High-risk Plaque Research Articles

Epicardial and pericoronary adipose tissue and coronary plaque burden in patients with Cushing's syndrome: a propensity score-matched study.

To assess coronary inflammation by measuring the volume and density of the epicardial adipose tissue (EAT), perivascular fat attenuation index (FAI) and coronary plaque burden in patients with Cushing's syndrome (CS) based on coronary computed tomography angiography (CCTA). This study included 29 patients with CS and 58 matched patients without CS who underwent CCTA. The EAT volume, EAT density, FAI and coronary plaque burden were measured. The high-risk plaque (HRP) was also evaluated. CS duration from diagnosis, 24-h urinary free cortisol (UFC), and abdominal visceral adipose tissue volume (VAT) of CS patients were recorded. The CS group had higher EAT volume (146.9 [115.4, 184.2] vs. 119.6 [69.0, 147.1] mL, P = 0.006), lower EAT density (- 78.79 ± 5.89 vs. - 75.98 ± 6.03 HU, P = 0.042), lower FAI (- 84.0 ± 8.92 vs. - 79.40 ± 10.04 HU, P = 0.038), higher total plaque volume (88.81 [36.26, 522.5] vs. 44.45 [0, 198.16] mL, P = 0.010) and more HRP plaques (7.3% vs. 1.8%, P = 0.026) than the controls. The multivariate analysis suggested that CS itself (β [95% CI], 29.233 [10.436, 48.03], P = 0.014), CS duration (β [95% CI], 0.176 [0.185, 4.242], P = 0.033), and UFC (β [95% CI], 0.197 [1.803, 19.719], P = 0.019) were strongly associated with EAT volume but not EAT density, and EAT volume (β [95% CI] - 0.037[- 0.058, - 0.016], P = 0.001) not CS was strongly associated with EAT density. EAT volume, FAI and plaque burden increased (all P < 0.05) in 6 CS patients with follow-up CCTA. The EAT volume had a moderate correlation with abdominal VAT volume (r = 0.526, P = 0.008) in CS patients. Patients with CS have higher EAT volume and coronary plaque burden but less inflammation as detected by EAT density and FAI. The EAT density is associated with EAT volume but not CS itself.

Abstract TP176: Radiological Reporting Frequencies of High-Risk Non-Stenosing Carotid Plaque Features: A Follow-Up Observational Study

Background: High-risk non-stenosing carotid plaque features are emerging as a possible source of embolism in the setting of ESUS. Unless there is a hemodynamically significant stenosis, neuroradiology reports tend to be rarely descriptive of these features. Methods: In our previous study published in September 2022, we analyzed a patient sample drawn from the stroke registry of the HFHS between June 2016 and June 2021. Our results showed a higher incidence of high-risk plaque features including plaque ulceration (19.08% vs 5.26%, p&lt;0.0001), plaque thickness &gt;3mm: (19.08% vs 7.24%, p=0.001), and length &gt;1cm (13.16% vs 5.92%, p=0.0218) ipsilateral to ESUS. In this subsequent study, we utilized the same patient dataset and used CTA reports on EPIC to explore how frequently neuroradiologists had mentioned those features. We utilized Fisher’s exact test to compare the frequencies of reporting each plaque characteristic. Results: We analyzed 152 CTA reports in depth. Our findings indicate that the frequency of reporting plaque ulceration compared to the frequency of reporting plaque calcification was significantly different (8.1% vs 100%, p&lt; 0.00001), this is also noticed with plaque length (4.6%, p&lt; 0.00001) and soft plaques (72.1%, p&lt; 0.00001). Notably, none of the CTA reports had commented on any plaque thickness or the presence of any “high-risk” features when encountering stroke ipsilaterally. Conclusion: When carotid plaques are not causing hemodynamically significant stenosis, neuroradiology reports frequently mention the density of plaques, but unfortunately overlook other characteristics. It is essential to conduct algorithms, scoring systems and prediction models to determine which plaque features are highly associated with embolism. These models should help prioritize the description of these features, alongside commonly reported metrics such as plaque density and the degree of stenosis.

