Background: Peripheral artery disease (PAD) is an under-recognised manifestation of systemic atherosclerosis and vascular aging. Homocysteine has been associated with PAD, but whether it marks an independent pathway or a broader renal-toxicant and inflammatory-aging context remains clinically uncertain. Methods: We analysed NHANES 1999-2002 participants with serum homocysteine, ABI-defined PAD, DNA methylation biomarkers, and survey weights. Sequential survey-weighted models examined homocysteine as a log2-transformed exposure and hyperhomocysteinemia as homocysteine greater than 15 umol/L. Mechanistic-marker models evaluated GrimAge2 and PhenoAge epigenetic age acceleration, DNAm-predicted beta-2 microglobulin (B2M), measured serum B2M, cystatin C-based eGFR, blood lead, and blood cadmium. Findings: The main analytic sample included 2103 participants, including 190 PAD cases. The crude association between homocysteine and PAD was positive (OR per doubling, 2.64; 95% CI, 1.28-5.42; p=0.010), but was not supported after adjustment for demographic, clinical, one-carbon, metal, and renal measures (OR, 0.75; 95% CI, 0.28-2.02; p=0.503). Homocysteine remained associated with measured serum B2M (beta, 0.249; 95% CI, 0.106-0.392; p=0.005), and DNAm-predicted B2M was associated with PAD (OR per SD, 1.49; 95% CI, 1.09-2.03; p=0.020). Interpretation: These findings do not support homocysteine as a standalone PAD driver in this NHANES setting. They instead identify a B2M-related biological-aging signal embedded in a renal-toxicant vascular context, a pattern that requires prospective validation before clinical risk-stratification use.

SUMOylation plays critical roles in both initiation and development of atherosclerosis. SUMO-specific protease 3 (SENP3), a SUMO-specific protease that targets SUMO2/3 for deSUMOylation, is involved in vascular remodeling and the modulation of macrophage functions. Here, we probed for the role of SENP3 in macrophages in the development of atherosclerosis. Stable and unstable plaques were collected from patients with atherosclerosis. A macrophage-specific SENP3 knockout mouse (Senp3Mac-KO) was generated and performed for a murine atherosclerosis model. Transcriptional sequencing was performed to identify potential mechanisms. SENP3 expression in macrophages was increased in unstable plaques, compared to stable plaques. The mean fluorescence intensity of SENP3 in macrophages infiltrating carotid plaques was positively correlated with circulating pro-inflammatory cytokines, low density lipoprotein (LDL-C), and triglycerides in atherosclerosis patients. Senp3Mac-KO mice exhibited a markedly reduced atherosclerotic plaque area in the aorta, compared to wild-type mice. Knockdown of SENP3 in macrophages resulted in decreased secretion of pro-inflammatory cytokines, increased secretion of anti-inflammatory factors, and reduced foam cell formation. Transcriptional analysis identified significant enrichment in Toll-like receptor (TLR4) signaling pathway modulated by SENP3. Genetic deletion of either TLR4 (Tlr4-/-) or Sterol O-Acyltransferase 2 (SOAT2) (Soat2-/-) attenuated the exacerbation of atherosclerosis development induced by SENP3 overexpression. Furthermore, SENP3 regulated TLR4 and SOAT2 expression indirectly via the transcription factor MYC rather than through direct deSUMOylation of TLR4 or SOAT2 themselves. Downregulation of SENP3 in macrophages suppresses pro-inflammatory cytokine release by inhibiting TLR4 signaling and reduces foam cell formation by impeding SOAT2 expression, both mediated by the transcription factor MYC, thereby attenuating the development of atherosclerosis. Hence, SENP3 may represent a potential therapeutic target in atherosclerosis.

