Carotid Artery Plaque Research Articles

Machine learning methods for adult OSAHS risk prediction

BackgroundObstructive sleep apnea hypopnea syndrome (OSAHS) is a common disease that can cause multiple organ damage in the whole body. Our aim was to use machine learning (ML) to build an independent polysomnography (PSG) model to analyze risk factors and predict OSAHS.Materials and methodsClinical data of 2064 snoring patients who underwent physical examination in the Health Management Center of the First Affiliated Hospital of Shanxi Medical University from July 2018 to July 2023 were retrospectively collected, involving 24 characteristic variables. Then they were randomly divided into training group and verification group according to the ratio of 7:3. By analyzing the importance of these features, it was concluded that LDL-C, Cr, common carotid artery plaque, A1c and BMI made major contributions to OSAHS. Moreover, five kinds of machine learning algorithm models such as logistic regression, support vector machine, Boosting, Random Forest and MLP were further established, and cross validation was used to adjust the model hyperparameters to determine the final prediction model. We compared the accuracy, Precision, Recall rate, F1-score and AUC indexes of the model, and finally obtained that MLP was the optimal model with an accuracy of 85.80%, Precision of 0.89, Recall of 0.75, F1-score of 0.82, and AUC of 0.938.ConclusionWe established the risk prediction model of OSAHS using ML method, and proved that the MLP model performed best among the five ML models. This predictive model helps to identify patients with OSAHS and provide early, personalized diagnosis and treatment options.

Relationship between Obesity Indices Measured with Body Composition Analyzer and Carotid Artery Plaques in Korean Middle-Aged Men

Relationship between Obesity Indices Measured with Body Composition Analyzer and Carotid Artery Plaques in Korean Middle-Aged Men

Effect of evolocumab on carotid plaque composition in asymptomatic carotid artery stenosis (EVOCAR-1) using magnetic resonance imaging

Background and AimsTo determine the effect of evolocumab treatment in patients with asymptomatic carotid artery stenosis ≥50 % on carotid plaque morphology and composition, as determined by magnetic resonance imaging. MethodsWe conducted a double-blind randomized controlled trial in patients with asymptomatic carotid artery plaque with ≥50 % stenosis and low-density lipoprotein-associated cholesterol (LDL-C) ≥1.8 mmol/L, despite standard lipid-lowering therapy, with 12 months of evolocumab or placebo injection every two weeks. The primary endpoint was the between group difference in the absolute change from baseline in carotid plaque lipid-rich necrotic core (LRNC), assessed by carotid magnetic resonance. ResultsDue to interrupted recruitment during the COVID-19 pandemic, 33 patients (36 % female) were randomised, which was less than the target of 52. Mean age was 68.7 years (SD, 8.5) and baseline LDL-C 2.4 mmol/L(SD, 0.7). LDL-C was reduced with evolocumab to 0.8 mmol/L (SD, 0.5) vs 2.2 mmol/L (SD, 0.7) with placebo at 3 months (between group absolute difference -1.3 mmol/L [95 % CI, -1.7 to -0.9], p < 0.001). Evolocumab treatment was associated with a favourable change in LRNC at 12 months of -16 mm3 (SD, 54) whereas the placebo group showed -4 mm3 (SD, 44). Between group differences did not show statistically significance with a placebo-adjusted LRNC change of -17 mm3 ([95 % CI, -45 to 12], p = 0.25). Percentage carotid plaque LRNC also numerically reduced at 12 months, however this did not reach statistical significance (-2.4 % vessel wall volume [95 % CI, -5.7 to 0.9], p = 0.16). ConclusionIntensive LDL-C lowering with the addition of evolocumab to maximally tolerated lipid-lowering therapy did not lead to a statistically significant change in vulnerable plaque phenotype characteristics in patients with asymptomatic carotid artery stenosis, but the study was underpowered due to under-recruitment in the context of the COVID-19 pandemic.

