OBJECTIVE:Stent graft induced aortic intimo-intimal intussusception (SAoII) during thoracic endovascular aortic repair (TEVAR) of type B aortic dissection (TBAD) is a rare complication. This study aimed to report reliable imaging features of SAoII to avoid such a potentially catastrophic event. This retrospective, multicentre observational analysis was registered as a Chinese Clinical Trial (ChiCTR2300073780). METHODS:Patients undergoing TEVAR for TBAD in three centres were reviewed from January 2014 to December 2022. SAoII was defined as intra-procedural partial or circumferential disruption of the aortic intima because of TEVAR, excluding those created by natural disease progression. The imaging features and management of SAoII were summarised. RESULTS:1 643 patients undergoing TEVAR for TBAD were reviewed. Among them, SAoII was observed in 20 patients (mean age, 44.5 ± 11.8 years; 16 men). TEVAR was performed in the acute phase (8 of 20), subacute phase (11 of 20), or chronic phase (1 of 20). Imaging features including displacement of the intima, wire, or delivery system were observed in eight (40%), floating endograft in 17 (85%), intussusception of the intima layer in 13 (65%), true lumen occlusions and visceral artery loss in three (15%), and a single lumen without intimal septa in three (15%) patients. SAoII was observed in 60% (12 of 20) after deployment of the stent graft, in 20% (4 of 20) after introduction of a stent graft delivery system, and in 20% (4 of 20) after the introduction of a super stiff wire. All patients who developed SAoII were endovascularly managed by an additional stent graft; no aortic related death was observed among these patients with SAoII during the median follow up of 51.5 months. CONCLUSION:SAoII is a rare but potentially fatal iatrogenic complication during or after TEVAR; endovascular interventions could be effective to manage this acute complication. Timely and accurate identification of decisive imaging features are key to successful treatment.

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.

Atherosclerosis-induced critical limb ischemia, characterized by impaired neovascularization and high susceptibility to infection, remains a major therapeutic challenge. Here, we developed a fungi-like biomimetic nanoparticle-based delivery system by loading adipose-derived stem cell exosomes (ADSC-exos) into chitosan (CS) via flash nanocomplexation (FNC), yielding ADSC-exo@CS nanoparticles. This approach leveraged the electrostatic interactions to complex exosomes with CS, thereby enhancing exosome stability and cellular uptake, while also capitalizing on the inherent antibacterial properties of CS shell. The resulting ADSC-exo@CS nanoparticles exhibited excellent structural stability for over 20 days and achieved a 2.9-fold increase in cellular internalization compared to free ADSC-exos. Both in vitro and in vivo assessments demonstrated that ADSCexo@CS possessed strong antibacterial activity, promoted angiogenesis, and modulated immune responses by facilitating macrophage polarization toward the M2 phenotype. In a murine model of hindlimb ischemia, ADSCexo@CS treatment led to rapid restoration of blood perfusion, reduced tissue fibrosis, and a 100% limb salvage rate, significantly outperforming the control and monotherapy groups. These results highlight a biomimetic synergistic therapeutic strategy that promotes angiogenesis while preventing infection, precisely disrupting the vicious cycle and facilitating in situ repair in ischemic limb disease with a minimally invasive and scalable approach.

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.

OBJECTIVE:Acute type B aortic dissection (ATBD) is a severe cardiovascular event with potential impact on health related quality of life (HRQoL). Evidence on post-operative rehabilitation and exercise guidance remains limited. This study evaluated HRQoL among patients with ATBD after thoracic endovascular aortic repair (TEVAR), focusing on follow up duration, sex, and age. METHODS:This single centre, cross sectional survey study initially screened 625 patients who underwent TEVAR for ATBD between 1 January 2016 and 31 July 2023. HRQoL was assessed using the Chinese versions of the Medical Outcomes Study 36 Item Short Form Health Survey (SF-36v2). Physical Component Summary (PCS) and Mental Component Summary (MCS) scores were compared with sex specific Shanghai normative values, and factors associated with PCS and MCS were analysed. RESULTS:Three hundred and six patients completed interviews. PCS was lower than sex specific Shanghai normative values in both men and women, whereas MCS was not significantly lower than the corresponding normative values. In multivariable analyses, being a woman was associated with lower PCS (β = -2.77, 95% confidence interval [CI] -5.49 - -0.06; p = .045), and increasing age was associated with lower PCS (β = -0.18 per year, 95% CI -0.26 - -0.10; p < .001). For MCS, follow up duration of 13 - 24 months compared with ≤ 12 months was associated with lower scores (β = -3.34, 95% CI -5.61 - -1.08; p = .004). CONCLUSION:Patients with TEVAR treated ATBD had lower PCS than sex specific Shanghai normative values, while MCS was not significantly lower. Increasing age and being a woman were associated with lower PCS, suggesting that physical HRQoL after TEVAR may differ across patient subgroups. These findings support incorporating patient reported outcomes and individualised assessment of physical recovery into post-TEVAR follow up.

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.

