Background: Ultraviolet B exposure may influence vascular homeostasis and extracellular matrix remodeling. Thoracic aortic aneurysm (TAA) is characterized by progressive aortic wall degeneration; however, its relationship with sunburn susceptibility remains unclear.Objective:This study was aimed at investigating whether genetically predicted sunburn susceptibility might be associated with TAA risk, and to explore potential genomic and transcriptomic mechanisms. Methods: We performed two-sample Mendelian randomization on sunburn susceptibility and TAA GWAS data from 350,232 and 19,646 individuals of European ancestry. PheWAS and pigmentation-locus sensitivity analyses were conducted to assess instrument architecture. Genetic loci were annotated using FUMA SNP2GENE and GTEx eQTL mapping, and molecular evidence was explored using ssGSEA, differential-expression analysis, functional enrichment, PPI analysis, and exploratory candidate-gene prioritization. Results: Genetically predicted sunburn susceptibility was inversely associated with TAA (inverse-variance weighted OR = 0.403, 95% CI = 0.216-0.752, P = 0.004). However, this association was attenuated after exclusion of 11 pigmentation-related SNPs. Transcriptomic analyses implicated UV-response signatures, matrix and vascular remodeling, immune trafficking, ERK signaling, cell junctions, and vesicle-related processes. Integrated analyses identified HYAL1 and PREPL as priority candidates for further exploration. Conclusion: The association between sunburn susceptibility and TAA appeared to be largely driven by the pigmentation and tanning-response genetic architecture. Exploratory evidence linked phototype-related variation to matrix turnover, intracellular trafficking, and vascular remodeling.

Background: An integrated evaluation of medical therapy and surgical intervention for mitral regurgitation (MR) regression is necessary. Methods: Eligible studies in five electronic databases were screened by two independent reviewers. Relative risk (RR) was calculated for an echocardiographic MR grade ≤ 2+, and the standard mean difference (SMD) was calculated for the percentage change in MR severity and left ventricular/atrial volume with random-effects models. Results: A total of 24 RCTs including 3711 patients were collected. Overall medical therapy decreased MR area (SMD = −1.13) and volume (SMD = −0.76), whereas angiotensin receptor and neprilysin inhibitors (SMD = −0.49) and sodium glucose cotransporter-2 inhibitors (SMD = −0.70) had better performance, on the basis of decreased left atrial volume. Transcatheter mitral valve repair (TMVr) performed similarly to mitral valve surgery (MVS) (RR = 0.99) but better than nonsurgical controls (RR = 3.02), according to 12-month MR grade ≤ 2+. The addition of MVS to coronary artery bypass grafting was associated with more ≤ 2+ MR (RR = 1.66) and lower left ventricular volume (SMD = −0.49) (all P < 0.05). A network meta-analysis supported the 12-month benefits of TMVr and MVS for nonrecurrent MR. Conclusion: TMVr and MVS were associated with nonrecurrent MR, and medical therapy also decreased MR. The combination of medication and surgery might potentially be beneficial to reduce left heart size and to preserve its output.

Obesity, given its strong association with cardiovascular diseases (CVDs), is a major global public health issue attracting increasing attention. This comprehensive review systematically synthesizes clinical and basic research progress in elucidating the complex relationship between obesity and CVDs. We explore the epidemiology, pathophysiology, clinical manifestations, and management strategies for obesity-related CVDs. Drawing on recent studies, we highlight the effects of obesity on atherosclerotic disease, cardiomyopathy, heart failure, arrhythmias, hypertension, and venous thromboembolism. Understanding these mechanisms is essential for developing effective prevention and treatment strategies to decrease the cardiovascular burden associated with obesity. Furthermore, this review summarizes current therapeutic approaches for obesity-related CVDs, such as lifestyle interventions, pharmacotherapy, and metabolic surgery, and discusses future research directions, including precision medicine, exploration of novel therapeutic targets, and single-cell spatiotemporal omics.

Dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) increases the risk of upper gastrointestinal bleeding (UGIB). Proton pump inhibitors (PPIs) are widely used for gastroprotection but have limitations including delayed onset of action and potential interactions with clopidogrel. Potassium-competitive acid blockers (P-CABs) might provide an alternative with more rapid and consistent acid suppression. This systematic review and meta-analysis of observational studies compared P-CABs versus PPIs for the prevention of UGIB in patients receiving DAPT after PCI. Major literature databases were searched for articles published until March 2026. Risk of bias was assessed with ROBINS-I, and pooled odds ratios (ORs) were estimated with random-effects models. Six cohort studies in 42,304 patients were analyzed. No significant difference in UGIB was observed between P-CABs and PPIs (OR 1.03, 95% CI 0.77-1.37; I² = 4%). Sensitivity analysis excluding studies with high risk of bias yielded consistent results (OR 0.96, 95% CI 0.70-1.30). No significant differences were observed in major adverse cardiovascular events or all-cause mortality. The certainty of evidence was very low because of confounding and imprecision. P-CABs appeared comparable to PPIs in preventing UGIB in this population; however, randomized trials are needed.

