Carotid Artery Plaque Research Articles

Ultrabright and ultrafast afterglow imaging in vivo via nanoparticles made of trianthracene derivatives.

Low sensitivity, photobleaching, high-power excitation and long acquisition times constrain the utility of afterglow luminescence. Here we report the design and imaging performance of nanoparticles made of electron-rich trianthracene derivatives that, on excitation by room light at ultralow power (58 μW cm-2), emit afterglow luminescence at ~500 times those of commonly used organic afterglow nanoparticles. The nanoparticles' ultrabright afterglow allowed for deep-tissue imaging (up to 6 cm), for ultrafast afterglow imaging (at short acquisition times down to 0.01 s) of naturally behaving mice with negligible photobleaching, even after re-excitation for over 15 cycles, and for the accurate visualization of subcutaneous and orthotopic tumours and of plaque in carotid arteries. We also show that an afterglow nanoparticle that is activated only in the presence of granzyme B allowed for the tracking of granzyme-B activity in the context of therapeutic monitoring. The high sensitivity and negligible photobleaching of the organic afterglow nanoparticles offer advantages for real-time in vivo monitoring of physiopathological processes.

Protein signatures associated with methylation patterns of heart failure phenotypes

Abstract Introduction The heart failure (HF) syndrome is highly susceptible to the exposome. The interplay between DNA methylation (DNAm), surrogate for exposomal influences, and the plasma proteome in the progression and development of phenotypes of heart failure is unclear. We investigated the relation between methylation patterns of HF phenotypes and proteins signatures. Methods Individuals with symptomatic HF (stage C/D with HFpEF, HFmrEF and HFrEF) of the MyoVasc cohort (N=3,289) were investigated. EDTA-Plasma and DNA were extracted from peripheral blood and stored in -80°C. DNAm was measured using the Infinium MethylationEPIC v2.0 methylation array. Concentrations for 538 proteins were measured using an immuno-qPCR assay in EDTA plasma. Multivariable regression models adjusted for age and sex were used to assess the relationship between DNAm signatures and individual proteins in each phenotype. Ridge-regularized linear regression was used to generate a phenotype-specific protein-signature in relation to each methylation signature, linear regression to estimate links between protein signatures and cardiovascular traits and Cox regression relate protein signatures to clinical outcome. Results Data from 1,317 individuals with symptomatic HF were analyzed. After FDR adjustment, 310 proteins were significantly related to HFpEF methylation signature, 314 to HFmrEF and 266 to HFrEF. Of associated proteins, 49.9% (198) were found in all phenotypes, 8.82% (35) only in HFpEF, 12.1% (48) in HFmrEF and 4.79% (19) in HFrEF. Tumor necrosis, arterial hypertension and T-cell regulation pathways were enriched in all three phenotypes. NT-proBNP had the strongest association with HFrEF (β=0.95 [0.82-1.08], p<0.0001) followed by presence of plaques in carotid artery and C-reactive protein, while left ventricular mass (LVM) had stronger association with HFpEF (β=0.22 [0.11-0.33], p=0.0001). All three signatures were associated with worsening of HF (HFpEF: HR=1.93 [1.61-2.30], p<0.0001; HFmrEF: HR=1.63 [1.29-2.04], p<0.0001; HFrEF: HR=1.64 [1.38-1.95], p<0.0001) and all-cause death in HF (HFpEF: HR=1.93 [1.65-2.26], p<0.0001; HFmrEF: HR=1.95 [1.58-2.42], p<0.0001; HFrEF: HR=2.24 [1.86-2.69], p<0.0001). Methylation-associated protein signatures had stronger associations with clinical outcome than the methylation signatures themselves (p < 0.01). Conclusion This study revealed protein signatures associated with methylation patterns of HF phenotypes that shared common and unique features for HF phenotypes. Important common pathways were enriched in tumour necrosis, arterial hypertension and regulation of T cells. However, important differences between phenotypes were also revealed, e.g. NT-proBNP was strongly associated with the HFrEF protein signature and LVM with the HFpEF signature. The methylation-associated protein signatures emphasise the possible exposomal influence on HF syndrome.