Leukemia inhibitory factor receptor inhibition reduces stenosis grade and total serum cholesterol levels in a mouse model for atherosclerosis

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Dutch Heart Foundation Atherosclerosis is characterized by the accumulation of lipids and immune cells in the arterial wall and it is the main underlying pathology causing cardiovascular diseases (CVD). Cytokines are involved in all stages of atherosclerosis and most cytokines contribute to disease progression. For instance, IL-6 cytokine family members, such as IL-6, oncostatin-M and cardiotrophin-1, are closely related to CVDs. However, the role of leukemia inhibitory factor (LIF), a member of the IL-6 cytokine family, and its receptor (LIFR) in atherosclerosis remains unknown. Therefore, the aim of this study is to assess the contribution of LIFR signaling to atherosclerosis development by systemically inhibiting LIFR in an atherosclerotic mouse model. First, the expression of LIF and LIFR was examined using single-cell RNA sequencing data of human carotid artery plaques. Mast cells highly and exclusively express LIF, whereas LIFR was specifically expressed by activated endothelial cells. To validate LIFR signaling in vivo, female western-type diet fed Ldlr-/- mice were treated with LIFR inhibitor EC359 (5 mg/kg s.c., n=15) or control solvent (n=15) three times per week for eight weeks. During the experiment, weights of the mice did not differ between groups, whereas total serum cholesterol levels were significantly reduced in EC359 treated mice (p=0.03). In particular, EC359 treatment reduced VLDL levels. Additionally, EC359 treatment significantly reduced Sr1, Abca1 and Lrp1 expression in the liver, suggesting an altered lipid metabolism in EC359 treated mice. Furthermore, LIFR inhibition affected innate immunity, both systemically and locally in the plaque. Neutrophil numbers were significantly increased in the circulation (ctrl 18.7±1.7%; EC359 28.0±2.0%; p=0.002) and aortic plaques (ctrl 3.9±0.8%; EC359 9.9±1.9%; p=0.003) of mice treated with EC359 compared to control mice. Moreover, LIFR inhibition affected circulating monocytes resulting in less inflammatory monocytes. The adaptive immune cells, such as T and B cells, remained largely unaffected. Collectively, the reduction of serum total cholesterol and increase in neutrophil numbers in EC359 treated mice resulted in a trend towards reduced atherosclerotic stenosis grade compared to control mice (39.8±1.4% versus 34.9±1.9%; p=0.054), but it did not affect plaque collagen and monocyte/macrophage content in the aortic root. Conclusively, LIFR signaling inhibition reduces atherosclerotic stenosis grade, lowers plasma total cholesterol levels and affects innate immunity.

Diagnostic potential of TSH to HDL cholesterol ratio in vulnerable carotid plaque identification.

This study aimed to investigate the predictive value of the thyroid-stimulating hormone to high-density lipoprotein cholesterol ratio (THR) in identifying specific vulnerable carotid artery plaques. In this retrospective analysis, we included 76 patients with carotid plaques who met the criteria for admission to Zhejiang Hospital from July 2019 to June 2021. High-resolution magnetic resonance imaging (HRMRI) and the MRI-PlaqueView vascular plaque imaging diagnostic system were utilized to analyze carotid artery images for the identification of specific plaque components, including the lipid core (LC), fibrous cap (FC), and intraplaque hemorrhage (IPH), and recording of the area percentage of LC and IPH, as well as the thickness of FC. Patients were categorized into stable plaque and vulnerable plaque groups based on diagnostic criteria for vulnerable plaques derived from imaging. Plaques were categorized based on meeting one of the following consensus criteria for vulnerability: lipid core area over 40% of total plaque area, fibrous cap thickness less than 65 um, or the presence of intraplaque hemorrhage. Plaques meeting the above criteria were designated as the LC-associated vulnerable plaque group, the IPH-associated group, and the FC-associated group. Multivariate logistic regression was employed to analyze the factors influencing carotid vulnerable plaques and specific vulnerable plaque components. Receiver operating characteristic (ROC) curves were used to assess the predictive value of serological indices for vulnerable carotid plaques. We found that THR (OR = 1.976; 95% CI = 1.094-3.570; p = 0.024) and TSH (OR = 1.939, 95% CI = 1.122-3.350, p = 0.018) contributed to the formation of vulnerable carotid plaques. THR exhibited an area under the curve (AUC) of 0.704 (95% CI = 0.588-0.803) (p = 0.003), and the AUC for TSH was 0.681 (95% CI = 0.564-0.783) (p = 0.008). THR was identified as an independent predictor of LC-associated vulnerable plaques (OR = 2.117, 95% CI = 1.064-4.212, p = 0.033), yielding an AUC of 0.815. THR also demonstrated diagnostic efficacy for LC-associated vulnerable plaques. This study substantiated that THR and TSH have predictive value for identifying vulnerable carotid plaques, with THR proving to be a more effective diagnostic indicator than TSH. THR also exhibited predictive value and specificity in the context of LC-associated vulnerable plaques. These findings suggest that THR may be a promising clinical indicator, outperforming TSH in detecting specific vulnerable carotid plaques.