Abstract 42: Validation of a New Plaque-RADS Classification System to a Cohort of Embolic Stroke of Undetermined Source Patients

Introduction: A new Plaque-RADS classification (I-IV) is proposed to categorize the degree of carotid plaque instability and risk of embolic ischemic stroke. We tested the Plaque-RADS classification in a cohort of patients with embolic stroke of undetermined source (ESUS) and imaged with neck CTAs. Methods: Patients with unilateral anterior circulation ischemic stroke due to ESUS and neck CTAs showing &lt;50% carotid stenosis were retrospectively identified. Carotid total plaque thickness and ulceration were scored by a neuroradiologist blinded to stroke side. A semiautomated segmentation software measured intraplaque hemorrhage (IPH) volumes. The Plaque-RADS classification is defined as: I: no plaque; II: plaque thickness &lt;3mm ; III: plaque thickness ≥ 3mm or ulcerated; and IV: plaque with IPH&gt;50mL irrespective of thickness. Prevalence of Plaque-RADS subtypes was analyzed ipsilateral versus contralateral to stroke side. The proportion of low (subtypes I/II) versus high-risk (III/IV) carotid plaques on the ipsilateral versus contralateral stroke-side was tested using a McNemar’s test. Results: Ninety-four patients (N=52 female, mean age 65.4; N=188 plaques) met criteria. Plaque-RADS distribution was classified as: Plaque-RADS I: 18.1%; II: 44.7%; III: 36.7% (III ulc : 1.6%); IV: 0.5%. High-risk Plaque-RADS subtypes were significantly more prevalent on the ipsilateral (42.6%) compared to the contralateral side of stroke (31.9%, p=0.008). Conclusions: Carotid plaque ipsilateral to stroke side showed a higher proportion of Plaque-RADS III/IV subtypes. The Plaque-RADS classification may be used to risk-stratify carotid plaque phenotypes in patients with ESUS.

Circulating Sex-Specific Markers of Plaque Instability in Women and Men With Severe Carotid Atherosclerosis.

Sex-specific differences in plaque composition and instability underscore the need to explore circulating markers for better prediction of high-risk plaques. This cross-sectional study aims to (1) investigate differences in lipid, immune, and adipokine circulating profiles between men and women with stable versus unstable plaques and (2) identify circulating markers that can better classify men and women according to plaque instability. Preoperative blood samples and plaque specimens were collected from consecutive men and women with carotid artery stenosis ≥50% and who underwent a carotid endarterectomy between 2009 and 2018. Adipokine, lipid, and immune profiling was conducted. Plaque stability was determined by gold-standard histological classifications. Statistical analyses, including χ2, ANOVA, Kruskal-Wallis, and logistic regression, assessed differences in plaque features and blood parameters between men and women with stable and unstable plaques. Of 470 recruited patients (aged 70.8±9.2 years), the final study analyses included 317 men and 143 women (aged 71.0±9.0 years). Men exhibited more unstable plaques (P<0.001), characterized by increased plaque hemorrhage, larger lipid core, and inflammation (P<0.001), along with less favorable circulating profiles. Antagonistic interactions between sex and white blood cell (WBC) counts, basophil-to-WBC ratio, and platelet counts influenced plaque instability. In men, low WBC counts, high monocyte-to-WBC ratio, low basophil-to-WBC ratio, and high LDL-C (low-density lipoprotein cholesterol) levels were associated with greater plaque instability (odds ratio, 0.827 [95% CI, 0.713-0.926], 1.158 [95% CI, 1.027-1.305], 0.495 [95% CI, 0.281-0.871], and 1.564 [95% CI, 1.001-2.443], respectively) and more unstable features (ie, inflammation, foam cells, and neovascularization). In women, a high basophil-to-WBC ratio was associated with greater plaque instability (3.142 [95% CI, 1.220-8.093]), hemorrhage, and thrombosis, while a high molecular weight-to-total adiponectin ratio was associated with decreased instability (0.014 [95% CI, 0.000-0.646]) and inflammation. Our findings demonstrated sex-specific differences, with women displaying more stable plaque phenotypes and favorable circulating profiles compared with men. This proof-of-concept study was also designed as the key first step in exploring novel sex-specific associations between circulating lipid, immune, and adipokine profiles and carotid plaque instability.

Invasive coronary imaging of inflammation to further characterize high-risk lesions: what options do we have?