OBJECTIVE:The factors influencing patency loss after iliocaval and iliofemoral venous stenting remain incompletely understood. We therefore conducted a systematic review and meta-analysis to synthesize the available evidence. METHODS:PubMed, Embase, and Cochrane Library were searched to December 2025. Studies reporting associations between potential risk factors and stent outcomes were included. Data were synthesized narratively, and random-effects meta-analyses with Hartung-Knapp adjustment were performed when comparable multivariable-adjusted estimates were available. RESULTS:A total of 49 studies were included, predominantly involving retrospective cohorts. The meta-analysis suggested that post-thrombotic disease, stent extension across or below the inguinal ligament, and hyperlipidemia were associated with an increased risk of patency loss, whereas increasing age showed a modest inverse association with patency loss. The narrative evidence suggested that greater anatomical disease extent was associated with poorer stent patency, whereas the evidence regarding impaired venous inflow was heterogeneous and varied according to the disease phenotype, anatomical segment, and inflow definition. Pooled analyses did not identify statistically significant associations of sex, stent length, or number of stents with patency loss. Evidence regarding anticoagulation discontinuation and adjunctive antiplatelet therapy was insufficient and inconsistent. CONCLUSIONS:Patency loss after iliocaval and iliofemoral venous stenting appears to be associated with the disease phenotype, higher anatomical disease burden, and stent landing strategy. Venous inflow impairment may also be associated with poorer stent patency, although the evidence was heterogeneous. The predominantly retrospective evidence precludes causal inference. Prospective studies with standardized definitions and robust adjustment are needed to improve risk stratification and optimize post-stenting management.

Objective: To evaluate the long-term safety and efficacy of endovascular treatment in patients with subclavian artery stenosis or occlusion (SAS/SAO) and the resultant disease prognosis. Methods: This single-center retrospective study analyzed 232 consecutive patients undergoing endovascular treatment for SAS/SAO between June 2017 and June 2024. The end points included technical success, complication rate, and rates of freedom from cardiovascular death (CVD), restenosis, and reintervention. Multivariable analysis was performed to determine the independent predictors. Results: The technical success rate was significantly higher in patients with stenosis than in patients with occlusion (99.4% vs 90.8%, P < .001). The perioperative complication rate was 5.2%. Over the mean follow-up time of 48.2 months, the rates of freedom from CVD, restenosis, and reintervention were 97.1%, 89.1%, and 97.0% at 5 years and 88.7%, 77.7%, and 89.0% at 7 years, respectively. Predictors (hazard ratio, 95% confidence interval; P) of CVD included upper limb ischemia (6.845, 1.108-42.301; P = .038), age (1.148, 1.001-1.316; P = .048), and prior coronary revascularization (8.683, 1.311-57.511; P = .025). Predictors of restenosis included upper limb ischemia (2.408, 1.007-5.757; P = .048) and smaller stent diameter (0.665, 0.461-0.958; P = .029). Predictors of reintervention included transbrachial access (3.494, 1.278-9.551; P = .015) and right-sided lesion (6.080, 1.457-25.376; P = .013). Conclusions: Endovascular treatment is a safe and effective revascularization strategy for SAS/SAO, demonstrating favorable long-term patency and a low complication rate. This study identified the risk factors for CVD, restenosis, and reintervention, which may benefit the management of patients at risk. (JVS-Vascular Insights 2026;4:100420.)

BACKGROUND:This study aimed to compare the efficacy of the Conformable TAG Thoracic Endoprosthesis (CTAG) and the Valiant Captivia System Stent Graft in thoracic endovascular aortic repair (TEVAR) for type B aortic dissection (TBAD). METHODS:TBAD patients treated from 2016 to 2022 at a Chinese tertiary center with a CTAG or Captivia stent graft were eligible for inclusion, and their data were retrospectively collected and analyzed. Intraoperative characteristics, short-term outcomes during hospitalization, mid-term outcomes during follow-up, and aortic remodeling were analyzed and compared between 2 groups. RESULTS:In total, the study included 617 patients (372 CTAG and 245 Captivia). The baseline characteristics of both groups were comparable. Procedural details showed that the CTAG group had larger stent diameter (P < 0.001) and higher oversize ratio (P < 0.001) than the Captivia group and led to less intraoperative type I endoleak cases (P = 0.01). Complications during hospitalization, especially stroke, occurred more commonly in the Captivia group (P = 0.033). Mid-term outcomes, including readmission rate and aortic-related mortality, were comparable between the 2 groups. And CTAG performed better in aortic remodeling with higher expansion rate of true lumen than Captivia in the stented segment of aorta (P < 0.001). CONCLUSION:Both CTAG and Captivia offered comparable and favorable mid-term survival rates and freedom from readmission in patients with TBAD. CTAG performed better during TEVAR operations and in short-term outcomes, including reducing intraoperative type I endoleak and avoiding complications during hospitalization. In addition, CTAG achieved an improved aortic remodeling effect in expanding the true lumen of aorta.

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.