Puerarin alleviates atherosclerosis via the inhibition of Prevotella copri and its trimethylamine production

ObjectivePuerarin (PU) is a natural compound that exhibits limited oral bioavailability but has shown promise in the treatment of atherosclerosis (AS). However, the precise mechanisms underlying its therapeutic effects remain...

Increased TMEM166 Level in Patients with Postoperative Stroke after Carotid Endarterectomy

Postoperative stroke is a challenging and potentially devastating complication after elective carotid endarterectomy (CEA). We previously demonstrated that transmembrane protein 166 (TMEM166) levels were directly related to neuronal damage after cerebral ischemia–reperfusion injury in rats. In this subsequent clinical study, we aimed to evaluate the prognostic value of TMEM166 in patients suffering from post-CEA strokes. Thirty-five patients undergoing uncomplicated elective CEA and 8 patients who suffered ischemic strokes after CEA were recruited. We evaluated the protein level and expression of TMEM166 in patients diagnosed with postoperative strokes and compared it to those in patients who underwent uncomplicated elective CEA. Blood samples and carotid artery plaques were collected and analyzed. High expressions of TMEM166 were detected by immunofluorescence staining and Western Blot in carotid artery plaques of all patients who underwent CEA. Furthermore, circulating TMEM166 concentrations were statistically higher in post-CEA stroke patients than in patients allocated to the control group. Mean plasma concentrations of inflammatory markers, including interleukin 6 (IL-6) and C-reactive protein (CRP), were also elevated in patients with postoperative strokes. Therefore, based on these findings, we hypothesize that elevated TMEM166 levels, accompanied by a strong inflammatory response, serve as a useful biomarker for risk assessment of postoperative stroke following CEA.

Impact of androgenic anabolic steroid use on cardiovascular and mental health in Danish recreational athletes: protocol for a nationwide cross-sectional cohort study as a part of the Fitness Doping in Denmark (FIDO-DK) study

IntroductionThe use of androgenic anabolic steroids (AASs) among recreational athletes is steadily increasing. However, knowledge regarding the potentially harmful effects of AAS primarily originates from case reports and small observational...

Abstract 2079: Single-cell And Spatially Resolved Transcriptome Analysis Reveals A Novel Lncrna Regulator Of Human Atherosclerosis