Background and purpose: The global burden of peripheral artery disease (PAD) attributable to high fasting plasma glucose (HFG) has not been comprehensively characterized. This study aimed to quantify the global deaths and disability-adjusted life years (DALYs) of PAD attributable to HFG and to project their trends through 2036.Methods: Data on PAD-related deaths and DALYs were obtained from the Global Burden of Disease 2021 Study. Temporal trends were evaluated using estimated annual percentage change (EAPC) and age-period-cohort (APC) models, while future projections were derived from a Bayesian (Bayesian APC) model. Cross-national inequalities were assessed in relation to the sociodemographic index (SDI). All analyses were performed in 2024.Results: Globally, from 1990 to 2021, the overall age-standardized mortality rate (ASMRs) and DALY rate (age-standardized disability rates [ASDRs]) for all-cause PAD decreased by 35.9% and 30.1%, respectively. However, the ASMRs and ASDRs for PAD specifically attributable to HFG increased by 15.3% (95% uncertainty interval [95% UI]: 6.6-24.7) and 20.0% (95% UI: 11.9-29.1). This rise was more pronounced in women, with increases of 15.9% (95% UI: 5.0-26.9) in ASMRs and 21.9% (95% UI: 13.2-31.5) in ASDRs, compared to 12.5% (95% UI: 2.0-24.4) and 17.1% (95% UI: 7.3-27.2) in men, respectively. In 2021, HFG was responsible for 67,744 (95% UI: 59,937-74,257) PAD-related deaths and 1,558,243 (95% UI: 1,266,999-2,045,869) DALYs. Absolute inequality (slope index of inequality) in PAD burden widened over time, with the burden disproportionately concentrated in low- and middle-SDI countries. Projections to 2036 indicate a continued increase in the HFG-attributable PAD burden among women, while a slight decline is projected for men.Conclusions: The global burden of PAD is increasingly driven by HFG, with a disproportionate and growing impact on women and populations in low- and middle-SDI countries. Our findings underscore an urgent need for targeted public health policies that address gender and socioeconomic disparities. Implementing evidence-based interventions focused on glycemic control is critical to mitigating the rising global burden of HFG-attributable PAD.

Although hydrophobic drugs demonstrate the promising therapeutic efficacy for peripheral artery disease in vitro, their in vivo performance is often hindered by low bioavailability due to inherent hydrophobicity. To address this, an injectable, self-healing and curcumin-sustained-release hydrogel (CGP hydrogel) using a gelatin/polyvinyl alcohol hydrogel (GP hydrogel) was developed. The CGP hydrogel effectively preserved the DPPH radical-scavenging activity of curcumin at room temperature. Meanwhile, in the murine hindlimb ischemia model, a single intramuscular injection of CGP following femoral artery ligation significantly improved the motor function of the ischemic limb compared to curcumin suspension. This superior therapeutic outcome is attributed to the sustained release of curcumin from the CGP hydrogel. Mechanistically, we found that CGP, but not GP, inhibited the expression of Atp6v0d2 in ischemic skeletal muscle cells and suppressed ischemia-induced autophagy. The inhibition of autophagy may mitigate tissue and cellular necrosis and promote the expression of Myogenin. Furthermore, CGP reduced the expression of pro-fibrotic factors such as Tgfb1 and Ctgf and prevented skeletal muscle fibrosis. In summary, the CGP hydrogel, through its sustained release of curcumin, inhibits ischemia-induced autophagy, alleviates necrosis and fibrosis in skeletal muscle tissue and preserves motor function in the ischemic limb.

Carotid plaque vulnerability drives ischemic stroke, yet preoperative assessment remains imprecise. A retrospective multi-center study was conducted using carotid CT angiography (CTA) datasets with pathology-validated carotid endarterectomy cases for radiomics analysis and an independently annotated CTA dataset for image-based deep learning. Radiomic features were screened using ANOVA–Kruskal–Wallis analysis, correlation filtering, and LASSO followed by development of Random Forest, Support Vector Machine, k-Nearest Neighbor, Naïve Bayes and Logistic Regression models. Image-based models included MLP, CNN and ImageNet-pretrained VGG16, VGG19, and ResNet50. Model performance was evaluated using ROC/AUC, calibration analysis and external validation. The main cohort comprised 260 consecutive CEA patients (200 for model development/internal validation and 60 for external validation), while an independent annotated CTA dataset of 236 cases (7394 ROIs) was used for image-based deep learning. On the internal test set, radiomics achieved AUCs of 0.858 (RF), 0.857 (SVM), 0.855 (Naïve Bayes), 0.843 (KNN) and 0.821 (Logistic Regression) with small train–test gaps. External validation confirmed comparable discrimination: SVM 0.839, Logistic Regression 0.835, KNN 0.830, Naïve Bayes 0.817, Random Forest 0.817; calibration curves showed close predicted–observed agreement. Image models reached test AUCs of 0.767 (VGG16), 0.754 (ResNet50), 0.718 (VGG19), 0.669 (MLP) and 0.654 (CNN); external AUCs were 0.776, 0.751, 0.719, 0.684, and 0.687, respectively. Grad-CAM localized hyperattenuating regions consistent with pathology, most clearly for VGG16/ResNet50. Radiomics classifiers particularly SVM/Logistic Regression and transfer-learning backbones (VGG16/ResNet50) offer reproducible plaque stability prediction from CTA with good calibration and external generalizability, supporting their potential use in stroke risk stratification. This framework may aid in preoperative risk stratification and guide surgical decision-making.

