Venous thromboembolism (VTE) is a leading preventable cause of in-hospital mortality in older adults, yet early risk stratification remains a key clinical challenge. This study aimed to develop and internally validate an explainable machine learning model for incident VTE prediction in hospitalized older adult patients. We enrolled 28,231 patients aged ≥65 years admitted between January 2023 and December 2024, excluding those with VTE on admission. The primary endpoint was imaging-confirmed incident in-hospital VTE. Patients were split into training/test sets (7:3) via outcome-stratified sampling. Missing data were handled with multivariate imputation by chained equations imputation (training set only). Five machine learning models were constructed with 10-fold cross-validation and hyperparameter tuning, evaluated by pooled area under the curve (AUC), calibration curves, and decision curve analysis, with SHAP for model interpretation. 1797 (6.38%) incident VTE events were recorded. XGBoost showed optimal performance, with a training AUC of 0.753 and a test AUC of 0.712, favorable calibration, and stable clinical net benefit. Top predictors included diabetic nephropathy, triglycerides, great saphenous vein varicosity, fatty liver, cerebrovascular accident and age. We developed and validated an explainable XGBoost model for VTE risk prediction in older inpatients, enabling early risk stratification to support individualized thromboprophylaxis. Multicenter prospective external validation is warranted for clinical implementation.

Blood eosinophil count has been associated with prognosis in patients with cardiovascular disease. However, its prognostic value among critically ill patients with atrial fibrillation (AF) remains unclear. This study aimed to investigate the association between admission blood eosinophil count and 28-day all-cause mortality in this population. This retrospective cohort study used data from the Medical Information Mart for Intensive Care IV database, version 3.1. Multivariable Cox regression, restricted cubic spline analysis, threshold-effect analysis, and Kaplan-Meier survival analysis were used to evaluate the association between blood eosinophil count and 28-day mortality. A total of 2787 critically ill patients with AF were included, of whom 1948 (69.9%) were male. The mean age was 70.4 ± 10.9 years, and the overall 28-day mortality rate was 9.8% (n = 273). Compared with patients in the lowest eosinophil count quartile (Q1), the adjusted hazard ratios for 28-day mortality were 0.51 (95% confidence interval [CI]: 0.37-0.70; P < .001) for Q2, 0.37 (95% CI: 0.25-0.55; P < .001) for Q3, and 0.45 (95% CI: 0.32-0.63; P < .001) for Q4. Restricted cubic spline analysis showed an L-shaped association between blood eosinophil count and 28-day mortality (P for nonlinearity <.001). Threshold-effect analysis identified an inflection point at 0.08 × 109/L. Below this threshold, a higher eosinophil count was associated with lower 28-day mortality (hazard ratio per 0.01 × 109/L increase, 0.864; 95% CI: 0.794-0.940; P < .001), whereas no significant association was observed above the threshold. In critically ill patients with AF, blood eosinophil count showed an L-shaped association with 28-day mortality. Lower eosinophil count was associated with a higher risk of short-term mortality.

In recent years, with a growing understanding of coronary microvascular dysfunction, myocardial infarction with nonobstructive coronary arteries (MINOCA) has been proposed as a distinct type of myocardial infarction. The management of atrial fibrillation (AF) coexisting with myocardial infarction remains a major challenge in clinical practice. This study aims to explore the association between the inflammatory marker aggregate index of systemic inflammation (AISI) and new-onset AF (NOAF) in patients with MINOCA. In this single-center, retrospective study, we consecutively enrolled patients with MINOCA from January 2019 to June 2025. AISI was calculated as (Neutrophil count × Platelet count × Monocyte count)/Lymphocyte count from procedural complete blood count. NOAF was defined as new-onset AF after admission in patients with no previous history of AF. Multivariable logistic regression was employed to screen for factors associated with NOAF. Restricted cubic spline was used to characterize the dose-response relationships between AISI and NOAF. Receiver operating characteristic curves were constructed to evaluate the discriminative performance of AISI. Among 409 patients with MINOCA, 38 (9.3%) developed NOAF. In multivariable analysis, AISI (odds ratio 2.335, 95% confidence interval [CI] 1.532-3.560, P < .001) and C-reactive protein (odds ratio 1.009, 95% CI 1.002-1.017, P = .015) remained independently associated with NOAF, which suggests that AISI provides additional information independent of the traditional inflammatory marker C-reactive protein in relation to NOAF. Restricted cubic spline analysis suggested an initial nonlinear dose-response relationship between AISI and NOAF in the unadjusted model; however, this association was no longer statistically significant after adjustment for relevant clinical covariates. In receiver operating characteristic analysis, AISI yielded an area under the curve of 0.712 with an optimal cutoff of 750 (sensitivity 0.737, specificity 0.650, 95% CI 0.617-0.808, P < .001). Higher AISI is independently associated with in-hospital NOAF in patients with MINOCA, although its discriminative performance is moderate, suggesting that AISI may serve as an adjunctive rather than a standalone risk marker.