Cardiovascular diseases, such as atherosclerosis, are the major cause of death in Western societies. Still, molecular mechanisms of plaque destabilization remain unclear. Vascular Smooth Muscle Cells (VSMCs) are the most abundant cell type in atherosclerotic lesions. These cells keep their plasticity also with disease progression and are, therefore, an ideal target cell type for potential therapies. Long non-coding RNAs (lncRNAs) are one example of highly cell type- and disease-state-specific novel molecular modulators. We utilized combined total (bulk) RNA and single cell (sc) RNA sequencing of advanced human carotid artery lesions (patients who underwent carotid endarterectomy in our vascular surgery clinic) to discover novel regulators. Additionally, we performed hybridization-based RNA in situ sequencing (HybRISS, Xenium) to indicate where these genes are located within the plaques. We also performed scSeq in our inducible carotid artery plaque rupture mice ( ApoE-/- ). In vivo and in vitro modulation (KD; knock-down) of the newly identified lncRNA DLX6-AS1 ( D istal- L ess Homeobo x 6 A nti s ense 1 ) using Antisense LNA (Locked nucleic acid) GapmeRs is performed in this mouse model as well as in primary human VSMC culture. DLX6-AS1 shows a highly specific expression pattern in a distinct sub-cluster of VSMCs, as well as a striking location within human atherosclerotic lesions shown by spatial transcriptomics in advanced plaques. DLX6-AS1 is mainly expressed in the nucleus of cells, and KD of this lncRNA leads to changes in VSMC behavior in vitro and in vivo . The KD also has only little effect on the other genes of this locus, DLX6 and DLX5 ( D istal- L ess Homeobo x 6 and 5 ) We found Dlx6os1 ( D istal- l ess homeobo x 6, o pposite s trand 1 ) in our scRNA-seq dataset of the inducible carotid artery plaque rupture mice ( ApoE-/- ) where the KD leads to an increased plaque rupture rate. Taken together, our datasets, methods, and animal models demonstrate that utilizing bulk- and scRNA-seq data, together with spatially resolved sequencing methods, are powerful tools to identify and characterize novel lncRNA regulators that can facilitate fate decisions in VSMCs in atherosclerosis. DLX6-AS1 is one of these novel regulators and will be further analyzed in vivo and in vitro .

High-risk carotid artery plaque: the histological images and a review of the literature

High-risk carotid artery plaque: the histological images and a review of the literature

Deep learning-based fully automatic screening of carotid artery plaques in computed tomography angiography: a multicenter study

To develop and validate a deep learning (DL) algorithm for the automated detection and classification of carotid artery plaques (CAPs) on computed tomography angiography (CTA) images. This retrospective study enrolled 400 patients (300 in the Center Ⅰ and 100 in Ⅱ). Three radiologists co-labeled CAPs, and their revised calcification status (noncalcified, mixed, and calcified) was regarded as ground truth. Center Ⅰ patients were randomly divided into training and internal validation datasets, while Center Ⅱ patients served as the external validation dataset. Carotid artery regions were segmented using a modified 3D-UNet network, followed by CAPs detection and classification using a ResUNet-based architecture in a two-step DL system. The DL model's detection and classification performance were evaluated on the validation dataset using precision-recall curve, free-response receiver operating characteristic (fROC) curve, Cohen's kappa, and ROC curve analysis. The DL model had achieved 83.4% sensitivity at 3.0 false positives (FPs)/CTA scan in internal validation and 78.9% in external validation. F1-scores were 0.764 and 0.769 at the optimal threshold, and area under fROC curves were 0.756 and 0.738, respectively, indicating good overall accuracy for CAP detection. The DL model also showed good performance for the ternary classification of CAPs, with Cohen's kappa achieved 0.728 and 0.703 in both validation datasets. This study demonstrated the feasibility of using a fully automated DL-based algorithm for the detection and ternary classification of CAPs, which could be helpful for the workloads of radiologists.

Carotid artery ultrasonography and shear wave elastography in Takayasu's arteritis: a comparative analysis with diabetes mellitus.