Atherosclerosis is respectively correlated with interleukin-6/interleukin-6 receptor (IL6/IL6R) mediated inflammation signaling and macrophages ferroptosis. Nonetheless, the underlying mechanism of IL6/IL6R signaling mediated macrophages ferroptosis in atherosclerosis remains unknown. This study aims to investigate whether IL6/IL6R signaling mediated macrophages ferroptosis through mitochondrial fragmentation and mitophagy impairment. Two human atherosclerotic transcriptomic datasets were used to conduct bioinformatic analysis. In vitro, counting kit-8 (CCK-8) assays, flow cytometry, immunofluorescence staining, malondialdehyde (MDA) and glutathione (GSH) assay kits were employed to evaluate reactive oxygen species (ROS) levels and macrophages ferroptosis. Transmission electron microscopy (TEM), laser confocal microscope and seahorse experiments were used to evaluate changes of mitochondrial morphology and mitochondrial function. Western blotting (WB) was used to quantify key markers of mitophagy and ferroptosis. In vivo, histological stainings and WB were used to determine the effects of IL6R deficiency on atherosclerosis, mitophagy and ferroptosis. Integrated bioinformatic analysis revealed that the IL6 expression could stratify early and advanced plaques. IL6 induced macrophages ferroptosis by increasing ROS and MDA levels, depleting GSH level, promoting lipid peroxidation and suppressing glutathione peroxidase 4 (GPX4) expression. Dynamin-related protein 1 (Drp1) mediated excessive mitochondrial fragmentation in IL6-induced macrophages, resulting in more shortened mitochondria, impaired oxidative phosphorylation (OXPHOS) and ROS accumulation. Activation of mitophagy, the process of mitochondrial fragmentation clearance, could increase GPX4 expression and attenuate the lipid peroxidation level in IL6 induced macrophages. Aggravation of ferroptosis further compromised mitophagy-related proteins expression. Targeting IL6R signaling attenuated atherosclerotic burden in ApoE−/− mice, mitigated mitochondrial fragmentation, suppressed macrophages ferroptosis and promoted mitophagy. In atherosclerosis progression, IL6/IL6R signaling induces susceptibility of macrophages to ferroptosis by exacerbating mitochondrial fragmentation and impairing mitophagy. Ferroptosis further aggravates mitophagy impairment, contributing to a detrimental cycle. Our study supports the rationale of anti-IL6/IL6R signaling interventions in atherosclerosis therapy. IL6 causes macrophages ferroptosis through excessive ROS accumulation, lipid peroxidation and suppressed GPX4 expression. IL6/IL6R signaling induces the activation of p-Drp1Ser616 resulting in mitochondrial fragmentation and mitochondrial dysfunction. Defective mitophagy sensitizes IL6-induced macrophages to ferroptosis and and ferroptosis further aggravates mitophagy impairment, contributing to a detrimental cycle. IL6R deficiency attenuates atherosclerotic plaques by mitigating mitochondrial fragmentation, suppressing macrophages ferroptosis and activating mitophagy in vivo.

