Wei Wang

Background: Aberrant splenic artery (SA), defined as the SA arising from the superior mesenteric artery (SMA) rather than the celiac axis, is a rare anatomical variant with a prevalence of less than 1% in the general population. Although clinical observations suggest that individuals with this variant are highly susceptible to developing SA aneurysms (SAAs), the underlying pathophysiological mechanisms remain poorly understood. Objectives: This study aimed to systematically investigate the morphological and hemodynamic features of aberrant SA anatomy and their contributions to SAA formation, and to develop a predictive model for individualized risk stratification. Methods: This multi-center retrospective cohort study enrolled 195 patients with aberrant SA anatomy from 16 centers across China between January 2008 and June 2026, including 94 patients with concomitant SAAs and 101 without. In addition, 100 patients with common SAAs and 100 non-aneurysmal controls with normal vascular anatomy were enrolled for comparative analysis. Three-dimensional vascular models were reconstructed from computed tomography angiography? (CTA) images, and twelve morphological parameters were measured. Computational fluid dynamics simulations were performed to analyze fourteen hemodynamic parameters. A two-stage machine learning model based on five morphological parameters was developed to predict SAA occurrence and location. Results: Aberrant SAAs were significantly larger and predominantly located in the proximal SA, whereas common SAAs were mainly located in the distal splenic hilum. Morphological analysis revealed that the aberrant SA exhibited a smaller branching angle with its parent vessel, an increased SA/SMA cross-sectional area ratio, and a higher tortuosity index. Hemodynamic analysis demonstrated significantly lower time-averaged wall shear stress (TAWSS) at the proximal SA in aberrant anatomy, whereas the SA-parent vessel junction showed elevated oscillatory shear index (OSI), which was inversely correlated with the branching angle. Longitudinal follow-up of non-aneurysmal patients (n=14; mean follow-up, 36.8 months) showed stable vessel dimensions over time. The KNN-based predictive model achieved an AUROC of 0.828 for predicting SAA occurrence and was deployed as an interactive web application (the zs_abeSA model) for clinical use. Conclusions: Aberrant SA anatomy is an independent risk factor for SAA formation. The pathogenic mechanism involves a cascade from morphological remodeling to hemodynamic derangement, ultimately leading to aneurysm formation at the proximal SA. The zs_abeSA model provides a practical tool for individualized risk assessment and clinical decision-making, with direct implications for screening, surveillance, and therapeutic strategies.

Abdominal aortic aneurysm (AAA) is a life-threatening cardiovascular disease for which no effective pharmacological treatments exist. Histone deacetylases (HDACs) have emerged as critical regulators of cardiovascular pathophysiology; however, the contributions of individual HDAC isoforms to AAA formation remain largely undefined. Here, we identified sirtuin 7 (SIRT7) as the most markedly downregulation isoform among 18 HDAC family members in human AAA tissues. Global and vascular smooth muscle cell (VSMC)-specific Sirt7 knockout exacerbated AAA formation, whereas SIRT7 overexpression attenuated aneurysm progression. Mechanistically, SIRT7 deacetylates serum response factor (SRF) at lysine 154, thereby preventing SRF nuclear-to-cytoplasmic translocation and ubiquitin-mediated degradation and preserving the VSMC contractile phenotype. Consequently, SIRT7 deficiency enhances SRF acetylation, accelerates its degradation, and promotes VSMC phenotypic switching, ultimately facilitating AAA progression. Pharmacological activation of SIRT7 with the NAD⁺ precursor nicotinamide mononucleotide attenuated aortic dilation. Collectively, our findings reveal a crucial role for SIRT7-mediated SRF-K154 deacetylation in limiting AAA progression and suggest that nicotinamide mononucleotide supplementation may represent a promising therapeutic strategy for AAA.

Introduction: Peripheral arterial disease (PAD) is a significant contributor to global morbidity, with regional burdens exhibiting considerable heterogeneity. The PAD burden attributable to metabolic risks across regions with varying socioeconomic levels has yet to be adequately characterized. Methods: This study analyzes PAD burden attributable to metabolic risks across different socioeconomic regions using data from the Global Burden of Disease (GBD) 2021 study. We analyzed data on PAD attributable to metabolic risks, including high systolic blood pressure (SBP), high fasting plasma glucose (FPG), kidney dysfunction (KD), and high body mass index (BMI), across four health systems, four world bank income levels, five Socio-demographic Index (SDI) levels, and 21 GBD regions, from 1990 to 2021. We presented age-standardized mortality rates (ASMR), age-standardized disability-adjusted life year rates (ASDR) and estimated annual percentage changes (EAPC) to assess burden and trends. Results: In 2021, the burden of PAD due to metabolic risks remained high in regions with higher socioeconomic levels, though it showed a declining trend. Conversely, the burden in regions with lower socioeconomic levels was also high but exhibited an increasing trend. High FPG has become a significant factor in the burden of PAD, particularly in higher socioeconomic regions. Gender disparities in the burden of PAD attributable to metabolic risks were evident, with males exhibiting higher ASMR and ASDR, although females in middle-income regions had slightly elevated ASDRs. Finally, an inverted "U" relationship was observed between SDI and burden, with regions around an SDI of 0.75 exhibiting a higher burden of PAD attributable to metabolic risks. Discussion: These findings underscore the urgent need to tailor region-specific public health strategies that account for socioeconomic disparities in metabolic risk exposures contributing to the PAD burden. Conclusions: Effective public health interventions targeting these metabolic risks are urgently needed, especially in low-socioeconomic regions where the burden remains disproportionately high. Enhanced blood glucose control and early intervention strategies should be prioritized to mitigate the growing impact of PAD globally.

Aortic arch pathologies are complex to treat. Alternatives include open surgery, hybrid surgery (endovascular aortic stent-grafting and open surgical debranching procedures) and total endovascular solutions with branched stent-grafts. Branched stent-grafts are the mainstream approach for endovascular repair, but they are primarily available only as dedicated custom-made devices. The aim of this study was to evaluate the safety and effectiveness of a non-customized modular aortic arch stent-graft. This trial was led by the Chinese PLA General Hospital and 16 additional aortic centres in China. All included patients were treated with a non-customized modular inner branched stent-graft (Endonom Medtech, Hangzhou, China). The study endpoints were 30-day death and stroke, technical success, clinical success, early and late complications, reintervention, and death during follow-up. Follow-up via clinical examination and CT angiography scan were scheduled post surgery at 1, 6, and 12 months, and annually thereafter. From June 2021 to December 2024, a total of 88 patients were enrolled in this study. Technical success rate was 100%. The mean follow-up was 28.6 ± 11.7 months. The overall 30-day mortality rate was 3%, and the 30-day stroke rate was 9%. Overall survival was 91% ± 3%, 86% ± 4%, and 81% ± 4% at 12, 24, and 36 months respectively. A total of 10 patients developed endoleaks, none of which required reintervention. Modular branched stent-graft repair for aortic arch disease is feasible and with comparative rates of safety with custom made branched endovascular stent-grafts, hybrid techniques and open surgery. Long-term comparative effectiveness studies are required to establish whether it is superior to alternative interventions.

Background: Estimated pulse wave velocity (ePWV), a noninvasive marker of arterial stiffness, reflects vascular aging and has been associated with increased coronary artery disease (CAD) risk. However, the interplay between ePWV and genetic factors, including polygenic risk score (PRS) and apolipoprotein E genotypes, in determining CAD susceptibility remains unclear. Methods: We analyzed data from the HRS (Health and Retirement Study), including 5856 participants (4741 White and 1115 Black individuals) without baseline CAD. ePWV was calculated, and genetic risk was assessed using PRS and apolipoprotein E genotyping. Cox proportional hazards models evaluated the associations between ePWV, genetic predisposition, and CAD incidence, with stratified analyses by race and sex. Mediation analyses explored underlying mechanisms. Results: Elevated ePWV (≥10 m/s) was significantly associated with increased CAD risk (hazard ratio [HR], 1.50 [95% CI, 1.25–1.81], P P =0.032). Sex‐stratified analyses indicated that White women with high PRS and high ePWV had a lower‐than‐expected CAD risk. Additionally, changes in total cholesterol and high‐density lipoprotein cholesterol mediated the association between ePWV and CAD. Conclusions: Vascular aging and genetic predisposition interact in complex ways to influence CAD risk, with notable variations across racial and sex subgroups. These findings highlight the need for personalized prevention strategies incorporating both vascular health and genetic risk profiling.