Takayasu's arteritis (TAK) is a chronic inflammatory large vessel vasculitis with a grim prognosis due to the excessive risk for cardiovascular (CV) diseases. Its diagnosis relies on radiographic imaging and its differentiation particularly from atherosclerosis could be challenging. Hypothesising that vascular morphology observed in TAK would be comparable to that found in type 2 diabetes mellitus (T2DM), a prototype for advanced atherosclerosis, we compared two disease groups using carotid artery B mode US and shear wave elastography (SWE). A total of 72 patients with TAK (63F/9M; mean age: 42.7± 10.0 years) and 74 patients with T2DM (65F/9M; mean age: 50.2± 7.1 years) were studied. Intima-media thickness (IMT), outer diameter and arterial stiffness as assessed by SWE values were measured on the common carotid artery (CCA) and atherosclerotic plaques were recorded. Clinical characteristics, CV risk factors and previous history of CV diseases were determined. Framingham risk score was calculated. Patients with TAK exhibited significantly lower atherosclerotic risk but higher systolic blood pressure (BP) levels compared to those with T2DM. The mean values of CCA IMT, outer diameter, and stiffness were significantly elevated among patients with TAK compared to those with T2DM. Carotid artery plaques were evenly distributed between the study groups, but their anatomical localisation and composition differed significantly. While coronary artery disease (CAD) was more prevalent among T2DM patients, cerebrovascular diseases were more frequent among TAK patients. Our study revealed distinctive vascular alterations and atherosclerotic changes when compared to advanced atherosclerosis associated with T2DM. Apart from these, higher levels of systolic BP and significantly different distribution of CV diseases between TAK and T2DM also suggest that TAK should be handled with distinct assessment strategies than that employed in conventional atherosclerotic conditions.

Association of the trimethylamine N-oxide with cardiovascular risk and vascular alterations in middle-aged patients with risk factors for cardiovascular diseases.

Trimethylamine N-oxide (TMAO) is synthesized by the intestinal microbiota and is an independent predictor of cardiovascular disease (CVD). However, its underlying mechanisms remain unclear. We investigated TMAO levels across different CVD-risk patient groups, and evaluated associations between TMAO and vascular alterations (e.g., arterial stiffness, intima-media thickness [IMT], and the presence and grade of carotid artery plaques [CAPs]). We examined 95 patients (58.5 ± 7.3 years): 40 with clinical atherosclerotic cardiovascular disease (ASCVD), 40 with atherosclerosis risk factors (RF), and 15 controls. Arterial stiffness was measured by Carotid-Femoral Pulse Wave Velocity (C-F PWV). B-mode ultrasound was used to evaluate the presence and grade of CAPs and carotid IMT (CIMT). TMAO was measured by high performance liquid chromatography-tandem mass spectrometry (LC-MS/MS) and results were presented as the median (interquartile range). TMAO levels were higher in patients with ASCVD (251.5 [164.5] µg/l) when compared with patients with RFs (194.0 [174] µg/l, P=0.04) and controls (122.0 (77) µg/l, P<0.001). A significant correlation was observed between TMAO and PWV (r = 0.31, P=0.003), which was not confirmed after adjustment for RFs. TMAO levels were significantly correlated with plaque score (r = 0.46, P<0.001) and plaque height (r=0.41, P=0.003), and were independent predictors for grade III plaques (odds ratio [OR] = 1.002, confidence interval (CI) 95%: 1.000047-1.003, P=0.044). TMAO levels are increased with expanded CVD risk. Across different types of vascular damage, TMAO is associated with atherosclerotic changes.

Assessing radiation-induced carotid artery injury using ultrasound in patients with head and neck cancer

Background and purposeRadiotherapy (RT) can damage neck vessels in patients with head and neck cancer (HNC). This study investigated the early effects of RT on carotid artery, including the internal media thickness (IMT) and carotid plaques of the common carotid artery (CCA). Materials and methodsThis study included 69 patients with HNC who underwent RT at the First Hospital of Jilin University from March 2017 to September 2022, and 69 healthy participants as controls. Color Doppler ultrasound (CDUS) of the carotid artery was used to measure the CCA IMT and plaques. ResultsLeft CCA IMT increased from 0.60 mm (0.60, 0.70) before RT to 0.70 mm (0.60, 1.20) after RT (P < 0.0001). Right CCA IMT changed from 0.60 mm (0.60, 0.71) before RT to 0.60 mm (0.60, 1.10) after RT (P = 0.0002). CCA IMT was 0.60 mm (0.60, 0.70) and 0.80 mm (0.60, 1.20) in the ≤40 Gy and >40 Gy groups (P = 0.0004). The CCA plaques number increased significantly after RT on both the left and right sides (Pleft < 0.0001; Pright <0.0001). The CCA plaques volume increased from 0 mm3 (0, 11.35) and 0 mm3 (0, 8.55) before RT to 8.8 mm3 (0, 21.5) and 5.8 mm3 (0, 16.1) on the left and right sides. Correlation analysis revealed a correlation between CCA IMT and age (r = 0.283, P = 0.001), smoking status (r = 0.179, P = 0.020), and radiation dose (r = 0.188, P = 0.028). ConclusionRT significantly increased CCA IMT, and the growth was related to the radiation dose. The number and volume of the CCA plaques also increased after RT.