Coronary atherosclerosis remains a leading cause of morbidity and mortality worldwide. The underlying pathophysiology includes a complex interplay of endothelial dysfunction, lipid accumulation and inflammatory pathways. Multiple structural and inflammatory features of the atherosclerotic lesions have become targets to identify high-risk lesions. Various intracoronary imaging devices have been developed to assess the morphological, biocompositional and molecular profile of the intracoronary atheromata. These techniques guide interventional and therapeutical management and allow the identification and stratification of atherosclerotic lesions. We sought to provide an overview of the inflammatory pathobiology of atherosclerosis, distinct high-risk plaque features and the ability to visualize this process with contemporary intracoronary imaging techniques.

Proteomics associated with coronary high-risk plaques by optical coherence tomography.

Biomarkers are widely used for the diagnosis and monitoring of cardiovascular disease. However, markers for coronary high-risk plaques have not been identified.The aim of this study was to identify proteins specific to coronary high-risk plaques.Fifty-one patients (71.2 ± 11.1 years, male: 66.7%) who underwent intracoronary optical coherence tomography imaging and provided blood specimens for proteomic analysis were prospectively enrolled. A total of 1470 plasma proteins were analyzed per patient using the Olink® Explore 1536 Reagent Kit.In patients with thin-cap fibroatheroma, the protein expression of Calretinin (CALB2), Corticoliberin (CRH) and Alkaline phosphatase, placental type (ALPP) were significantly increased, while the expression of Neuroplastin (NPTN), Folate receptor gamma (FOLR3) and Serpin A12 (SERPINA12) were significantly decreased. In patients with macrophage infiltration, the protein expressions of Fatty acid-binding protein, intestinal (FABP2), and Fibroblast growth factor 21 (FGF21) were significantly decreased. In patients with lipid-rich plaques, the protein expression of Interleukin-17C (IL17C) was significantly increased, while the expression of Fc receptor-like protein 3 (FCRL3) was significantly decreased.These proteins might be useful markers in identifying patients with coronary high-risk plaques. Clinical Trial Registration: https://www.umin.ac.jp/ctr/ , UMIN000041692.

Pancoronary plaque characteristics in STEMI patients with rapid plaque progression: An optical coherence tomography study

BackgroundNon-culprit plaque progression is associated with recurrent cardiac ischemic events and worse clinical outcomes. Given that atherosclerosis is a systemic disease, the pancoronary characteristics of patients with rapid plaque progression are unknown. This study aims to identify pancoronary plaque features in patients with ST-segment elevation myocardial infarction (STEMI) with and without rapid plaque progression, focused on the patient level. Methods and resultsFrom January 2017 to July 2019, 291 patients underwent 3-vessel optical coherence tomography imaging at the time of the primary procedure and a follow-up angiography interval of 12 months. The final analysis included 237 patients. Overall, 308 non-culprit lesions were found in 78 STEMI patients with rapid plaque progression, and 465 non-culprit plaques were found in 159 STEMI patients without rapid plaque progression. These patients had a higher pancoronary vulnerability (CLIMA-defined high-risk plaque: 47.4% vs. 33.3%; non-culprit plaque rupture: 25.6% vs. 14.5%) and a significantly higher prevalence of other vulnerable plaque characteristics (i.e., lipid-rich plaque, cholesterol crystal, microchannels, calcification, spotty calcification, and thrombus) at baseline versus those without rapid plaque progression. Lesions with rapid progression were highly distributed at the LAD, tending to be near the bifurcation. In multivariate analysis, age ≥ 65 years was an independent predictor of subsequent rapid lesion progression at the patient level, whereas microchannel, spotty calcification, and cholesterol crystal were independent predictors for STEMI patients ≥65 years old. ConclusionsSTEMI patients with subsequent rapid plaque progression had higher pancoronary vulnerability and commonly presented vulnerable plaque morphology. Aging was the only predictor of subsequent rapid plaque progression.

The Role of Fluid Mechanics in Coronary Atherosclerotic Plaques: An Up-to-Date Review.