PURPOSE:To compare the periprocedural and 5-year outcomes between patients with very severe stenosis (80%-99% stenosis) and those with carotid near occlusion (CNO) with full collapse. MATERIALS AND METHODS:Data from patients with very severe stenosis and CNO with full collapse who underwent carotid artery stent (CAS) placement at a single center were retrospectively analyzed from January 2018 to December 2021. Unmatched and propensity score-matched (PSM) comparisons of periprocedural adverse events and 5-year follow-up rates for in-stent restenosis, ipsilateral ischemic stroke, myocardial infarction, and mortality were conducted between the 2 groups. RESULTS:A total of 555 patients (481 patients in the very severe stenosis group and 74 in the CNO with full collapse group) were included. PSM resulted in 61 patients from the CNO group being matched with 183 from the severe stenosis control group. The periprocedural adverse events did not differ significantly between the 2 groups after PSM. The 5-year follow-up results demonstrated no significant differences in outcomes between the 2 groups. Kaplan-Meier curves showed that the 5-year rate of freedom from stroke was 89% (CNO group) versus 92% (control group; P = .500). The 5-year rate of freedom from in-stent restenosis was 89% (CNO group) versus 91% (control group; P = .630), while that from death, myocardial infarction, and stroke incidence was 84% (CNO group) versus 87% (control group; P = .430). CONCLUSIONS:CNO with full collapse showed long-term outcomes comparable with those of very severe carotid stenosis following CAS placement.

BackgroundCarotid artery stenosis (CAS) is a common vascular condition that can impair retinal and optic nerve blood supply, leading to ocular ischemic damage. Optical coherence tomography angiography (OCTA) provides a non-invasive method to evaluate retinal microcirculation and detect vascular changes in CAS patients.MethodsThis study utilized OCTA to evaluate changes in retinal microcirculation in CAS patients before and after carotid artery angioplasty and stenting. A 6 × 6 mm OCTA scan was performed to analyze deep retinal vascular complex (DVC) blood flow density, foveal avascular zone area (FAZA), foveal density within a 300 μm-wide ring surrounding the FAZ (FD-300), and radial peripapillary capillary vessel density (RPC-VD). Additionally, ultra-wide-field OCTA imaging (24 × 20 mm) was employed to comprehensively assess perfusion in both the posterior pole and peripheral retina.ResultsFollowing carotid artery angioplasty and stenting, significant improvements were observed in the ipsilateral eye, including increased macular blood flow density (p = 0.004), FD-300 (p = 0.031), RPC-VD (p = 0.028) and decreased FAZA (p = 0.018) in the deep retinal vascular layer, indicating enhanced retinal microcirculation. No statistically significant changes were found in the contralateral eye. In some cases, ultra-wide-field OCTA revealed a reduction in macular non-perfusion areas in the ipsilateral eye, alongside an increase in non-perfusion areas near the vascular arcades.ConclusionCarotid artery angioplasty and stenting effectively improves retinal microcirculation in CAS patients, as evidenced by increased blood flow density and reduced non-perfusion areas in the ipsilateral eye. OCTA is a valuable non-invasive tool for assessing retinal circulation dynamics, identifying microvascular abnormalities, and monitoring treatment efficacy in CAS patients.

To investigate whether the number of superficial calcification clusters in target carotid plaque influences the prognosis of patients undergoing carotid artery stenting (CAS) by altering intraplaque stress distribution. Patients receiving CAS and occurring major adverse cardiovascular events (MACEs) more than 30 days after discharge during follow-up were screened from the carotid stenosis database. These were matched 1:2 with controls based on age, sex, BMI, symptom status, alcohol abuse, smoking history, and > 3 superficial calcification clusters in the target plaque. Finite element analysis simulated intraplaque stress distribution during balloon inflation and revealed significantly elevated intraplaque maximum principal stress in patients with numerous superficial calcification clusters. Subsequent analysis of all 42 patients in the case-control study using Conditional logistic regression demonstrated that maximum principal stress at the superficial calcification-tissue interface (PSSCT) > 110 kPa was significantly associated with MACEs [P = 0.0429; odds ratio (OR) = 5.31; 95% confidence interval (CI): 1.05–26.8]. Finally, analysis of maximum PSSCT in target plaques containing varying numbers of superficial calcification clusters revealed that plaques with more superficial calcification clusters exhibited an increased probability of developing elevated maximum PSSCT. Therefore, elevated maximum PSSCT is significantly associated with MACEs in patients receiving CAS, representing a likely mediating pathway through which the number of superficial calcification cluster influences long-term prognosis after CAS.