Does obstructive sleep apnea–induced intermittent hypoxia increase the incidence of solitary pulmonary nodules, thyroid nodules, and other disorders? A retrospective study based on 750 cardiovascular disease patients

BackgroundObstructive sleep apnea (OSA) has been shown to be an important risk factor for cardiovascular disease (CVD), and intermittent hypoxia is an important pathogenetic factor for it. In the clinic, it was found that most CVD patients combined with OSA were also combined with solitary pulmonary nodules (SPN) or thyroid nodules (TN). Are these disorders related to intermittent hypoxia? One study showed that intermittent hypoxia is a pathogenic factor for lung cancer in mice, but there have been no clinical reports. So we conducted a retrospective study to explore whether intermittent hypoxia caused by OSA increases the incidence of SPN, TN, and other disorders.MethodsWe selected 750 patients with cardiovascular disease (CVD), who were divided into the control group and the OSA group according to the result of portable sleep monitoring. Retrospectively analyzed the comorbidities that patients with OSA are prone to and explored the correlation between OSA and those comorbidities.ResultsThe incidence of SPN, TN, cervical spondylosis, and carotid-artery plaques was higher in the OSA group than in the control group. These diseases are significantly associated with OSA (p < 0.05), and their incidence increased with an elevated apnea–hypopnea index. After excluding interference from age, gender, BMI, smoking history, history of lung disease, and history of tumors, OSA showed a significant correlation with SPN. After excluding age, gender, BMI, and thyroid disease, OSA was associated with TN. Patients with comorbidities have lower nocturnal oxygen saturation and more extended periods of apnea. Logistic multiple regression results revealed that male, advanced age, obesity, CS, and nasal septum deviation were independent risk factors for OSA.ConclusionsPatients combined with OSA may further develop more comorbidities, such as SPN, TN, and carotid-artery plaques. It may be related to intermittent hypoxia caused by OSA.

Multiple techniques to evaluate the relationship between carotid artery plaque and acute stroke.

To evaluate the important characteristics of the plaque vulnerability using multimodal ultrasound imaging methods (2D, contrast-enhanced ultrasound, and elastography), and to explore the relationship between plaque and acute stroke. A total of 244 patients with carotid plaque were enrolled, including 104 patients with acute stroke ipsilateral to the plaque as the case group and 140 patients as the control group. All patients underwent conventional carotid ultrasound, contrast-enhanced ultrasound (CEUS) and elastography (SWE). The results of each examination were compared and analyzed, and the relationship between the results and the occurrence of stroke was discussed. In the acute stroke group, the men, with a history of alcohol consumption the direction of contrast media diffusion was higher than that in the control group, but the plaque gray value (GSM), maximum, average and minimum Young's elastic modulus imaging values (YM) were slightly lower than those in the control group (P < 0.05). Logistic regression analysis showed that waist to body ratio (WHtR), GSM, YM, neovascularization density and contrast diffusion direction were independent risk factors for predicting acute ischemic stroke. The influence degree of each factor from strong to weak was waist to body ratio, neovascularity density, GSM and YM, respectively. The area under the curve (AUC) for the diagnosis of acute ischemic stroke by regression model was 0.746. The combination of multiple ultrasound techniques to evaluate the vulnerability of carotid plaque and predict the occurrence of acute stroke provides valuable information for clinical decision making.

Matrix metallopeptidase 9 contributes to the beginning of plaque and is a potential biomarker for the early identification of atherosclerosis in asymptomatic patients with diabetes.