Cardiovascular disease (CVD) remains a global health challenge. The body roundness index (BRI) may better reflect abdominal fat distribution associated with metabolic disorders than traditional anthropometric measures. This study aimed to investigate the association between BRI and CVD, including congestive heart failure, coronary heart disease, angina, heart attack, and stroke, among adults in the United States. Data were obtained from the 2005 to 2016 National Health and Nutrition Examination Survey (NHANES). All analyses accounted for sampling weights, clustering, and stratification to ensure national representativeness. Weighted logistic regression models were used to evaluate association between BRI and CVD outcomes. Smoothing curve fitting, subgroup analyses, multiple imputation, and receiver operating characteristic curves analysis were also performed to assess robustness and predictive performance relative to body mass index. This cross-sectional study examined the association between BRI and CVD and its components, using nationally representative data from the NHANES (n = 23,812). The results revealed significant association between BRI and CVD, specifically, each 1-unit increase in BRI, the prevalence of CVD increased by 10% (odds ratio = 1.10, 95% confidence interval: 1.06-1.14, P < .001). Tertile analyses demonstrated a dose-response relationship. Compared with body mass index, BRI demonstrated superior predictive performance for CVD and its components. Smoothing curve analysis revealed a generally linear association between BRI and CVD, coronary heart disease, angina pectoris, and heart attack. Tests for nonlinearity were not significant (P for nonlinearity > .05), whereas the overall associations remained significant (P for overall < .05). However, a J-shaped association was observed between BRI and congestive heart failure. Subgroup analyses confirmed the robustness of these findings, with limited interaction effects. In this nationally representative cohort of US adults from the NHANES database, BRI demonstrated stronger, and dose-dependent associations with major cardiovascular outcomes. These findings suggested that BRI may serve as a useful marker for CVD risk assessment, however; further longitudinal validation is needed.

Atrial fibrillation (AF) is the most common arrhythmia requiring lifelong treatment. While the gut microbiota has been linked to several cardiovascular diseases, its direct causal relationship with AF remains unclear, and the underlying "gut-heart" axis hypothesis requires validation. This study aimed to explore the bidirectional association between gut microbial profiles and the risk of AF to clarify this potential etiologic pathway. Genetic summary statistics of gut microbiota and AF were obtained from MiBioGen consortium and FinnGen cohort, respectively. Bidirectional Mendelian randomization (MR) analysis was used to assess the causality. Inverse-variance weighted (IVW) MR was the main approach to generate the estimates, and a series of sensitivity analyses were performed to examine the robustness of results. The forward MR analysis identified 12 bacterial taxa associated with AF risk; specifically, Coprococcus (OR: 1.22; 95% CI: 1.05-1.41; P = .008) was positively associated with AF, whereas, Holdemania (OR: 0.87; 95% CI: 0.78-0.97; P = .011) and Alphaproteobacteria (OR: 0.85; 95% CI: 0.74-0.97; P = .013) were inversely associated with the risk. Reverse MR analysis found that the diagnosis of AF was related to the abundance of 17 bacterial genera, such as Coprococcus (OR: 1.06; 95% CI: 1.03-1.10; P = .001), Ruminococcus gnavus group (OR: 1.09; 95% CI: 1.03-1.16; P = .002), Erysipelotrichia (OR: 1.05; 95% CI: 1.02-1.09; P = .003) and so on. Bidirectional association was found between Coprococcus or Lachnospiraceae and AF. In this study, MR analysis showed that there was a potential mutually causality between gut microbiota and the risk of AF, which may provide new insights for further studies of the role of gut microbiota in AF pathophysiology and development.