Background The role of calcification in carotid atherosclerosis before and after carotid artery stenting (CAS) is contradictory. This study assessed the relationship between the extent of calcification in target carotid plaque and the prognosis of patients with carotid stenosis undergoing carotid artery stenting. Methods A total of 293 subjects with carotid stenosis after CAS were consecutively and retrospectively recorded in this cohort. All subjects underwent outpatient and telephone follow-up using major adverse cardiovascular event (MACE). Finally, 211 subjects who completed 2-year follow-up were included. χ2 test, Student’s t-test and Wilcoxon test was used between MACE and no-MACE groups. Cox proportional hazard models were used to figure out the risk factor of calcification characteristics. Result Over a median follow-up period of 1.92 years, 14 composite endpoints were recorded. The symptom status (P = 0.0116), abuse of alcohol (P = 0.0091), the amount of total calcification clusters (P = 0.0428) and superficial calcification clusters (P = 0.0022) showed statistics significance in univariable Cox models. After adjusting for demographic characteristics and surgical-related factors, the amount of superficial calcification clusters maintained its statistical significance [P = 0.0232, hazard ratio (HR) = 1.694, 95% CI (confidence interval): 1.0744–2.6720]. Conclusion The present study established that the amount of superficial calcification clusters independently serves as a prognostic risk factor in patients with carotid atherosclerosis underwent carotid artery stenting.

BackgroundThoracic aortic dissection (TAD) is one of the most fatal cardiovascular diseases. One of its important pathological characteristics is the local inflammatory response. Many studies have found that Macrophage polarization plays an extremely critical role in the inflammatory progression and tissue remodeling of TAD. Costunolide (CTD) has an improving effect on oxidative stress and inflammation in the body. However, whether it can promote the integrity of extracellular matrix in Aortic dissection and its mechanism are still unclear.MethodsThe male C57BL/6J mice were used to construct an animal model of TAD with β-aminopropionitrile (BAPN) (100 mg/kg/day, lasting for 28 days), and then CTD (10 mg/kg or 100 mg/kg) was injected intraperitoneally for 28 days to check the survival rate, TAD incidence, aortic morphology and other indicators of the mice. Using hematoxylin-eosin (HE), Masson, Elastin van Gieson (EVG) staining, immunofluorescence (IF), and immunohistochemical staining, the study aimed to determine the therapeutic effects of CTD on an animal model with BAPN-induced TAD. To enhance the examination of the regulatory mechanism of CTD, we conducted transcriptome sequencing on arterial tissues of mice in both the BAPN group and the BAPN + CTD100 group. Next, ANG II were used to construct TAD model in vascular smooth muscle cells (VMSCs). The effects of CTD on the proliferation, migration, invasion, and apoptosis of ANG II-induced cells are to be detected. The expression of MMP2, MMP9, P65, and p-P65 in each group will be examined using Western blot. Finally, the overexpression of IκB kinaseβ (IKKβ) will be established in VMSCs cells to further explore the protective function of CTD.ResultsThe result showed that CTD significantly inhibited BAPN induced mortality and TAD incidence in the animal model, improved aortic vascular morphology, promoted the integrity of extracellular matrix in TAD, reduced tissue inflammation, reduced the accumulation of M1 macrophage, promoted M2 macrophage polarization, and reduced the expression of NF-κB pathway related proteins. Mechanistically, CTD significantly weakened the proliferation, migration, invasion, and apoptosis. p-P65 protein expression of TAD cells were induced by ANG II and IKK-β.ConclusionCTD has the potential to alleviate inflammation, VSMC apoptosis, MMP2/9 levels, and enhance extracellular matrix integrity in TAD by inhibiting the NF-κB signaling pathway.

Background: There is currently no consensus regarding the optimal perioperative antiplatelet strategy for carotid artery surgery. This multicentre study aimed to analyse the association between preoperative aspirin monotherapy following postoperative dual antiplatelet therapy (DAPT) and the risk for stroke and death after carotid endarterectomy (CEA). Methods: This cohort study included 821 patients with carotid artery stenosis who underwent CEA. Primary outcomes included any stroke or death up to the one-month postoperative follow-up. Multilevel multivariate regression analyses and descriptive statistics were performed. Results: Patients were predominantly male (53 %), with a mean age of 66.2 years. The primary outcome occurred in 1.6 % of patients. Univariate and multivariate analyses revealed that patients with chronic obstructive pulmonary disease (COPD) exhibited a high risk for stroke or death (P = 0.011). The occurrence of any local complications in the neck was accompanied by an increase in diastolic blood pressure (DBP) (P = 0.007). Patients with a high systolic blood pressure (SBP) (P = 0.002) experienced a longer operative duration. The length of hospital stay was longer in the patients with COPD (P = 0.020), minor stroke (P = 0.011), and major stroke (P = 0.001). A positive linear correlation was found between SBP and operative duration in the overall population (β 0.4 [95 % confidence interval (CI) 0.1–0.7]; P = 0.002). The resultant curve for DBP and any local complications in the neck exhibited a two-stage change and one breakpoint in the entire population (k = 68 mmHg, <68; odds ratio [OR] 0.9 [95 % CI 0.7–1.1], P = 0.461; ≥68: OR 1.1 [95 % CI 1.0–1.1], P = 0.003). Conclusions: Preoperative aspirin monotherapy and postoperative DAPT were safe and effective antiplatelet treatments for patients who underwent CEA.

BackgroundCarotid body tumor (CBT) is the most common head and neck paraganglioma. Whether preoperative embolization benefits CBT patients who will receive surgical resection is still controversial.MethodsIn this multi-center retrospective study, we collected data from patients with CBT who received surgical treatment without (group A) or with preoperative embolization (group B) from 2011 to 2019. The primary outcome was the rate of death or stroke after 3 years of follow-up. The secondary outcomes of the study were length of operation (LOO), intraoperative blood loss (IBL), length of stay (LOS), rate of recurrence, and rate of cranial nerve (CN) injuries. Descriptive statistics were used to analyze the demographics, clinical characteristics, complications, and follow-up results of the patients.ResultsBetween January 2011 and October 2019, 261 consecutive patients (107 male and 154 female) entered analysis. After 3 years of follow-up, no patient died in both groups. Only three patients with stroke were detected: 2/226 (0.9%) in group A vs. 1/35 (2.9%) in group B (p = .308). The LOO in group A was 132.6 ± 64.6 min compared with 152.9 ± 40.4 min in group B (p = .072). IBL in group A was 375.4 ± 497.8 ml compared with 448.0 ± 270.8 ml in group B (p = .400). LOS in group A was 8.3 ± 2.0 days compared with 7.4 ± 1.7 days in group B (p = .016). Seventy-two CN injuries were detected: 65/226 (28.8%) in group A vs. 7/35 (20.0%) in group B (p = .281). There were 65 temporary CN injuries (59 in group A vs. 6 in group B) (p = .254) and seven permanent CN injuries (6 in group A vs. 1 in group B) (p = .945). Three most frequently injured cranial nerves were the pharyngeal branch and superior laryngeal nerve (12.3%), recurrent laryngeal nerve (7.7%) and vagus nerve (7.3%).ConclusionThere was insufficient evidence to support the efficacy of preoperative embolization. CBT resection alone had a similar rate of stoke, recurrence, and CN injuries when compared with CBT resection with preoperative arterial embolization. Meanwhile, CBT resection alone did not increase LOO and IBL.

Thrombotic complications pose serious health risks worldwide. A significant change in our understanding of the pathophysiology of thrombosis has occurred since the discovery of extracellular traps (ETs) and their prothrombotic properties. As a result of immune cells decondensing chromatin into extracellular fibers, ETs promote thrombus formation by acting as a scaffold that activates platelets and coagulates them. The involvement of ETs in thrombosis has been reported in various thrombotic conditions including deep vein thrombosis (DVT), pulmonary emboli, acute myocardial infarction, aucte ischemic stroke, and abdominal aortic aneurysms. This review summarizes the existing evidence of ETs in human and animal model thrombi. The authors described studies showing the existence of ETs in venous or arterial thrombi. In addition, we studied potential novel therapeutic opportunities related to the resolution or prevention of thrombosis by targeting ETs.