To determine the roles of matrix metallopeptidase-9 (MMP9) on human coronary artery smooth muscle cells (HCASMCs) in vitro, early beginning of atherosclerosis in vivo in diabetic mice, and drug naïve patients with diabetes. Active human MMP9 (act-hMMP9) was added to HCASMCs and the expressions of MCP-1, ICAM-1, and VCAM-1 were measured. Act-hMMP9 (n=16) or placebo (n=15) was administered to diabetic KK.Cg-Ay/J (KK) mice. Carotid artery inflammation and atherosclerosis measurements were made at 2 and 10 weeks after treatment. An observational study of newly diagnosed drug naïve patients with type 2 diabetes mellitus (T2DM n=234) and healthy matched controls (n=41) was performed and patients had ultrasound of carotid arteries and some had coronary computed tomography angiogram for the assessment of atherosclerosis. Serum MMP9 was measured and its correlation with carotid artery or coronary artery plaques was determined. In vitro, act-hMMP9 increased gene and protein expressions of MCP-1, ICAM-1, VCAM-1, and enhanced macrophage adhesion. Exogenous act-hMMP9 increased inflammation and initiated atherosclerosis in KK mice at 2 and 10 weeks: increased vessel wall thickness, lipid accumulation, and Galectin-3+ macrophage infiltration into the carotid arteries. In newly diagnosed T2DM patients, serum MMP9 correlated with carotid artery plaque size with a possible threshold cutoff point. In addition, serum MMP9 correlated with number of mixed plaques and grade of lumen stenosis in coronary arteries of patients with drug naïve T2DM. MMP9 may contribute to the initiation of atherosclerosis and may be a potential biomarker for the early identification of atherosclerosis in patients with diabetes. https://clinicaltrials.gov, identifier NCT04424706.

Intravascular lithotripsy to facilitate transcarotid artery revascularization in patients with heavily calcified carotid arteries

Transcarotid artery revascularization (TCAR) is an accepted and approved treatment for carotid artery stenosis in high-risk patients, and recently in standard risk patients under the guidelines of the recent CMS National Coverage Determination. However, it's applicability is limited by certain anatomic criteria, such as heavily calcified internal carotid arteries. We retrospectively reviewed two patients at our institution with heavily calcified internal carotid artery plaques who underwent intravascular lithotripsy and TCAR. These two cases demonstrate the feasibility of lithotripsy for modification of heavy, calcified plaque prior to TCAR for patients at high risk for carotid endarterectomy.

An integrated visual analytics system for studying clinical carotid artery plaques

An integrated visual analytics system for studying clinical carotid artery plaques

Risk factors and characteristics analysis of cognitive impairment in patients with cerebral infarction during recovery period

Objective To analyze the risk factors and characteristics of cognitive impairment in patients with cerebral infarction during the recovery period. Methods This retrospective case-control study included 183 patients with cerebral infarction in the recovery period. According to the MMSE score, they were divided into a cognitive impairment group of 79 cases and a cognitive normal group of 104 cases. Collect clinical data from all patients, including age, gender, body mass index, laboratory test results, past medical history, National Institute of Health Stroke Scale (NIHSS) score, modified Barthel index, Oxfordshire Community Stroke Project (OCSP) classification, and number of infarcted lesions. Multiple logistic regression analysis was used to identify risk factors related to cognitive impairment in patients with cerebral infarction. Result There were significant differences (p < 0.05) between the cognitive impairment group and the cognitive normal group in terms of age, body mass index, low-density lipoprotein level, NIHSS score, modified Barthel index, and number of infarcted lesions. Multivariate logistic regression analysis showed that age ≥ 65 years, stroke, carotid artery plaques, NIHSS score ≥ 5, anterior circulation infarction type, and multiple infarcted lesions were important risk factors for cognitive impairment. Conclusion Elderly age, presence of carotid artery plaques, high NIHSS score, multiple infarct lesions, and specific infarct types are important risk factors for cognitive dysfunction in patients during the recovery period of cerebral infarction.