Aging is an inevitable biological process marked by progressive functional decline and elevated risk of cardiovascular diseases (CVDs). This review systematically examines the clinical mechanisms linking aging to cardiovascular pathology, focusing on molecular, cellular, and physiological changes that contribute to cardiovascular aging, which in turn increases the incidence of heart failure, atherosclerosis, atrial fibrillation, and other diseases. Key mechanisms include metabolic dysregulation, mitochondrial dysfunction, chronic inflammation, cellular senescence, immune disorders, and epigenetic changes. Understanding these mechanisms is crucial for developing targeted interventions to delay cardiovascular aging and alleviate CVD burden in older people. Current therapeutic strategies, including lifestyle modifications, pharmacotherapy, gerotherapeutic interventions, and device-based management, are reviewed, along with future directions in precision medicine, development of novel therapeutic targets, multi-omics, and AI-powered strategies against cardiovascular aging.

Low consumption of fruits and vegetables (FV) is a major preventable contributor to cardiovascular disease (CVD). Insufficient FV intake has been estimated to account for nearly 3 million CVD deaths and more than 70 million disability-adjusted life years worldwide. This review examines global patterns of FV intake; evidence linking FV consumption to cardiovascular outcomes; underlying biological mechanisms determined through in vitro and in vivo studies; serving size frameworks; current global recommendations; barriers to FV intake; and practical advice to increase FV intake. Although global FV intake has modestly increased in recent decades, consumption remains substantially below recommended levels in all regions, and marked disparities exist among countries. Evidence from meta-analyses of randomized controlled trials and intervention studies of individual fruits and vegetables has shown that FV intake improves cardiometabolic risk factors, and large prospective cohort studies have consistently demonstrated inverse associations between FV intake and CVD incidence and mortality. Experimental mechanistic studies have further supported these findings by identifying shared cardioprotective mechanisms mediated by FV-derived bioactive compounds. However, several practical and theoretical constraints limit the recommendation of adequate FV intake. This review proposes a practical serving-size framework based on macronutrient content, wherein one serving of fruit provides approximately 15 g carbohydrates (~60 kcal), and one serving of vegetables provides approximately 5 g carbohydrates (~25 kcal). By addressing key barriers and presenting practical dietary strategies, this review highlights the importance of promoting FV consumption at both the individual and population levels to decrease CVD risk and improve cardiovascular health outcomes.

Objective: The global burden, secular trends, and future projections of ischemic cardio-cerebrovascular disease (ICCVD), a composite indicator of ischemic heart disease (IHD) and ischemic stroke (IS), have not been specifically described in women. This study was aimed at estimating the global ICCVD burden from 1990 to 2021, and the projected burden from 2022 to 2050, in women. Methods: Age-standardized incidence, prevalence, mortality, and disability-adjusted life years (DALYs) with 95% uncertainty intervals (UI), and corresponding average annual percentage change (AAPC) with 95% confidence intervals (CI) and associated P-values, were calculated for women at global, regional, and national levels according to data from Global Burden of Disease 2021. Age-specific patterns, DALYs attributable to risk factors, and DALY projections to 2050 were also examined. Results: In women, the global age-standardized prevalence of ICCVD increased from 3063 (95% UI: 2786 to 3339) per 100,000 population in 1990 to 3127 (2778 to 3476) per 100,000 population in 2021, and the AAPC was 0.03% (95% CI: 0.02% to 0.05%), whereas the incidence, mortality, and DALYs decreased (all P < 0.001). Notably, the age-standardized ICCVD incidence among women resurged in the past decade (0.29%), following a decline from 1990 to 2011 (−0.66%), whereas men experienced a consistent decline between 1990 and 2021. Low-middle Sociodemographic Index (SDI) countries consistently exhibited the highest age-standardized ICCVD incidence among women from 1990 to 2021, whereas only middle SDI countries demonstrated an increasing trend in age-standardized incidence over this period. Age-specific incidence rates increased among people younger than 60 years (0.14%) but decreased among people older than 60 years (−0.55%). High systolic blood pressure remained the leading risk factor for ICCVD in women, whereas high temperatures exhibited the most rapid relative increase in associated DALYs. DALYs for ICCVD in women are projected to continue declining through 2050, but the fatal burden will remain substantial, accounting for 87.4% of the total burden in 2050. Conclusions: ICCVD has posed a severe burden on women, largely driven by a notable resurgence in its incidence and prevalence over the past decade, alongside a pronounced increase in early-onset cases. Despite the projected decreasing trend in DALYs by 2050, the fatal burden is expected to remain the leading health threat. