Abdominal aortic aneurysm (AAA) is a life-threatening condition. Although the traditional risk factors for AAA have been identified, the evidence for other influencing factors (comorbidities, drugs, biomarkers, and biomechanical parameters) remains fragmented and lacks comprehensive stratified assessment. This umbrella review synthesized evidence from 36 meta-analyses on risk/protective factors for abdominal aortic aneurysm (presence, growth, and rupture). Conducted per PRISMA 2020 guidelines, it appraised methodological quality (AMSTAR-2) and evidence certainty (GRADE). Analysis of 39 factors identified several supported by moderate-quality evidence. Diabetes was a consistent protective factor against prevalence, growth, and rupture. Similarly, statins use slowed growth and reduced rupture risk, while metformin use reduced AAA growth. For risk factors, hypertension increased incidence, and the biomarkers D-dimer, fibrinogen, and hsCRP were positively associated with AAA presence. Associations for other factors, including various comorbidities, medications, and biomechanical parameters like peak wall rupture index, were less consistent or based on low/very low-quality evidence. This study confirms AAA’s multifactorial nature and establishes a clear evidence hierarchy, highlighting diabetes, statins, and metformin as key protective factors. It underscores that most factors lack high-quality evidence, necessitating standardized measurement and prospective studies to improve risk prediction and therapeutic strategies.

Peripheral artery disease (PAD) is a chronic arterial occlusive disease characterized by atherosclerosis affecting the lower extremity arteries, leading to luminal stenosis or occlusion, which in turn causes lower limb ischemia and necrosis. PAD not only significantly reduces a patient’s quality of life but also carries a non-negligible risk of amputation and mortality, imposing a heavy economic and health burden on both patients and society, especially among the elderly. Advanced age has been identified in multiple studies as a key risk factor for amputation and death in PAD patients. The prevalence of PAD increases significantly with age in the elderly, who often have multiple comorbidities such as coronary heart disease, renal insufficiency, and tumors. Their pathophysiological characteristics, treatment options, and prognostic assessments are more complex than those in younger patients. Diagnosis is challenging because symptoms in elderly patients are easily masked by comorbidities, requiring a comprehensive medical history, physical examination, and auxiliary examinations. Treatment difficulties, such as poor adherence and challenges in follow-up, further complicate management. Currently, there are no specific guidelines or consensus statements for the diagnosis and treatment of PAD in the elderly, either domestically or internationally. Therefore, this consensus, combining the latest evidence-based medicine and clinical experience from both domestic and international sources, focuses on key issues such as the characteristics of the disease in elderly patients, management of comorbidities, individualized treatment, and long-term follow-up. Its aim is to develop scientific and practical treatment guidelines to provide guidance for clinicians.

The human microbiome functions as a distributed superorganism that exerts profound systemic control over vascular homeostasis. Here, we systematically synthesize how microbial communities across five distinct anatomical niches—the gut, oral cavity, respiratory tract, skin, and reproductive tract—orchestrate vascular health and disease. While convergent pathways, such as pattern recognition receptor-mediated systemic inflammation, operate across niches, each compartment deploys specialized mechanisms, including gut-derived metabolic signaling, hematogenous dissemination of periodontal pathobionts, and niche-specific mucosal barrier crosstalk. We critically evaluate the mechanistic contributions of these inter-ecosystem networks to the pathogenesis of atherosclerosis, hypertension, and vascular inflammation, highlighting robust microbial signatures as emerging diagnostic biomarkers and risk predictors. Finally, we delineate precision therapeutic paradigms that target niche-specific dysbiosis—ranging from targeted microbiome modulation and periodontal interventions to systemic anti-inflammatory frameworks—and outline multi-omics-driven roadmaps to translate microbiome-vascular science into clinical cardiovascular medicine.