Thyroid hormones may accelerate heart rate and enhance cardiac contractility, improving both systolic and diastolic functions of heart, while reducing systemic vascular resistance at rest. Thyroid dysfunction may be associated with an increased risk of cardiovascular disease (CVD). However, current findings are not entirely consistent, and variations in thyroid hormone sensitivity may serve as a key factor underlying the inconsistent associations between thyroid function and CVD. Hence, the present narrative review synthesizes the association between thyroid hormone sensitivity and common CVDs, such as hypertension, coronary heart disease (CHD), and stroke. The possible molecular mechanisms of thyroid hormone sensitivity-mediated cardiovascular pathology are also summarized. We found that most studies failed to establish a significant relationship between peripheral, central thyroid hormone sensitivity and hypertension. Further, current studies generally suggest a positive correlation between reduced peripheral thyroid hormone sensitivity and an increased risk of stroke. Similarly, most studies indicate that reduced thyroid hormone sensitivity is associated with an elevated risk of adverse clinical outcomes after CHD.

Coronary artery lesions (CAL) complicating Kawasaki disease (KD) are a central concern affecting the long-term cardiovascular health of affected children. This study aimed to systematically depict the macro landscape, knowledge structure, and evolutionary dynamics of this field through bibliometric and knowledge graph methods, providing strategic guidance for future research.

Literature related to KD-CAL was retrieved from the Web of Science Core Collection. Quantitative and visual analyses of publication trends, countries/regions, institutions, authors, journals, references, and keywords were conducted using CiteSpace 6.3.R1, VOSviewer 1.6.20, and the Bibliometrix R package.

A total of 2655 publications were included. The annual publication volume showed an increasing trend, with acceleration after 2015. The United States emerged as the country with the highest productivity and influence (citation frequency, centrality), while China ranked first in publication output (909 articles) but had a lower rate of international collaboration (MCP_Ratio = 0.08). The core journal cluster comprised Circulation, Journal of Pediatrics, and Pediatric Cardiology, among others. A close international collaboration network was formed around key figures like Jane Carleton Burns and Adriana H. Tremoulet. Keyword and document co-citation analyses revealed 5 major research clusters: acute-phase management, immunopathological mechanisms, coronary complications, treatment of intravenous immunoglobulin resistance, and long-term follow-up. The research frontier has evolved from "epidemiology" and "diagnosis" to "biomarkers" and "IVIG resistance," and is now predominantly focused on "biologics" (e.g., infliximab, anakinra) and "artificial intelligence/machine learning."

The new phase of KD-CAL research may focus on precision medicine. Future efforts may focus on deepening immunological mechanism studies to develop targeted therapies, utilizing artificial intelligence to optimize risk stratification and imaging assessment, and establishing globally collaborative long-term cohorts to clarify cardiovascular outcomes in adulthood. Strengthening basic and clinical translation is essential to advance KD-CAL diagnosis and treatment into a new era of precision and efficiency.

Occupational therapy (OT) is an important component of stroke rehabilitation, but the global research landscape, collaboration patterns, research hotspots, and emerging trends in OT for stroke have not been systematically mapped. This bibliometric study aimed to analyze publications on OT for stroke from 2006 to 2025 and provide evidence for future clinical practice and research planning.

English-language articles related to OT for stroke were retrieved from the Web of Science Core Collection from January 1, 2006, to October 31, 2025. After applying predefined inclusion and exclusion criteria, bibliometric and visualization analyses were performed using VOSviewer and CiteSpace 6.4.R1. Publication trends, countries, institutions, authors, journals, keyword co-occurrence, keyword clustering, timeline evolution, and burst terms were analyzed.

A total of 770 publications were included. The annual number of publications showed a fluctuating but overall upward trend, with the highest output observed in 2021 and 2022, each with 60 publications. The United States, Australia, the United Kingdom, and China were the leading contributing countries, while Jikei University and La Trobe University were the most productive institutions. The most prolific authors were Masahiro Abo and Louise Gustafsson. The British Journal of Occupational Therapy and Topics in Stroke Rehabilitation were the leading journals in terms of publication output. Keyword analyses showed that early research mainly focused on upper-limb function, functional recovery, and basic rehabilitation interventions, whereas recent hotspots have expanded to neurorehabilitation, knowledge translation, virtual reality, clinical trials, mental health, and home-based rehabilitation.

