Yanhua Tang

Coronary artery aneurysms are focal dilatations that exceed the diameter of normal adjacent vessels by a factor of at least 1.5-fold. Multimodal imaging is essential when attempting to improve the efficacy of curative interventions in aneurysm patients as it can facilitate the comprehensive functional and anatomical characterization of these intricate vascular lesions. In this report, we describe the case of a patient with giant diagonal branch aneurysms accompanied by obstructive coronary artery disease. Successive coronary artery bypass grafting (CABG) and surgical resection were performed to effectively treat these conditions, and these procedures were aided by the use of three-dimensional (3D) printed models of the heart. Employing computed tomography-guided reconstruction procedures in combination with the use of multiplanar, multicolor 3D printed models can enable surgeons to better assess the dimensions, source, and relationships of target vessels with adjacent tissues, thereby ensuring that preoperative planning can be completed more effectively.

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.

Purpose: Patients with chronic obstructive pulmonary disease (COPD) and atrial fibrillation (AF) face elevated ischemic stroke (IS) risk. This study assessed the triglyceride-glucose (TyG) index as a metabolic marker for IS risk in this population. Patients and Methods: This retrospective analysis included 710 hospitalized patients with COPD and AF (2014– 2024). The TyG index (ln[fasting triglycerides (mg/dL)×fasting glucose (mg/dL)/2]) measured at admission was the exposure; new-onset IS occurring during the index hospitalization (median duration: 9 days, IQR: 6– 13) was the outcome. Univariate and multivariate logistic regression (adjusting for age, sex, smoking, blood pressure, diabetes, lipids, prior stroke) identified associations. Nonlinearity was assessed using generalized additive models (GAM). Predictive performance was evaluated via ROC analysis (AUC). Results: IS occurred in 32 patients (4.5%). Unexpectedly, and in contrast to findings in the general population, higher TyG index was associated with lower IS risk in univariate analysis (OR=0.49, 95% CI:0.26– 0.94). After full adjustment, each unit increase in TyG index was associated with lower IS risk (aOR=0.24, 95% CI:0.10– 0.57, P=0.001). However, the wide confidence interval and limited events (n=32) indicate this large effect estimate should be interpreted cautiously, as it may reflect statistical instability. The finding suggests a potential metabolic paradox in this population. GAM confirmed a linear inverse relationship after adjusting for stroke history (OR=0.50, 95% CI:0.30– 0.90, P=0.032). The TyG index predicted IS with an AUC of 0.614 (95% CI:0.513– 0.715). Conclusion: Contrary to observations in the general population, in hospitalized COPD and AF patients, a higher TyG index was associated with lower short-term ischemic stroke risk. However, this inverse association could reflect either a true inverse metabolic relationship or reverse causality whereby low TyG marks disease severity (malnutrition, poor metabolic reserve, chronic inflammation). Lack of comprehensive disease severity and nutritional assessments limits causal inference. The TyG index may serve as a potential biomarker in hospitalized patients, but population-based studies are essential to address selection bias.

Infective endocarditis (IE) is a disease caused by the involvement of pathogenic microorganisms in the endocardium, primarily characterized by the formatio

Acute myocardial infarction (AMI) remains the leading cause of mortality worldwide, posing a significant threat to global public health. Although revascularization strategies such as percutaneous coronary intervention represent the standard treatment for AMI, myocardial cell death caused by myocardial ischemia/reperfusion injury (MI/RI) significantly compromises clinical efficacy. The clinical application of anti-inflammatory and antioxidant therapeutic medicine for MI/RI is hindered by critical limitations, including poor targeting and low bioavailability. A novel mitochondria-targeted nanomedicine, VB@MOF/TA, was successfully constructed, utilizing a metal-organic framework (MOF) as a carrier to achieve synergistically antioxidant and anti-inflammatory activities of verbascoside (VB), and employing a tannic acid (TA)-based nanocomplex for specific mitochondrial localization. Cellular experiments demonstrate that VB@MOF/TA co-localizes with mitochondria, exerts potent antioxidant effects, significantly suppresses oxygen-glucose deprivation/reoxygenation-induced cardiomyocyte apoptosis, and effectively modulates macrophage polarization. In vivo studies confirm that, compared with VB monotherapy, the VB@MOF/TA group exhibits a 2.59-fold reduction in apoptosis rate, a 7.72% ± 3.71% improvement in left ventricular ejection fraction, and a 2.50-fold increase in vascular density. These findings indicate that VB@MOF/TA significantly mitigates MI/RI and promotes myocardial tissue remodeling through its targeted antioxidant and synergistic anti-inflammatory mechanisms, highlighting its substantial clinical translational potential.