Most acute coronary syndromes are due to a sudden luminal embolism caused by the rupturing or erosion of atherosclerotic plaques. Prevention and treatment of plaque development have become an effective strategy to reduce mortality and morbidity from coronary heart disease. It is now generally accepted that plaques with thin-cap fibroatheroma (TCFA) are precursors to rupturing and that larger plaques and high-risk plaque features (including low-attenuation plaque, positive remodeling, napkin-ring sign, and spotty calcification) constitute unstable plaque morphologies. However, plaque vulnerability or rupturing is a complex evolutionary process caused by a combination of multiple factors. Using a combination of medicine, engineering mechanics, and computer software, researchers have turned their attention to computational fluid mechanics. The importance of fluid mechanics in pathological states for promoting plaque progression, inducing plaque tendency to vulnerability, or even rupture, as well as the high value of functional evaluation of myocardial ischemia has become a new area of research. This article reviews recent research advances in coronary plaque fluid mechanics, aiming to describe the concept, research implications, current status of clinical studies, and limitations of fluid mechanic's characteristic parameters: wall shear stress (WSS), axial plaque shear (APS), and fractional flow reserve (FFR). Previously, most computational fluid dynamics were obtained using invasive methods, such as intravascular ultrasound (IVUS) or optical coherence tomography (OCT). In recent years, the image quality and spatial resolution of coronary computed tomography angiography (CCTA) have greatly improved, making it possible to compute fluid dynamics by noninvasive methods. In the future, the combination of CCTA-based anatomical stenosis, plaque high-risk features, and fluid mechanics can further improve the prediction of plaque development, vulnerability, and risk of rupturing, as well as enabling noninvasive means to assess the degree of myocardial ischemia, thereby providing an important aid to guide clinical decision-making and optimize treatment.

Evaluation of Turbulence Index and Flow Pattern for Atherosclerotic Carotid Stenosis: A High-Frame-Rate Vector Flow Imaging Study

ObjectiveThe emerging high-frame rate vector flow imaging (H-FRV Flow) provides a new way of hemodynamic evaluation for complex blood flow. This study aimed to explore quantitatively the characteristics of complex flow with turbulence (Tur) index and analyze flow pattern in atherosclerotic internal carotid artery stenosis (ICAS) using H-FRV Flow. MethodsThis study prospectively included 60 patients with ICAS. Tur values in different segments of stenosis and cardiac phases were compared. Meanwhile Spearman correlation analysis was performed between clinical plaque characteristics with turbulence grading by ln (Tur). Three complex flow patterns were qualitatively drawn on vector flow mode, and the detection rate of flow patterns in different stenosis groups and ulceration groups were compared. ResultsHighly disordered blood flow was observed in the stenosis (Tur (%) (M, QR) =12.5, 21.5) and distal segment (15.4, 27.2), particularly during systole (21.0, 30.7/ 33.3, 38.7, P<0.05). Spearman correlation analysis showed that stenosis rate was correlated with turbulence grading in the stenosis (ρ=0.65, P<0.05) and distal segment (ρ=0.79, P<0.05), and ulcer formation was correlated with turbulence grading in the stenosis segment (ρ=0.58, P<0.05). The overall detection rate of three flow patterns was higher respectively in the severe stenosis group (22/22) versus mild to moderate stenosis group (21/38) (P<0.001) and the ulcer group (21/23) versus non-ulcer group (23/37) (P<0.001). ConclusionH-FRV Flow was helpful for assess the severity and characteristics of flow turbulence. Lumen geometric factors could affect the flow turbulence and blood flow patterns around the plaque. This would provide important hemodynamic information for the detection of high-risk plaque.

Relationship of Coronary Angiography-Derived Radial Wall Strain With Functional Significance, Plaque Morphology, and Clinical Outcomes

BackgroundCoronary angiography-derived radial wall strain (RWS) is a newly developed index that can be readily accessed and describes the biomechanical features of a lesion. ObjectivesThe authors sought to investigate the association of RWS with fractional flow reserve (FFR) and high-risk plaque (HRP), and their relative prognostic implications. MethodsWe included 484 vessels (351 patients) deferred after FFR measurement with available RWS data and coronary computed tomography angiography. On coronary computed tomography angiography, HRP was defined as a lesion with both minimum lumen area <4 mm2 and plaque burden ≥70%. The primary outcome was target vessel failure (TVF), a composite of target vessel revascularization, target vessel myocardial infarction, or cardiac death. ResultsThe mean FFR and RWSmax were 0.89 ± 0.07 and 11.2% ± 2.5%, respectively, whereas 27.7% of lesions had HRP, 15.1% had FFR ≤0.80. An increase in RWSmax was associated with a higher risk of FFR ≤0.80 and HRP, which was consistent after adjustment for clinical or angiographic characteristics (all P < 0.05). An increment of RWSmax was related to a higher risk of TVF (HR: 1.23 [95% CI: 1.03-1.47]; P = 0.022) with an optimal cutoff of 14.25%. RWSmax >14% was a predictor of TVF after adjustment for FFR or HRP components (all P < 0.05) and showed a direct prognostic effect on TVF, not mediated by FFR ≤0.80 or HRP in the mediation analysis. When high RWSmax was added to FFR ≤0.80 or HRP, there were increasing outcome trends (all P for trend <0.001). ConclusionsRWS was associated with coronary physiology and plaque morphology but showed independent prognostic significance.

Evaluation of the Correlation Between Distribution Location and Vulnerability of Carotid Plaque in Patients with Transient Ischemic Attack.

To analyze the relationship among distribution location, characteristics, and vulnerability of carotid plaque using CTA and provide more information on the risk factors of carotid atherosclerotic plaque. We retrospectively analyzed the CTA images of the head and neck of 93 patients with carotid atherosclerosis. Atherosclerosis was developed in 148 carotid arteries. The plaques were divided into a high-risk plaque group and a low-risk plaque group according to whether the plaques had high-risk characteristics. The maximum cross-sectional area of carotid artery bifurcation plaque on the axial image was selected, and the cross-sectional lumen was equally divided into four 90-degree sectors, ventral side wall, dorsal side wall, inner side wall, and outer side wall. The differences in the characteristics and distribution locations of the plaques in the two groups were analyzed. The characteristic parameters of the cross-sectional plaques at the bifurcation of the carotid artery. The logistic regression analysis was used to further analyze the risk factors associated with plaque vulnerability. Among 148 carotid arteries,80 were classified as high-risk and 68 as low-risk groups. There were significant differences between the two groups concerning the thickness, length, maximum cross-sectional area, burden, and cross-sectional distribution of the plaques (P < 0.05). The plaque distribution on the dorsal side wall of the carotid bifurcation was higher in the high-risk group than that in the low-risk group (P < 0.05), dorsal side wall plaque-independent risk factors for the development of vulnerability of plaques in transient ischemic attack (TIA) patients (95% CI:1.522~6.991, P<0.05). High-risk plaques tend to occur on the dorsal side wall of the carotid bifurcation, whereas low-risk plaques tend to occur on the outer side wall of the carotid bifurcation.

Age-related Pancoronary Characteristics in Patients with ST-segment Elevation Myocardial Infarction

Background: Age-related vulnerable characteristics of pancoronary plaques in patients with ST-segment elevation myocardial infarction (STEMI) have not been systemically evaluated by optical coherence tomography (OCT). Therefore, we sought to explore the discrepancies in pancoronary characteristics between younger and older patients with STEMI through OCT. Methods: This retrospective single-center study included 588 patients who had STEMI and underwent three-vessel OCT through emergency percutaneous coronary intervention between October 2016 and September 2018. With a median age of 56 years as a cutoff, the patients were divided into a younger group (≤56 years, n = 298) and an older group (&gt;56 years, n = 290). Results: A total of 795 non-culprit plaques were found in 298 of the younger patients, whereas 858 non-culprit plaques were identified in 290 of the older patients. Fewer high-risk OCT plaques (15.8% vs. 23.1%; P = 0.025), as well as other structures (cholesterol crystals, P = 0.001; microchannels, P = 0.032; calcifications, P &lt; 0.001; spotty calcifications, P &lt; 0.001; large calcifications, P &lt; 0.001; and thrombi, P = 0.001) were identified in younger patients than older patients, at the patient level. In addition, pancoronary vulnerability in younger patients was independently predicted by culprit plaque rupture {CLIMA-defined high-risk plaques (odds ratio [OR]: 3.179; 95% CI: 1.501 to 6.733; P = 0.003), non-culprit rupture (OR: 3.802; 95% CI: 1.604 to 9.014; P = 0.002), non-culprit thin-cap fibroatheroma (OR: 3.536; 95% CI: 2.051 to 6.094; P &lt; 0.001)}, hypertension (OR: 1.920; 95% CI: 1.099 to 3.355; P = 0.022), and total cholesterol (OR: 1.094; 95% CI: 1.002 to 1.195; P = 0.045). In older patients with STEMI, the predictor was male sex (OR: 3.031; 95% CI: 1.352 to 6.795; P = 0.007). Conclusions: Among patients with STEMI, younger patients had limited vulnerable plaque characteristics, and pancoronary vulnerability was associated with culprit plaque rupture, hypertension, and total cholesterol. In contrast, older patients had greater pancoronary vulnerability with the single predictor of male sex, thus suggesting that traditional risk factors have limited applicability in predicting pancoronary vulnerability in older patients.