Deletion of the asialyloglycoprotein receptor-1 (ASGR1) causes atheroprotective effects in vitro and in vivo

Abstract Introduction The asialoglycoprotein receptor 1 (ASGR1) is a hepatic receptor that clears desialylated glycoproteins from the circulation. A loss-of-function mutation in ASGR1 was reported to associate with a 34% reduction in coronary artery disease (CAD) risk, suggesting a role for ASGR1 in CAD. Aim To determine the role of ASGR1 in atherosclerosis and whether deletion of ASGR1 elicits atheroprotective effects. Methods Western blotting, mass spectrometry and flow cytometry assessed ASGR1 expression in cultured macrophages or immune cells collected from the blood and aortas of wildtype mice. Bone marrow-derived macrophages (BMDMs) from wildtype and Asgr1-/- mice were subjected to cholesterol efflux and oxidised low-density lipoprotein (oxLDL) uptake in vitro functionalassays. ELISA and qPCR measured changes in lipid regulators in BMDMs. Asgr1-/- mice were crossed with atherosclerosis-prone apolipoprotein (Apo)e-/- mice (Apoe-/-Asgr1-/-). Stable plaque area was assessed histologically in the aortic sinuses of mice fed a high-cholesterol diet for 8 weeks (n=16/group). Using the tandem stenosis surgical model, unstable plaque was assessed in carotid arteries (n=10/group). Human ASGR1 was measured by ELISA in peripheral blood mononuclear cells (PBMCs) isolated from patient samples (n=18). Results Western blotting and mass spectrometry discovered ASGR1 is expressed in macrophages. Immunofluorescence identified the presence of ASGR1 in aortic sinus plaque. Flow cytometry revealed ASGR1 is expressed in both inflammatory and patrolling monocytes, neutrophils, macrophages and dendritic cells of blood and aortas. Asgr1-/- BMDMs elicited greater cholesterol efflux (+39%, P<0.05) and decreased oxLDL uptake (-15%, P<0.05), compared to wildtype BMDMs. Moreover, Asgr1-/- BMDMs had significantly higher LDL receptor protein levels (+2-fold), and Lxra (+2-fold) and Pparg (+1.5-fold) mRNA levels than wildtype BMDMs, P<0.001. Plasma from Asgr1-/- mice had lower total (-25%, P<0.05) and LDL (-36%, P<0.05) cholesterol concentrations than wildtype mice. Apoe-/-Asgr1-/- mice developed less stable plaque in aortic sinuses (-37%, P<0.001) than Apoe-/- controls, as well as smaller unstable plaques in carotid arteries (-49%, P<0.05). Finally, in a human population, ASGR1 protein levels were higher in PBMCs from patients with coronary plaque (+61%, P<0.05), than those without plaque, determined from coronary angiograms. Conclusion ASGR1 is expressed on monocytes, macrophages and in plaques, and human PBMC ASGR1 associates with coronary plaque. Deletion of ASGR1 causes atheroprotective functions in macrophages in vitro and reduced plaque burden in vivo. Our findings demonstrate ASGR1 is important in atherosclerosis with implications for ASGR1 as a therapeutic target.

Relationship of cumulative low-density lipoprotein cholesterol with atherosclerosis

Abstract Background The relationship between cumulative low-density lipoprotein cholesterol (LDL-C) exposure and progression of atherosclerosis remains uncertain. Objective The aim of this study was to determine the relationship between cumulative LDL-C level and flow-mediated vasodilation (FMD), nitroglycerine-induced vasodilation (NID) and the presence of plaque in the common carotid artery (CCA). Methods This was a cross-sectional study. We measured FMD in 8208 subjects, NID in 1822 subjects, and CCA plaque in 591 subjects who were not taking lipid-lowering drugs. The subjects were divided into four groups based on cumulative LDL-C exposure: <4000 mg･year/dL, 4000-4999 mg･year/dL, 5000-5999 mg･year/dL, and ≥6000 mg･year/dL. Results The odds ratio of the lower quartile of FMD in the cholesterol-year-score <4000 mg･year/dL group was significantly higher than the odds ratios in the other groups (Figure 1A). The odds ratio of the lower quartile of NID in the <4000 mg・year/dL group was significantly higher than the odds ratios in the 5000-5999 mg･year/dL and ≥6000 mg･year/dL groups (Figure 1B). The odds ratio of the prevalence of CCA plaque in the <4000 mg・year/dL group was significantly higher than that in the ≥6000 mg･year/dL group (Figure 1C). Conclusions Endothelial dysfunction occurred from cumulative LDL-C exposure of 4000 mg・year/dL, vascular smooth muscle dysfunction occurred from cumulative LDL-C exposure of 5000 mg･year/dL, and prevalence of CCA plaque occurred from cumulative LDL-C exposure of 6000 mg･year/dL.Graphical abstractFigure 1