随着医疗技术的不断发展，微创技术，包括腔镜和辅助机器人，在临床外科领域的应用已愈加广泛，被越来越多的医生所认可，也被诸多患者接受和推崇。然而，目前血管外科仅部分开放手术可以实现机器人辅助，而辅助血管腔内手术虽有报道但并不成熟。本综述旨在总结机器人系统在血管外科的应用与研究进展。

Objective:To evaluate the safety and efficacy of carotid artery stenting (CAS) in the treatment of non-circumferential severe calcification using the distal embolic protection device.Methods:Clinical data of patients with severe calcification lesions in cervical carotid artery treated by CAS from Jan 2018 to Dec 2020 at our center was analyzed retrospectively.Results:226 consecutively admitted patients of cervical carotid artery stenosis and non-circumferential severe calcification (CR>270°) underwent CAS using the distal embolic protection device. The technical success rate was 90.26%. No death or myocardial infarction occurred during the perioperative period. Two patients had ipsilateral hemiparesis ischemic stroke during post-dilatation. The incidence of perioperative bradycardia/hypotension was 25.34%. Patients were followed up for 6-36 months, with median follow-up period of 17.3 months. The incidence of mild or moderate in-stent restenosis (<70%) was 16.59%, and the incidence of severe in-stent restenosis or occlusion (>70%) was 3.22%.Conclusions:For carotid artery stenosis with non-circumferential severe calcification in high risk for CEA patients, carotid artery stenting is safe and effective with the aggressive pre-dilation strategies, strict stent selections and implantation standards. The incidence of perioperative death, myocardial infarction or ipsilateral hemiparesis ischemic stroke was low. The patency rate of the carotid stent in the calcification lesion is satisfactory during the mid-term follow-up.

Objective:To investigate the effect of diabetes on the occurrence of stroke and death after carotid endarterectomy.Methods:According to the inclusion and exclusion criteria, 795 patients who were diagnosed with carotid stenosis and underwent carotid endarterectomy from January 2017 to January 2019 were included in 3 centers, Zhongshan Hospital affiliated to Fudan University, Changhai Hospital affiliated to Naval Medical University, and the Shanghai Seventh People's Hospital affiliated to Shanghai University of Traditional Chinese Medicine. The patients were divided into diabetes mellitus (DM) group (n=215) and non-diabetes mellitus (NDM) group (n=580) according to whether they had diabetes. The clinical data of patients were collected and analyzed with univariate, multivariate, and survival analysis of stroke and death events 30 days after operation and within 3 years of follow-up. Logistic regression analysis was used for univariate analysis of categorical outcome variables. Cox regression equation was used for multivariate analysis, and survival curves were plotted by using the Kaplan-Meier method.Results:The success rate of CEA surgery is 100%. The incidence of adverse events at 30 days after surgery showed: stroke and death in 4 cases (0.5%), serious stroke and death in 3 cases (0.4%), stroke and TIA in 7 cases (0.9%), and no patient died. Adverse events at 3-year follow-up showed: 13 (1.6%) stroke and death, 6 (0.8%) serious stroke and death, 15 (1.9%) stroke or TIA, and 1 patient died (0.1%). The univariate and multivariate results of stroke and death 30 days after surgery did not significantly associated risk factors. The results of univariate analysis of adverse events during the 3-year postoperative follow-up showed that chronic obstructive pulmonary disease was a high risk factor for stroke or death after CEA (HR=13.8, 95%CI: 1.8-106.0, P=0.011). Multivariate analysis after adjusting for variables showed that age (HR: 1.0; 95%CI: 0.9-1.0; P=0.034), previous alcohol consumption (HR: 13.1; 95%CI: 1.7-100.3; P=0.013), and chronic Obstructive pulmonary disease (HR: 13.1; 95%CI: 1.7-100.3; P=0.013) were independent risk factor for stroke or death after CEA. The results of 3-year follow-up survival analysis showed that the 1-year, 2-year and 3-year survival rates of DM group were 99.5%, 99.0% and 98.3%; And that in the NDM group were 99.5%, 99.5% and 97.7%, respectively.Conclusion:The risk of stroke and death after CEA in patients with carotid artery stenosis in the diabetic group was higher than that in the non-diabetic group, but there was no significant correlation between diabetes and the occurrence of stroke and death within 3 years after CEA.