Tannic acid-poloxamer self-assembled nanoparticles for advanced atherosclerosis therapy by regulation of macrophage polarization.

Atherosclerosis (AS) is a significant contributor to cardiovascular events. Advanced AS is particularly concerning, as it leads to the formation of high-risk vulnerable plaques. Current treatments for AS focus on antithrombotic and lipid-lowering interventions, which are effective in treating early-stage AS. Recent studies have shown that macrophage polarization plays a crucial role in the development of AS. This study presents a new biomedical application of natural tannic acid as an anti-inflammatory nanoplatform for advanced AS. Tannic acid-poloxamer nanoparticles (TPNP) are fabricated through self-assembly of tannic acid (TA) and poloxamer. TPNP has the potential to provide effective treatment for advanced AS. According to in vitro studies, TPNP has been found to suppress the inflammatory response in lipopolysaccharide-stimulated macrophages by scavenging reactive oxygen species (ROS), downregulating the expression levels of inflammatory cytokines (such as interleukin-10 and tumor necrosis factor-α) and regulating polarization of macrophages. In vivo studies further reveal that TPNP can retard the development of advanced atherosclerotic plaques by reducing ROS production and promoting M2 macrophage polarization in the aorta of ApoE-/- mice. Overall, these findings suggest that TPNP could be used to develop natural multifunctional nanoplatforms for molecular therapy of AS and other inflammation-related diseases.

The Ability of Near-Infrared Spectroscopy to Identify Vulnerable Patients and Plaques: A Systematic Review and Meta-Analysis.

Previous studies have analyzed the efficacy of near-infrared spectroscopy-derived lipid core burden index (LCBI) in quantifying and identifying high-risk plaques and patients at increased risk of future major adverse cardiac outcomes/major adverse cardiovascular and cerebrovascular events. A maxLCBI4mm of 400 or greater seems to be an effective threshold for classifying at-risk plaques. This meta-analysis provides a more precise odds ratio with a narrow standard deviation that can be used to guide future studies.

Lipid Content Distribution and its Clinical Implication in Patients with Acute Myocardial Infarction-Plaque Erosion: Results from the Prospective OCTAMI Study.

Plaque erosion (PE) is one of the main plaque phenotypes of acute coronary syndrome (ACS). However, the underlying plaque component and distribution have not been systematically analysed. This study aims to investigate the distribution of lipid and calcium content in culprit lesions assessed by optical coherence tomography (OCT) in patients with PE and explore its relationship with prognosis in a cohort of ST segment elevation myocardial infarction (STEMI) patients. A prospective cohort of 576 patients with STEMI was enrolled in our study. After exclusion, 152 PE patients with clear underlying plaque components were ultimately analysed. The culprit lesion was divided into the border zone, external erosion zone and erosion site in the longitudinal view. Each pullback of the culprit lesions was assessed by 3 independent investigators frame-by-frame, and the quantity and distribution of lipid and calcium components were recorded. Of the 152 PE patients, lipid and calcium contents were more likely to exist in the external erosion zone than in the other regions. In particular, a high level of lipid content proximal to the erosion site was significantly associated with plaque vulnerability and a higher incidence of MACEs. This study revealed that high level of lipid content in the proximal external erosion zone was related to high-risk plaque characteristics and poor prognosis, which provided a novel method for risk stratification and precise management in patients with plaque erosion.