Experimental evidence on colchicine's mode of action in human carotid artery plaques

Abstract Background and aims Atherosclerosis driven by inflammation is a major cause of cardiovascular events. Recent clinical trials have demonstrated the therapeutic potential of anti-inflammatory treatments. Consequently, colchicine is recommended in current guidelines as a second-line therapy for secondary prevention, although the drug's mechanism of action is not fully understood. Methods To this end, we performed a multiomic study of the effect of colchicine on human carotid plaques. Sections from endarterectomy specimens were exposed ex vivo to colchicine at concentrations of 2 ng/ml and 10 ng/ml for 24 hours and compared with untreated segments of the same plaque. Changes in gene expression were analyzed by RNA sequencing, and plaque secretomes were subjected to proteomic analysis by mass spectrometry. In situ cell proliferation was examined histologically. Results Our data suggest that colchicine primarily suppresses neutrophil and platelet degranulation, collagen degradation, and macrophage proliferation in atheromatous plaques in a dose-dependent manner, while stimulating myofibroblast activation. Conclusion Our study demonstrates multifactorial pathways by which colchicine, the first anti-inflammatory drug recommended by cardiovascular guidelines, acts on human atherosclerotic lesions. Targeting neutrophil and platelet degranulation, collagen degradation and macrophage proliferation could provide significant therapeutic benefit in atherosclerotic cardiovascular disease without the adverse side effects of colchicine.

Adverse outcomes following carotid artery stenting in echolucent plaques: a systematic review and meta-analysis

Abstract Objective Conflicting evidence exists regarding carotid artery stenting (CAS) interventions on echolucent plaques and adverse outcomes. This meta-analysis aims to assess the relationship between carotid plaque echogenicity and adverse outcomes following CAS. Methods We conducted a systematic search of electronic databases (PubMed, MEDLINE, EMBASE and Cochrane Center Register) up to January 2024. Two researchers independently assessed the eligibility of studies that used ultrasound to assess carotid artery plaque echogenicity and its relationship with adverse outcomes after CAS. We used web-based systematic review production software RevMan to conduct the analysis. Results Eight studies including 810 patients’ data that have reported on in-stent restenosis, distal embolization and stroke after CAS were meta-analyzed. Mean age of the participants was 68±11 years and 43% were females. CAS performed on echolucent plaques demonstrated a higher frequency of association with distal microembolization OR=3.64 (95% CI 2.11-6.30, p<0.001), in-stent restenosis OR=2.87 (95% CI 1.84-4.47, p=0.003) and stroke OR=3.80 (95% CI 1.93-7.44, p<0.001). In the pooled analysis covering all adverse outcomes following CAS, the OR was 3.28 (95% CI 2.41-4.45, p<0.001, I2=25%). Conclusions Arterial stenting performed on echolucent carotid plaques was more frequently associated with adverse outcomes, such as stroke, distal microembolization, and in-stent restenosis.

Association of ethanolamine desaturase TMEM189-plasmalogen axis with the stability of atherosclerotic plaque and cardiovascular events after acute coronary syndrome