Stanford type B aortic dissections often exhibit helical morphology. However, the influences of structural helicity on periprocedural and mid-to long-term adverse events after thoracic endovascular aortic repair (TEVAR) remain unclear. In this article, a total of 197 patients who underwent TEVAR between October 2019 and December 2020 were studied. Among them, 93 patients were excluded, and 104 patients were analyzed. The maximum helical angles and the maximum twists were measured using an efficient morphological method based on computed tomography angiography images. The whole dissecting aorta was divided into five zones. The visceral aortic zone exhibited the most pronounced structural helicity compared with other zones. Patients with the maximum helical angle larger or smaller than 200° were categorized into two groups, i.e., the groups of strong helicity and weak helicity. The patients in the strong helicity group exhibited a greater likelihood of experiencing adverse events after TEVAR.

Background: The efficacy of excimer laser ablation (ELA) in de novo atherosclerotic lesions of lower extremity artery disease (LEAD) is unknown. Objectives: This real-world study aimed to evaluate the safety and efficacy of ELA combined with drug-coated balloon (DCB) versus DCB alone in LEAD patients. Methods: In this prospective, multicenter, real-world trial (ChiCTR2100051263), patients with de novo atherosclerotic lesions of LEAD were enrolled and allocated to either ELA + DCB or DCB-alone group in a 1:1 ratio. The primary endpoint was 12-month primary patency, with secondary endpoints including technical success, clinically driven target lesion reintervention (CD-TLR), and changes in ankle-brachial index (ABI). Results: A total of 136 patients were enrolled in the study. At baseline, patients in the ELA + DCB group presented significantly higher Rutherford classification (3.7 ± 0.9 vs. 4.2 ± 1.0, p = 0.007) and longer mean lesion lengths (7.4 ± 2.5 cm vs. 8.4 ± 1.9 cm, p = 0.012). The ELA + DCB group demonstrated significantly superior 12-month primary patency (87.5% vs. 71.2%, p = 0.03) and technical success rates (92.7% vs. 79.4%, p = 0.046) compared to the DCB-alone group. Kaplan-Meier analysis further confirmed sustained patency benefit with ELA + DCB (p = 0.015). Conclusion: In this real-world trial, ELA appears to be a promising therapy for LEAD in terms of safety and efficacy. However, these findings need to be corroborated by larger, randomized studies. ### Competing Interest Statement The authors have declared no competing interest. ### Clinical Trial URL: https://www.chictr.org.cn/. Unique identifier: ChiCTR2100051263 ### Funding Statement This study was supported by Noncommunicable Chronic Diseases-National Science and Technology Major Project (grant no. 2023ZD0504300), the Postdoctoral Fellowship Program and China Postdoctoral Science Foundation (grant no. BX20250267), Youth Fund of Fudan University Affiliated Zhongshan Hospital (grant no. ZSZP202413), Outstanding Resident Clinical Postdoctoral Program of Zhongshan Hospital Affiliated to Fudan University, and the National Natural Science Foundation of China (grant no. 82270507). ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: This study design was approved by the Ethics Committee for the Protection of Human Subjects at Zhongshan Hospital, Fudan University, Shanghai, China. All included patients were informed about the nature of the study and gave their written informed consent. I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes The datasets analyzed during this study are available from the corresponding author on reasonable request.

OBJECTIVE:The prevalence of peripheral artery disease (PAD) is on the rise due to an aging population. This study aimed to gain insight into the clinical role of infrared thermography (IRT) as a diagnostic method and prognostic tool for below-the-knee (BTK) PAD patients. MATERIALS AND METHODS:The study prospectively recruited 64 patients who received lower limb revascularization for symptomatic BTK PAD (ChiCTR2400083847). IRT was used to detect lower limb skin temperature. Locations on the lower extremity sampled with IRT were dorsal areas, plantar areas, and medial and lateral areas of the calves. RESULTS:One hundred twenty-eight limbs of 64 patients were divided into normal (n=35), mild (n=22), moderate (n=55), and severe (n=16) groups based on the ankle-brachial index (ABI) testing. Limbs in the moderate and severe groups showed an obvious decrease in surface temperature when compared to the normal baseline measurements, particularly in the dorsal areas (all p values <0.01). Further analysis revealed IRT increased the sensitivity of ABI from 75.8% (69/91) to 96.7% (88/91) in PAD diagnosis. In addition, our results showed maximum temperature variations (ΔTEMP) on treated limbs decreased significantly after endovascular treatment. Further analysis revealed showed a negative correlation between maximum ΔTEMP on treated limbs and walking distance. CONCLUSIONS:Our findings showed the use of IRT increased the diagnostic efficacy of ABI in BTK PAD patients. This noninvasive technique has the potential to be applied in PAD diagnosis, preoperative, and postoperative evaluation.Clinical ImpactAn ankle-brachial index (ABI) is the most commonly used diagnostic method for evaluating vascular disorders in the lower limb. The high prevalence of medial sclerosis, which can render arteries incompressible upon cuff inflation, may lead to falsely elevated ABI values (ABI>1.4) in patients with diabetes mellitus. Infrared thermography (IRT) is a novel potential diagnostic method that does not require physical contact. The use of IRT may increase the diagnostic efficacy of ABI in BTK PAD patients. This non-invasive technique has the potential to be applied in PAD diagnosis, preoperative, and postoperative evaluation.

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.