BackgroundInflammation plays an important role in the progression of sporadic aortic dissection (AD). Immune cells, especially macrophages, infiltrate the aorta and secrete inflammatory cytokines and matrix metalloproteinases to cause degradation of the extracellular matrix, thereby contributing to the pathogenesis of AD. However, the cellular heterogeneity within these immune cells has not been fully characterized.MethodsWe used single-cell RNA sequencing to profile the transcriptomes of all immune cells in AD tissue and normal aorta. Using magnetic-activated cell sorting gating on CD45, we obtained a higher resolution identification of the immune cell subsets in the aorta.ResultsWe observed significant differences in the proportion of major immune cell subpopulations between AD and normal aorta tissues. Macrophages accounted for a higher percentage in the normal aorta, while the proportions of T cells, B cells and natural killer (NK) cells were all increased in AD tissues. Macrophage clusters that expanded in AD tissues originated primarily from circulating monocytes and expressed genes encoding proinflammatory cytokines and molecules involved in tissue repair. T and NK cells in AD tissues exhibited enhanced cytotoxic properties. A cluster of CD4+ T cells that had expanded in AD tissues was Th17-like and might contribute to the pathogenesis of AD. Cell–cell interaction analysis highlighted the increased communication between macrophages and T cells, which primarily regulated the costimulation of T cells.ConclusionsOur study provides a comprehensive characterization of immune cells in the dissected aorta with an emphasis on the role of macrophages and T cells. The information from our study improves our understanding of immune mechanisms in AD formation and helps to identify additional useful targets for early diagnosis or therapy of AD.

Background: The purpose of this study was to identify the independent risk factors for ipsilateral new ischemic lesions (NILs) during carotid artery stenting (CAS). Methods: In patients treated with CAS, the association between postoperative ipsilateral NILs on diffusion-weighted imaging (DWI) and patient demographics, intraoperative factors, the presence of plaque components, the semiquantitative grading of component size on multicontrast magnetic resonance imaging (MRI) were retrospectively analyzed. Results: Ipsilateral NILs on DWI were detected in 85 (39.2%) patients. The debris was observed on the surface embolic protection devices in 70.97% of patients. Univariate analysis showed that different stages of intraplaque hemorrhage (IPH) (along with lipid-rich necrotic core [LRNC]) ( P < 0.001), size of IPH ( P < 0.001), calcification (CA) ( P = 0.045), and LRNC (without IPH) ( P < 0.001) as well as postdilation ( P < 0.001)), stent type ( P = 0.001), and aortic arch ulcer ( P = 0.004) were associated with postoperative ipsilateral NILs. Multivariate logistic regression analysis showed that the acute and recent IPH (along with LRNC) (odds ratio [OR]: 5.77, P < 0.002 and OR: 28.66, P < 0.001, respectively), LRNC size in Grade 2 (OR: 6.10, P < 0.001) were independent risk factors for ipsilateral NILs. Aortic arch ulcer (OR: 3.44, P = 0.002), postdilation (OR: 4.72, P = 0.04) and open cell stent (OR: 2.88, P < 0.016) were also significantly related to ipsilateral NILs on DWI after CAS. There was a significant correlation between IPH at different stages and their grade of size (correlation coefficient: 0.89; P < 0.001). Conclusion: The IPH and larger LRNC along with the aortic arch ulcer, postdilation and open cell stent are associated with increased risk of ipsilateral NILs on DWI after CAS procedure. Preoperative staging of IPH and semiquantitative grading of size of plaque components based on multi-contrast MRI may be useful for predicting ipsilateral cerebral ischemic events after CAS.