Abstract Background Patients with acute coronary syndrome (ACS) are still at high risk of recurring major adverse cardiovascular events (MACE). Disorders of lipid metabolism play an important role in the pathogenesis and progression of ACS. However, whether there are lipid components that can play an early warning role on the recurrence of MACE in patients with ACS and its potential mechanism is not yet known. Purpose To explore the changes of lipid profile before recurrent MACE in ACS patients, screen lipid molecules related to recurrent MACE, and explore their effects on pathological changes of atherosclerotic plaque. Methods We selected 44 Chinese ACS patients from the ‘Peking and Rotterdam on Mission to Reduce Coronary Artery Disease’ (PRoMISS) study. Among them, patients with recurrent MACE within 1 year after first onset of ACS were defined as MACE group, and the control group was recruited through 1:1 matching. The lipid profile of patients was analyzed by liquid chromatography-mass spectrometry. The effects of the screened potential lipid biomarkers and their synthesis enzymes were evaluated by real-time PCR, Western blot, IHC staining and ELISA. The enzyme knockout mice and ApoE knockout mice were hybridized and bred to obtain double gene knockout mice to determine whether the enzyme deficiency affects atherosclerotic plaque. Results Lipomic analysis showed that in the MACE group, plasmalogens and their 12 subtypes continued to decrease three months before the MACE recurrence. The most critical ethanolamine desaturase in the synthesis pathway of plasmalogen, transmembrane protein 189 (TMEM189) was also significantly lower in the MACE group than in the control group, and the level of TMEM189 was positively correlated with plasmalogen. Analysis of single-cell RNA sequencing results in human carotid artery plaques shows that TMEM189 is enriched in endothelial cells and smooth muscle cells (VSMC). In VSMC, treatment with oxLDL reduced TMEM189 expression. Overexpression of TMEM189 significantly improved oxLDL induced reduction in collagen synthesis, expression of alpha-smooth muscle actin (alpha-SMA) and smooth muscle protein 22 (SM22). Overexpression of TMEM189 in VSMC, significantly reduced the content of plasmalogens in the cells. After 12 weeks of feeding with high-fat and high-cholesterol diet, it was found that the content of smooth muscle cells and vulnerability index in the aortic plaque in TMEM189 -/-ApoE -/- mice were significantly decreased than in ApoE -/- mice. Conclusions Before the recurrence of MACE in ACS patients, the synthesis pathway of plasmalogen was gradually damaged, and the reduction of plasmalogen was a potential marker for predicting the recurrence of MACE in ACS patients. The deficiency of TMEM189 - plasmalogen axis aggravates atherosclerosis, it can regulate the phenotype transformation of smooth muscle cells, inhibit their collagen synthesis, and thus affect plaque stability.

Imaging signs of carotid plaque vulnerability predict subclinical neurological events in asymptomatic patients: the carotid artery multi-modality imaging prognostic study

Abstract Background Carotid artery plaques should be considered for invasive treatment if diameter stenoses is ≥60%, in the presence of clinical and/or imaging characteristics associated with an increased risk of ipsilateral stroke, such as intraplaque haemorrhage (IPH) or lipid-rich necrotic core (LRNC). However, little is known about plaque’s characteristics in patients with <60% stenoses. Purpose To evaluate the prevalence and significance of imaging signs of plaque vulnerability in patients with asymptomatic <60% carotid artery stenoses. Methods In the Carotid Artery Multi-modality imaging Prognostic (CAMP) study (granted by Bando Ricerca Salute 2018 - Regione Toscana) we prospectively enrolled 200 patients with asymptomatic, mild/moderate (40-60%) carotid artery stenoses, as assessed at Doppler ultrasound (DUS). All patients were evaluated with multimodality imaging, including computed tomography angiography (CTA), magnetic resonance angiography (MRA) and brain magnetic resonance imaging (MRI), whenever not contraindicated. A subgroup of 75 patients underwent also a 18[F]-fluorodeoxyglucose (FDG) positron emission tomography (PET). A thorough clinical, biochemical, cardiological and neurological evaluation was performed in all patients. Results Imaging signs of plaque vulnerability were frequent (IPH and/or LRNC at MRA were found in 26.3% patients, plaque ulceration at CTA was found in 36.7% of patients). No difference in the prevalence of cardiovascular risk factors was noted in those with and without signs of vulnerability. Subclinical embolic brain infarctions at brain MRI were found in 8.8% of patients at enrollment. These patients had more frequently a LRNC at MRA than patients without subclinical embolic brain infarctions (50% vs 17%, p<0.05), lower estimated glomerular filtration rate (55±8 vs 73±23 mL/min/1.73mq, p<0.001), higher troponin HS values (16±4 vs 12±8 ng/ml, p<0.05). Presence of LRNC at MRA was the only predictor of embolic lesions at MRI (odds ratio 4.86, 95% confidence interval 1.08-21.8, p<0.05). Conclusions Imaging signs of vulnerability are highly prevalent in patients with asymptomatic intermediate carotid artery stenosis. Presence of a LRNC at MRA is associated with subclinical embolic brain infarcts. The use of non-invasive multi-imaging can better characterize carotid plaques, independent of the degree of stenosis, and help identifying a subgroup of patients at higher risk of events.

Arterial floating mural thrombi are a characteristic imaging pattern in SARS-CoV-2-related ischemic stroke.