Low-Attenuation Coronary Plaque Volume and Cardiovascular Events in Patients with Distinct Metabolic Phenotypes with or without Diabetes.

Diabetes mellitus (DM) plays a key role in the pathophysiology of metabolic syndrome (MetS). This study aimed to investigate the association among DM, low-attenuation plaque (LAP) volume, and cardiovascular outcomes across metabolic phenotypes in patients with suspected coronary artery disease (CAD) who underwent coronary computed tomography angiography (CCTA). We included 530 patients who underwent CCTA. MetS was defined as the presence of a visceral adipose tissue area 100 in patients with DM (n = 58) or two or more MetS components excluding DM (n = 114). The remaining patients were categorised as non-MetS patients with DM (n = 52) or without DM (n = 306). A CCTA-based high-risk plaque was defined as a LAP volume of 4%. The primary endpoint was the presence of a major cardiovascular event (MACE), which was defined as a composite of cardiovascular death, acute coronary syndrome, and coronary revascularization. The incidence of MACE was the highest in the non-MetS with DM group, followed hierarchically by the MetS with DM, MetS without DM, and non-MetS without DM groups. In the multivariable Cox hazard model analysis, DM as a predictor was associated with MACE independent of LAP volume 4% (hazard ratio, 2.68; 95% confidence interval, 1.16-6.18; p = 0.02), although MetS did not function as an independent predictor. A LAP volume 4% functioned as a predictor of MACE, independent of each metabolic phenotype or DM. This study demonstrated that DM, rather than MetS, is a predictor of coronary events independent of high-risk plaque volume in patients who underwent CCTA.

Cholesterol crystals at the culprit lesion in patients with acute coronary syndrome are associated with worse cardiovascular outcomes at two years follow up - results from the translational OPTICO-ACS study program

BackgroundCholesterol crystals (CCs) represent a feature of advanced atherosclerotic plaque and may be assessed by optical coherence tomography (OCT). Their impact on cardiovascular outcomes in patients presenting with acute coronary syndromes (ACS) is yet unknown. MethodsThe culprit lesion (CL) of 346 ACS-patients undergoing preintervention OCT imaging were screened for the presence of CCs and divided into two groups accordingly. The primary end-point was the rate of major adverse cardiac events plus (MACE+) consisting of cardiac death, myocardial infarction, target vessel revascularization and re-hospitalization due to unstable or progressive angina at two years. ResultsAmong 346 patients, 57.2% presented with CCs at the CL. Patients with CCs exhibited a higher prevalence of ruptured fibrous caps (RFC-ACS) (79.8% vs. 56.8%; p < 0.001) and other high-risk features such as thin cap fibroatheroma (80.8% vs. 64.9%; p = 0.001), presence of macrophages (99.0% vs. 85.1%; p < 0.001) as well as a greater maximum lipid arc (294.0° vs. 259.3°; p < 0.001) at the CL as compared to patients without CCs. MACE+ at two years follow-up occurred more often in CC-patients (29.2% vs. 16.1%; p = 0.006) as compared to patients without CCs at the culprit site. Multivariable cox regression analysis identified CCs as independent predictor of MACE+ (HR 1.705; 1.025–2.838 CI, p = 0.040). ConclusionsCCs were associated with conventional high-risk plaque features and associated with increased MACE+-rates at two years follow up. The identification of CCs might be useful as prognostic marker in patients with ACS and assist “precision prevention” in the future.

Symptomatic Non-stenotic Carotid Disease in Embolic Stroke of Undetermined Source : Analysis of the ESCAPE-NA1 Trial.