Emerging research has highlighted the significant role of the gut microbiota in atherosclerosis (AS), with microbiota‐targeted interventions offering promising therapeutic potential. A central component of this process is gut‐derived metabolites, which play a crucial role in mediating the distal functioning of the microbiota. In this study, a comprehensive microbiome‐metabolite analysis using fecal and serum samples from patients with atherosclerotic cardiovascular disease and volunteers with risk factors for coronary heart disease and culture histology is performed, and identified the core strain Bacteroides ovatus ( B. ovatus ). Fecal microbiota transplantation experiments further demonstrated that the gut microbiota significantly influences AS progression, with B. ovatus alone exerting effects comparable to volunteer feces from volunteers. Notably, B. ovatus alleviated AS primarily by restoring the intestinal barrier and enhancing bile acid metabolism, particularly through the production of indole‐3‐acetic acid (IAA), a tryptophan‐derived metabolite. IAA inhibited the TLR4/MyD88/NF‐κB pathway in M1 macrophages, promoted M2 macrophage polarisation, and restored the M1/M2 polarisation balance, ultimately reducing aortic inflammation. These findings clarify the mechanistic interplay between the gut microbiota and AS, providing the first evidence that B. ovatus , a second‐generation probiotic, can improve bile acid metabolism and reduce inflammation, offering a theoretical foundation for future AS therapeutic applications involving this strain.

Advances in synthetic biology have enabled the development of tumor-targeted live bacterial therapeutics. In a recent study published in Nature , Redenti et al. engineered Escherichia coli Nissle 1917(EcNcΔlon/ΔompT/LLO+ nAg), which exploits the advantages of living medicines to deliver arrays of tumor-specific neoantigenic epitope in optimal environments, thereby providing a novel strategy for developing effective and durable cancer immunotherapies.

Background: Hyperuricemia is independently associated with a poor prognosis in patients with myocardial infarction (MI). Furthermore, MI induces activation of the repair response in local fibroblasts, resulting in extracellular matrix accumulation that generates a stable fibrotic scar in the infarcted area. However, researchers have not determined whether hyperuricemia affects fibroblast activation and its involvement in postinfarction cardiac remodeling. Objectives: We aimed to trigger hyperuricemia by administering potassium oxonate in a mouse model of MI to evaluate the role of hyperuricemia in MI pathogenesis. Methods: Microarray datasets and single-cell sequencing data from gout patients, heart failure patients, and model mice were used to identify the underlying mechanisms responsible for the effect of hyperuricemia on MI progression. A hyperuricemia-related MI mouse model was established. Cardiac function was assessed, followed by sample collection and a uric acid assay. We conducted an enzyme-linked immunosorbent assay, histological detection, immunofluorescence, sequencing data processing, single-cell RNA-seq, and functional enrichment analysis. We then isolated and cultured cardiac fibroblasts and performed Western blotting, quantitative real-time polymerase chain reaction, and shRNA-mediated lumican knockdown assays. Results: Hyperuricemia decreased cardiac function, increased mortality, and aggravated adverse fibrosis remodeling in mice after MI. These outcomes were closely related to reduced levels of fibroblast-derived lumican. This reduction activated the TGF-β/SMAD signaling pathway to induce aberrant myofibroblast activation and extracellular matrix deposition in the infarcted area. Furthermore, lumican supplementation or uric acid-lowering therapy with allopurinol alleviated hyperuricemia-mediated abnormal cardiac remodeling. Conclusion: Hyperuricemia aggravates postinfarction cardiac remodeling by reducing lumican expression and promoting fibroblast phenotype transition. We highlight the clinical importance of lowering uric acid levels in hyperuricemia-related MI to prevent adverse ventricular remodeling.

Schematic diagram of the effect of B. animalis subsp. lactis LPL-RH on postoperative gastrointestinal symptoms, gut microbiota, and other clinical indicators in patients with VHD.