Acute ischemic stroke (AIS) is a complication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. We aimed to explore neurovascular imaging patterns in patients with SARS-CoV-2-related AIS. We retrospectively analyzed clinical and radiological data of patients hospitalized with AIS and a positive PCR test for SARS-CoV-2 prior to AIS onset. The control group comprised of AIS patients from a pre-COVID-19 pandemic period matched for gender and age. Thirty-five SARS-CoV-2-related stroke patients, and 35 controls were included. Fifty-seven percent of SARS-CoV-2 patients had either mild or asymptomatic disease. A distinctive imaging pattern of floating arterial mural thrombus was detected in 5 patients of the SARS-CoV-2 group. In 4 patients thrombus was attached to a stenotic atherosclerotic plaque in the proximal internal carotid artery. In the 5th patient a cardiac CTA showed multiple floating thrombi in the descending aorta. In the control group, floating thrombus was only detected in one patient. Treatment with dual antiplatelet therapy was associated with thrombus dissolution and good clinical outcome. Patients with floating thrombi had a longer time from SARS-CoV-2 diagnosis to stroke onset (mean 7.4 versus 3.4 days). Floating arterial mural thrombi attached to atherosclerotic plaques are unique characteristic source of AIS in SARS-CoV-2 patients. They may lead to ischemic stroke in patients with mild or asymptomatic infection up to 1-2 weeks from SARS-CoV-2 diagnosis. Patients with embolic AIS and SARS-CoV-2 diagnosis should perform high resolution cranio-cervical vascular imaging to evaluate floating thrombi as a potential embolic source.

Analysis of risk factors for carotid artery plaque in asymptomatic adults

ObjectiveThis study aimed to investigate the risk factors affecting the presence of carotid plaque in asymptomatic adults.MethodsAsymptomatic adults (age > 40 years, no symptoms of cardiovascular and cerebrovascular diseases) undergoing routine health examinations from physical examination department were included in this study. Carotid plaque was measured by Resona 7OB and Resona 8EXP color Doppler ultrasound and L9-3U and L4-5WU probes. The focal carotid intima–media thickness was greater than 1.1 mm, and the local protrusion of the artery wall into the artery lumen suggested the presence of carotid atherosclerotic plaque. According to their ultrasound results, 1077 asymptomatic adults were divided into a group with carotid plaque (477) and a group without carotid plaque (600).ResultsA total of 1077 asymptomatic adults were included in this study, of whom 44.3% had carotid plaque. The proportion of men with carotid plaque was 84.5%. Multifactorial logistic analysis suggested that age, fasting blood glucose (FBG), total cholesterol (TC), homocysteine (Hcy) and male gender were risk factors for carotid atherosclerosis. The predictive probability of these risk factor indicators derived from the multifactorial model was calculated using receiver operating characteristic (ROC) curves with SPSS 25.0 software. The calculated area under the receiver operating characteristic curve (AUC) was 0.715 (95% CI, 0.685–0.746).ConclusionAge, FBG, TC, Hcy and male gender are risk factors for carotid atherosclerosis in asymptomatic adults. Gender differences in carotid atherosclerosis deserve further attention.

High expression of PLA2G2A in fibroblasts plays a crucial role in the early progression of carotid atherosclerosis

BackgroundIn mouse models of atherosclerosis, knockout of the PLA2G2A gene has been shown to reduce the volume of atherosclerotic plaques. Clinical trials have demonstrated the potential of using the sPLA2 inhibitor Varespladib in combination with statins to reduce lipid levels. However, this approach has not yielded the expected results in reducing the risk of cardiovascular events. Therefore, it is necessary to further investigate the mechanisms of PLA2G2A.MethodsSingle-cell transcriptome data from two sets of carotid plaques, combined with clinical patient information. were used to describe the expression characteristics of PLA2G2A in carotid plaques at different stages. In order to explore the mechanisms of PLA2G2A, we conducted enrichment analysis, cell–cell communication analysis and single-cell regulatory network inference and clustering analyses. We validated the above findings at the cellular level.ResultsOur findings indicate that PLA2G2A is primarily expressed in vascular fibroblasts and shows significant cell interactions with macrophages in the early-stage, especially in complement and inflammation-related pathways. We also found that serum sPLA2 levels have stronger diagnostic value in patients with mild carotid artery stenosis. Subsequent comparisons of single-cell transcriptomic data from early and late-stage carotid artery plaques corroborated these findings and predicted transcription factors that might regulate the progression of early carotid atherosclerosis (CA) and the expression of PLA2G2A.ConclusionsOur study discovered and validated that PLA2G2A is highly expressed by vascular fibroblasts and promotes plaque progression through the activation of macrophage complement and coagulation cascade pathways in the early-stage of CA.

Comparative analysis of retinal microvascular parameters in healthy individuals with or without carotid artery stenosis or plaque.