Abdominal aortic aneurysm (AAA) is a progressive degenerative vascular disorder associated with substantial rupture-related mortality and persistent lack of effective pharmacological therapy. Traditionally regarded as a localized structural disease, AAA is now recognized as a systemic inflammatory and remodeling disorder. Key processes include inflammation, oxidative stress, endothelial dysfunction, vascular smooth muscle cell apoptosis and switching, extracellular matrix degradation, and thrombo-inflammatory remodeling. The gut microbiota–metabolite–vascular wall axis has emerged as a candidate upstream regulator of these processes. In this review, this axis refers to the biological continuum through which intestinal microbial dysbiosis and microbial or host–microbial metabolites influence immune activation, endothelial injury, thrombosis, and matrix remodeling in aneurysmal wall. This review synthesizes advances in understanding gut microbiota dysbiosis and microbiota-derived metabolites in AAA, with emphasis on mechanistic, translational, and clinically relevant developments. Current evidence suggests that gut microbial imbalance may promote aneurysm progression through immune and inflammatory pathways. One important mechanism is enhanced neutrophil extracellular trap formation. Among microbial mediators, trimethylamine N-oxide has become the most intensively studied candidate, with growing evidence linking elevated circulating levels to AAA occurrence, growth rate, and progression-related events, alongside experimental data supporting inflammatory and apoptotic mechanisms. In contrast, short-chain fatty acids may exert protective immunometabolic and barrier-supportive effects, whereas lipopolysaccharide may function as a key inflammatory amplifier linking intestinal barrier dysfunction to vascular injury. Insights from related disorders, including atherosclerosis, hypertension, metabolic syndrome, and inflammatory bowel disease, further strengthen the biological plausibility of microbiota-mediated aneurysmal remodeling. Despite this progress, major challenges remain, including taxonomic inconsistency, cohort heterogeneity, analytical standardization, and unresolved causality. Future studies should prioritize function-oriented microbiome analysis, integrated multi-omics, imaging-linked phenotyping, and mechanism-based intervention trials. Collectively, emerging evidence supports a conceptual shift in which AAA is viewed within a broader microbiome–metabolite–immune–matrix framework, opening new possibilities for biomarker development and non-surgical disease modification.

This review aims to break through the theoretical framework of traditional risk factors for vascular diseases, systematically elucidate the core role of gut microbiota in vascular health regulation, and focus on the three key bottlenecks currently facing research: difficulty in establishing causal relationships, unclear functional cell targets, and lack of near-physiological validation systems. To this end, we propose and construct a closed-loop research path of “discovery → prediction → localization → verification” supported by advanced technology: using high-throughput sequencing for microbial ecological map discovery, combining machine learning for risk prediction and biomarker screening, integrating multiple omics to construct gene–metabolite–target causal chains; using single-cell sequencing to accurately anchor microbial signals to key subgroups such as vascular smooth muscle cells and macrophages; using Raman spectroscopy to capture metabolic phenotypes in situ to compensate for the incompleteness of genomic information; and relying on organoid platforms to establish a humanized intestinal-vascular dynamic interaction verification system. The core purpose of this review is to systematically demonstrate how this technology loop can systematically reveal the microecological and etiological mechanisms of vascular diseases, promote research from correlation to causal mechanisms, and provide theoretical basis and methodological framework for precise prevention and treatment strategies based on individual microbial community characteristics, thus opening up new directions for the diagnosis and treatment of vascular diseases.

Introduction: To report a rare case of right iliac vein compression syndrome (IVCS) and secondary right lower extremity deep venous thrombosis (DVT) caused by internal iliac artery pseudoaneurysm (IIPA), and summarize the diagnosis and minimally invasive endovascular treatment experience.

Case Presentation: We retrospectively analyzed a 70-year-old female patient with right lower limb edema, fever and pain. Laboratory and imaging examinations confirmed right deep venous thrombosis and a compressive right IIPA. After endovascular therapy, anticoagulants and antibiotics were given, and routine imaging follow-up was conducted.

Results: Favorable clinical and angiographic results were achieved. The IIPA resolved completely, right hydronephrosis subsided, and both DVT and iliac venous stenosis improved significantly. No major complications occurred during follow-up.

Discussion: This rare case supplements limited literature on IIPA-induced right-sided IVCS-DVT. It recommends pelvic imaging for patients presenting with unexplained right°sided DVT and endorses endovascular intervention. In contrast to technically challenging open surgery, endovascular therapy offers the advantages of minimal trauma and faster recovery. Additional evidence is still needed to formulate standardized treatment protocols for this rare clinical entity.Conclusion: Right IVCS and DVT induced by IIPA are extremely rare clinical conditions. Endovascular therapy is safe and effective for this disease, which can relieve vascular compression and thrombotic symptoms and achieve a satisfactory long-term outcome. However, this conclusion remains to be verified by more clinical studies.