Non-stenotic (< 50%) carotid disease may play an important etiological role in ischemic stroke classified as embolic stroke of undetermined source (ESUS). We aimed to assess the prevalence of non-stenotic carotid disease and its association with ipsilateral ischemic stroke. Data are from ESCAPE-NA1, arandomized controlled trial investigating the neuroprotectant nerinetide in patients with acute ischemic stroke and large vessel occlusion (LVO). The degree of stenosis of the extracranial internal carotid artery (ICA) and high-risk plaque features were assessed on baseline computed tomography (CT) angiography. We evaluated the association of non-stenotic carotid disease and ipsilateral stroke by age-adjusted and sex-adjusted logistic regression and calculated the attributable risk of ipsilateral stroke caused by non-stenotic carotid disease. After excluding patients with non-assessable imaging, symptomatic > 50% carotid stenosis and extracranial dissection, 799/1105 (72.1%) patients enrolled in ESCAPE-NA1 remained for this analysis. Of these, 127 (15.9%) were classified as ESUS. Non-stenotic carotid disease occurred in 34/127 ESUS patients (26.8%) and was associated with the presence of ipsilateral ischemic stroke (odds ratio, OR1.6, 95% confidence interval, CI 1.0-2.6, p = 0.049). The risk of ipsilateral ischemic stroke attributable to non-stenotic carotid disease in ESUS was estimated to be 19.7% (95% CI -5.7% to 39%), the population attributable risk was calculated as 4.3%. Imaging features such as plaque thickness, plaque irregularity or plaque ulceration were not different between non-stenotic carotids with vs. without ipsilateral stroke. Non-stenotic carotid disease frequently occurs in patients classified as ESUS and is associated with ipsilateral ischemic stroke. Our findings support the role of non-stenotic carotid disease as stroke etiology in ESUS, but further prospective research is needed to prove acausal relationship.

Lower extremity arterial plaque in patients with type 2 diabetes mellitus: A cross-sectional study of 25-(OH)D3 and other risk factors

ObjectiveThe occurrence of chronic vascular complications in individuals with type 2 diabetes mellitus(T2DM) is influenced by multiple factors. This study aims to analyze the correlation between serum 25-(OH)D3 levels and other risk factors with the formation and severity of arterial plaques in the lower extremities, and explore its role in clinical diagnosis and treatment. MethodsA total of 628 Chinese patients with T2DM were included in this study. Based on the intima-media thickness (IMT) and plaque echogenicity measured by lower extremity vascular ultrasound, the patients were divided into the no plaque group(NP), low-risk plague group(LP), moderate-risk plague group(MP), and severe-risk plague group(SP). Based on 25-(OH)D3 levels, patients were categorized as vitamin D deficient group (VDD，25-(OH)D3 ≤ 20 ng/mL), vitamin D insufficient group (VDI，25-(OH)D3 between>20 ng/mL and < 30 ng/mL), and vitamin D sufficient group (VDS，25-(OH)D3 ≥ 30 ng/mL). The correlation between the severity of lower extremity arterial plaques and serum 25-(OH)D3 levels was analyzed, as well as the risk factors for lower extremity arterial plaque formation in patients with T2DM. ResultsThe levels of 25-(OH)D3 in patients with arterial plaques were significantly lower than those in the NP (p = 0.002). Additionally, with the increasing severity of lower extremity arterial plaques, 25-(OH)D3 levels also decreased significantly (p = 0.01). The proportion of patients with sufficient 25-(OH)D3 levels was highest in NP, while the proportion of deficient and insufficient groups was higher in LP (p<0.001). Multivariate logistic regression analysis showed that low levels of 25-(OH)D3 were an independent risk factor for lower extremity arterial plaques in T2DM patients. Compared to patients with 25-(OH)D3>20 ng/mL, the odds ratios for the formation of moderate-risk plaques were 2.525 (95 % CI: 1.45–4.39) in patients with 25-(OH)D3 ≤ 20 ng/mL, and 2.893 (95 % CI: 1.59–5.26) for the formation of high-risk plaques. ConclusionSerum 25-(OH)D3 levels may be correlated with the occurrence and severity of lower extremity arterial plaques in patients with T2DM. Low serum 25-(OH)D3 concentration is a risk factor for lower extremity vascular lesions.

CT Coronary Angiography: Technical Approach and Atherosclerotic Plaque Characterization.

Coronary computed tomography angiography (CCTA) currently represents a robust imaging technique for the detection, quantification and characterization of coronary atherosclerosis. However, CCTA remains a challenging task requiring both high spatial and temporal resolution to provide motion-free images of the coronary arteries. Several CCTA features, such as low attenuation, positive remodeling, spotty calcification, napkin-ring and high pericoronary fat attenuation index have been proved as associated to high-risk plaques. This review aims to explore the role of CCTA in the characterization of high-risk atherosclerotic plaque and the recent advancements in CCTA technologies with a focus on radiomics plaque analysis.