To evaluate the correlations between retinal microvascular changes and carotid artery stenosis (CAS) with and without plaques using fundus photography. Patients who had undergone bilateral carotid ultrasonography and bilateral fundus photography were divided into the following groups based on the carotid intima-media thickness (IMT) determined via ultrasonography in this retrospective, observational study: the control and CAS (comprising CAS with and without plaque subgroups) groups. The following retinal indicators were determined via fundus photography based on a deep learning algorithm: the arteriole-to-venule ratio (AVR), whole retinal fractal dimension (FD), arteriolar fractal dimension (AFD), venular fractal dimension (VFD), vascular density (VD), and VD within 3 mm (VD3mm) and 5 mm (VD5mm) from the macular fovea. The correlations between these indicators and IMT were also assessed. In total, 715 participants, comprising 313 participants with CAS (CAS group; 91 with plaque and 222 without plaque) and 402 participants without CAS (control group), participated in this study. AFD, VFD, and FD in the CAS group were significantly lower than those in the control group (all p < 0.001). VD, VD3mm, and VD5mm showed significant differences between the groups (all p < 0.05). VFD in the CAS with plaque group was lower than that in the group without plaque (p = 0.014). VD3mm, and VD5mm showed significantly negative correlations with IMTmin in the CAS subgroup. AFD, VFD, FD, VD, VD3 mm, and VD5 mm decreased, and fundus photography based on deep learning algorithm may provide new approaches for screening of CAS.

Duplex ultrasonography for screening and monitoring of carotid artery stenosis for risk stratification of ischemic stroke

Aim: To evaluate the efficiency of Duplex Ultrasonography (DUS) for monitoring and screening of Carotid Artery Stenosis (CAS).Methods: PubMed, Web of Science, Cochrane, and SCOPUS were searched for relevant articles. The quality assessment of the included studies was conducted according to the Cochrane Risk of Bias Tool.Results: Our meta-analysis included six articles. We found that carotid DUS could detect mild CAS in 25%, moderate CAS in 13%, severe CAS in 14.5% of the examined vessels, detection of carotid artery plaques in 36.5% of the examined vessels, and abnormal intima thickness in 21.5% of the examined vessels.Conclusion: DUS is an important exam in the identification of patients with symptomatic CAS. It can improve clinical practice and provide cost-effective management for CAS. Carotid DUS showed high specificity and sensitivity in the diagnosis of CAS, especially a severe degree of stenosis

Prediction of carotid artery plaque area based on parallel multi-gate attention capture model.

Cardiovascular disease (CVD) is a group of conditions involving the heart or blood vessels and is a leading cause of death and disability worldwide. Carotid artery plaque, as a key risk factor, is crucial for the early prevention and management of CVD. The purpose of this study is to combine clinical application and deep learning techniques to design a predictive model for the carotid artery plaque area. This model aims to identify individuals at high risk and reduce the incidence of cardiovascular disease through the implementation of relevant preventive measures. This study proposes an innovative multi-gate attention capture (MGAC) model that utilizes data such as risk factors, laboratory tests, and physical examinations to predict the area of carotid artery plaque. Experimental findings reveal the superior performance of the MGAC model, surpassing other commonly used deep learning models with the following metrics: mean absolute error of 4.17, root mean square error of 10.89, mean logarithmic squared error of 0.21, and coefficient of determination of 0.98.

Development and approval of a mobile test bench for the study of the mechanical properties of biological tissues

The determination of the mechanical properties of vessel walls and atherosclerotic plaques is a recurring issue in the numerical modelling of vessel sections. Testing machines are usually located in specialised laboratories outside medical facilities, and transporting samples from the clinic is difficult. Therefore, the task of developing mobile testing devices that can be installed directly in the clinic to perform tests immediately after surgery is relevant. This paper presents the results of the development and validation of a mobile test bench for performing mechanical experiments on uniaxial compression and tension of biological tissues. The purpose of the work is to perform mechanical tests on tissues in the clinic, avoiding their transport to the laboratory and/or freezing. Arduino UNO hardware platform is used as the control element of the test bench, which controls the main elements (motor, load cell), records data on SD card and displays information about the experiment on the computer screen. Structurally, the test bench is an analogue of a two-column testing machine. All mechanisms are assembled in a portable case, the control module is in the form of a remote plastic box. Verification of the test bench was carried out using an Instron 3342 universal testing machine with a 500 N load cell. A total of 121 soft tissue tests (including arterial wall and atherosclerotic plaque) were performed on the bench. The Young's modulus and ultimate strength values obtained are summarised in a table. The mean Young's modulus for the wall of the internal carotid artery was 0.32 ± 0.24 MPa, for soft plaque 0.30 ± 0.17 MPa, and for hard plaque 0.85 ± 0.39 MPa; a tensile strength of 1.12 ± 0.67 MPa was also determined for hard plaques in carotid arteries. The result is a unique database of tissue Young's moduli obtained from freshly collected material. The methodology and its implementation on the mobile test bench show good agreement with literature data.

