1980 Black and White participants in the ARIC study (Atherosclerosis Risk in Communities), a prospective cohort conducted in 4 US communities. Magnetic resonance imaging examinations included high-resolution vessel wall magnetic resonance imaging and magnetic resonance angiography to identify ICAD. Of these participants, 1590 without dementia, without missing covariates, and with adequate magnetic resonance imaging image quality were followed through 2019 for incident dementia. Associations between ICAD and incident dementia were assessed using Cox proportional hazard ratios adjusted for CSVD (characterized by white matter hyperintensities, lacunar infarctions, and microhemorrhages), APOE4 genotype, and cardiovascular risk factors.
UNASSIGNED: The mean age (SD) of study participants was 77.4 (5.2) years. ICAD was detected in 34.6% of participants. After a median follow-up of 5.6 years, 286 participants developed dementia. Compared with participants without ICAD, the fully adjusted hazard ratios (95% CIs) for incident dementia in participants with any ICAD, with ICAD only causing stenosis ≤50%, and with ICAD causing stenosis >50% in ≥1 vessel were 1.57 (1.17-2.11), 1.41 (1.02-1.95), and 1.94 (1.32-2.84), respectively. ICAD was associated with dementia even among participants with low white matter hyperintensities burden, a marker of CSVD.
UNASSIGNED: ICAD was associated with an increased risk of incident dementia, independent of CSVD, APOE4 genotype, and cardiovascular risk factors. The increased risk of dementia was evident even among participants with low CSVD burden, a group less likely to be affected by vascular dementia, and in participants with ICAD causing only low-grade stenosis. Our results suggest that ICAD may partially mediate the effect that cardiovascular risk factors have on the brain leading to dementia. Both ICAD and CSVD must be considered to understand the vascular contributions to cognitive decline.

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UNASSIGNED: Premature atherosclerosis is associated with systemic lupus erythematosus (SLE). We have previously shown an association of anti-Ro60/La/Ro52 with antioxidized low-density lipoprotein (LDL) in SLE. Here, we hypothesized that carotid intima-media thickening (CIMT) would be associated with antioxidized LDL (anti-oxLDL)/antilipoprotein lipase (ALPL) in a specific SLE autoantibody subset (anti-Ro60 positive, anti-RNP positive, anti-SmRNP positive, or extractable nuclear antigen antibody negative).
UNASSIGNED: We carried out a case-control study (one time-point testing) of CIMT, ALPL, anti-oxLDL, anti-low density lipoprotein (ALDL), and anti-LDL in 114 SLE patients and 117 age/sex-matched controls. The levels of total cholesterol, LDL, high-density lipoprotein (HDL), triglycerides, and HDL-Trig were also measured. A student\'s t-test was used for statistical analysis.
UNASSIGNED: Interestingly, the level of CIMT was highest in the SLE subset with anti-Ro60 (23/114). CIMT and anti-oxLDL were statistically significantly elevated in the anti-Ro60 SLE subset (1.3 ± 1.66, p < 0.01; 0.26 ± 0.16, p < 0.002, respectively) compared with controls (0.54 ± 1.26; 0.165 ± 0.13, respectively), but not anti-LPL/anti-LDL. CIMT was significantly elevated (0.9 ± 1.71; p < 0.05) in the SLE subset without antiextractable nuclear antigen (ENA) (63/114) compared with controls. The other antibodies in this subset were not statistically different from other SLE subsets or controls. Only antioxLDL was significantly elevated (0.29 ± 0.27; p < 0.005) in the SLE subset with anti-RNP (14/114) compared with controls, while none were elevated in the anti-SmRNP subset (6/114). We did not find any significant differences in lipids between the various SLE subsets.
UNASSIGNED: CIMT segregates in anti-Ro and ENA negative groups either with or without anti-oxLDL. It will be clinically important if cardiovascular events are augmented in the SLE anti-Ro subset having elevated antioxidized LDL antibodies.