Research on OT for stroke has increased overall over the past 2 decades, with evolving hotspots from impairment-oriented rehabilitation toward broader, occupation-centered, participation-oriented, technology-assisted, and home-based rehabilitation approaches. However, collaboration among countries, institutions, and authors remains relatively fragmented. Future studies should strengthen international and interdisciplinary cooperation and generate high-quality clinical evidence to support OT practice in stroke rehabilitation.

A large number of functional disorders and uncomfortable symptoms often remain following ischemic stroke (IS). Existing drug therapy is not ideal for the direct improvement of symptoms, which often leads to poor patient compliance with physical rehabilitation therapy. Buyang Huanwu Decoction (BYHWD) is a famous prescription that is effective in treating IS, especially during the sequela stage of IS. We analyzed the therapeutic mechanism of BYHWD through network pharmacology. This study aims to investigate the potential active ingredients, targets, and signaling pathways of BYHWD for the treatment of IS, utilizing network pharmacology and molecular docking technology. The active ingredients of 7 Chinese herbs in BYHWD were obtained from the Traditional Chinese Medicine Systems Pharmacology and HERB databases, and IS-related disease targets were searched in the DisGeNET, GeneCards, and OMIM databases. The protein-protein interaction network was constructed using the STRING database and analyzed by Cytoscape 3.10.2 software. Additionally, the target genes were uploaded to the Database for Annotation, Visualization, and Integrated Discovery website for Gene Ontology alongside Kyoto Encyclopedia of Genes and Genomes analyses. With the assistance of AutoDockTools and PyMOL software (Schrödinger, Inc.), a validation of molecular docking results and a visualization of the results were performed. The results showed that there were 190 intersection targets between the active drug components and IS, corresponding to 61 active components, among which the top 5 target genes were tumor suppressor protein 53, Jun proto-oncogene, AKT serine/threonine kinase 1, mitogen-activated protein kinase 1, and estrogen receptor alpha. The PI3K-Akt signaling pathway is one of the top 10 pathways. The molecular docking results indicated that most of the top 5 targets had good affinities for the 8 core compounds. This computational analysis suggests that BYHWD may treat IS through multiple targets and pathways. It may play a neuroprotective role by regulating the inflammatory response, oxidative stress, apoptosis, autophagy, and vascular endothelial homeostasis. The identification of core effective components provides a theoretical foundation and candidate compounds for further investigation into new drugs for the treatment of sequelae after IS.

Coffee is one of the most widely consumed beverages worldwide, yet its biological effects have often been attributed primarily to caffeine. Emerging evidence suggests that coffee contains a complex array of bioactive compounds, including chlorogenic acids, trigonelline, diterpenes, and melanoidins that collectively exert pleiotropic effects on cellular metabolism. However, a comprehensive framework linking the full spectrum of coffee-derived bioactives to mitochondrial health and chronic disease prevention is still lacking.

This review proposes an integrated perspective on coffee as a systemic "mitochondrial network optimizer." We present this model as an integrative framework and hypothesis rather than an established causal model. We synthesize molecular, pre-clinical, and clinical evidence suggesting that coffee bioactives converge on key regulatory nodes, namely the AMPK/SIRT1/PGC-1α axis, Nrf2/ARE antioxidant pathway, PINK1/Parkin-mediated mitophagy, and mitochondrial calcium signaling to coordinately enhance mitochondrial biogenesis, quality control, redox defense, and metabolic efficiency. These multi-targeted mechanisms provide a plausible biological basis for the consistent epidemiological associations between moderate coffee consumption and reduced risk of metabolic diseases (type 2 diabetes, non-alcoholic fatty liver disease), neurodegenerative disorders (Parkinson's, Alzheimer's), and cardiovascular conditions. Furthermore, we critically examine key determinants of response heterogeneity, including non-linear hormetic dose-response relationships, inter-individual variability (CYP1A2 genotype, gut microbiota, sex), and the impact of coffee processing and brewing methods on bioactive composition.

Collectively, these findings support the hypothesis that coffee may serve as a paradigm of polypharmacological dietary intervention that targets fundamental pathways of mitochondrial resilience. Moving beyond reductionist views centered on single compounds, we propose that the holistic effects of coffee are best understood through systems-level modulation of mitochondrial homeostasis. Future research should prioritize precision nutrition approaches stratified by genotype, microbiome, and metabolic phenotype, to translate these mechanistic insights into personalized dietary recommendations and the development of mitochondria-targeted nutraceuticals. We caution that this integrative framework requires direct validation in human causal studies.