Research on carotid artery plaque anomaly detection algorithm based on ultrasound images

Carotid artery plaque is a key factor in stroke and other cardiovascular diseases. Accurate detection and localization of carotid artery plaque are essential for early prevention and treatment of diseases. However, current carotid artery ultrasound image anomaly detection algorithms face several challenges, such as scarcity of anomaly data in carotid arteries and traditional convolutional neural networks (CNNs) overlooking long-distance dependencies in image processing. To address these issues, we propose an anomaly detection algorithm for carotid artery plaques based on ultrasound images. The algorithm innovatively introduces an anomaly sample pair generation method to increase dataset diversity. Moreover, it employs an improved adaptive recursive gating pyramid pooling module to extract image features. This module significantly enhances the model’s capacity for high-order spatial interactions and adaptive feature fusion, thereby greatly improving the neural network’s feature extraction ability. The algorithm uses a Sigmoid layer to map each pixel’s feature vector to a probability distribution between 0 and 1, and anomalies are detected through probability threshold binarization. Experimental results show that our algorithm’s AUROC index reached 90.7% on a carotid artery dataset, improving by 2.1% compared to the FPI method. This research is expected to provide robust support for the early prevention and treatment of cardiovascular diseases.

Application of machine learning algorithms in predicting carotid artery plaques using routine health assessments.

Cardiovascular diseases (CVD) constitute a grave global health challenge, engendering significant socio-economic repercussions. Carotid artery plaques (CAP) are critical determinants of CVD risk, and proactive screening can substantially mitigate the frequency of cardiovascular incidents. However, the unequal distribution of medical resources precludes many patients from accessing carotid ultrasound diagnostics. Machine learning (ML) offers an effective screening alternative, delivering accurate predictions without the need for advanced diagnostic equipment. This study aimed to construct ML models that utilize routine health assessments and blood biomarkers to forecast the onset of CAP. In this study, seven ML models, including LightGBM, LR, multi-layer perceptron (MLP), NBM, RF, SVM, and XGBoost, were used to construct the prediction model, and their performance in predicting the risk of CAP was compared. Data on health checkups and biochemical indicators were collected from 19,751 participants at the Beijing MJ Health Screening Center for model training and validation. Of these, 6,381 were diagnosed with CAP using carotid ultrasonography. In this study, 21 indicators were selected. The performance of the models was evaluated using the accuracy, sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), F1 score, and area under the curve (AUC) value. Among the seven ML models, the light gradient boosting machine (LightGBM) had the highest AUC value (85.4%). Moreover, age, systolic blood pressure (SBP), gender, low-density lipoprotein cholesterol (LDL-C), and total cholesterol (CHOL) were the top five predictors of carotid plaque formation. This study demonstrated the feasibility of predicting carotid plaque risk using ML algorithms. ML offers effective tools for improving public health monitoring and risk assessment, with the potential to improve primary care and community health by identifying high-risk individuals and enabling proactive healthcare measures and resource optimization.

Acute Vision Impairment Caused by Internal Carotid Artery Plaque Hemorrhage Combined With Thrombosis.

Atherosclerosis (As) is an important pathologic basis for ischemic cerebrovascular disease and easily causes stenosis of the origin of the internal carotid artery (ICA). As the main source of intracranial blood supply, the ICA accounts for 70% to 80% of blood flow. This stenosis can cause various ocular symptoms in patients. In the existing literature, it is rare to report cases with only acute vision loss caused by ICA plaque hemorrhage combined with thrombosis. The authors report a case of acute vision impairment caused by ICA plaque hemorrhage. The clinical manifestations, imaging characteristics, differential diagnosis, and treatment methods were discussed based on relevant literature, and the diagnosis and differentiation of the disease were considered to deepen the understanding of the disease.

Relationship between triglyceride-glucose index and carotid artery plaques in ischemic stroke patients: Based on blood pressure status, sex, and age

BackgroundNumerous studies have shown that the triglyceride-glucose (TyG) index is a reliable substitute marker for insulin resistance. Nevertheless, its correlation with carotid artery plaques (CAPs) among patients with ischemic stroke (IS) remains to be elucidated. Methods9248 IS patients hospitalized at the First Teaching Hospital of Tianjin University of Traditional Chinese Medicine were grouped according to the quartiles of TyG index. Patients were further stratified by blood pressure status, sex, age and hypertension control status. Employing logistic regression to examine the connection between the TyG index and CAPs.Additionally, analyzing the receiver operating characteristic (ROC) curve to evaluate the predictive value of the TyG index for CAPs. ResultsParticipants with an elevated TyG index had an increased prevalence of CAPs. The TyG index was positively correlated with CAPs (OR: 1.26, CI: 1.14-1.40, P<0.001). Compared with normal blood pressure and prehypertensive patients, the TyG index was markedly correlated with CAPs among hypertensive patients (OR: 1.29, 95% CI: 1.15-1.44, P<0.001). Females had a higher OR value than males(OR: 1.31, 95% CI: 1.11-1.54, P=0.001 versus OR: 1.24, 95% CI: 1.09-1.41, P=0.001). Older patients (>60 years) had a higher OR value than their middle-aged counterparts (≤60 years) (OR: 1.35; 95% CI: 1.16-1.58, P<0.001 versus OR: 1.20; 95% CI: 1.05-1.37, P=0.007). Patients with poorly-controlled hypertension had a higher OR value than patients with well-controlled hypertension(OR: 1.36; 95% CI: 1.14-1.63, P=0.001 versus OR: 1.24; 95% CI: 1.07-1.44, P=0.003). After adjusting for potential confounding factors, the area under the ROC curve (AUC) value in the overall population, sex-stratified group, hypertensive patients and hypertension control status-stratified group were all above 0.7 (P<0.01), demonstrating good forecasting capability. ConclusionsIn IS patients, the TyG index was significantly associated with CAPs. Additionally, this correlation was more pronounced in hypertensive patients, females, older individuals and patients with poorly-controlled hypertension.

Abstract P454: Screening of risk genes for carotid vulnerable plaque based on transcriptomics and experimental verification

Purpose and background: This study aims to conduct an in-depth analysis of human carotid atherosclerotic plaques using transcriptomic data to elucidate the relationship between hypoxia-related genes and the stability of carotid artery plaques and explore their connection with immune infiltration. Methods: Four GEO datasets (GSE21545, GSE24495, GSE159677, and GSE189300) were used. Initially, gene expression data from carotid artery plaque samples in GSE21545 and GSE24495 were analyzed. Hypoxia-related gene sets were obtained from MSigDB, and the "HALLMARK_HYPOXIA" gene set was explicitly selected. GSEA software was used for ultimately selecting CDKN1C and HAS1 as characteristic genes. Subsequently, sample clustering analysis was conducted to determin the optimal number of clusters. Gene set enrichment and differential analysis were performed. Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting experiments were conducted for preliminary validation of CDKN1C and HAS1 expression levels in ApoE knockout mice at 16 and 6 weeks. Subsequently, single-cell data from GSE159677 were processed to determine the differential localization of CDKN1C in carotid atherosclerotic plaques, with functional analysis conducted using GSE189300. Results: CDKN1C and HAS1 genes were found to exhibit differential expression in plaques and were correlated with hypoxia and immune scores. Clustering analysis revealed two main clusters, with patients in cluster A showing a higher risk of adverse events and a stronger association with immunity. Genes with a positive effect on atherosclerosis were highly expressed in poorer prognosis cluster A. Validation dataset GSE24495 also confirmed the grouping ability of CDKN1C and HAS1 genes, showing enrichment in atherosclerosis-related pathways. RT-qPCR and protein immunoblotting experiments demonstrated no significant differences in HAS1 expression levels, while CDKN1C showed lower protein expression in 16-week ApoE knockout mice compared to 6 weeks. Single-cell data from GSE159677 localized differential expression of CDKN1C in plaque cells. Finally, immunofluorescence validation confirmed the coexistence of CDKN1C and vascular smooth muscle cells. Conclusion: This study comprehensively analyzed transcriptomics data from carotid atherosclerotic plaques, revealing the significant roles of CDKN1C and HAS1 genes. Immunofluorescence validation further supported the crucial role of these genes in carotid atherosclerosis.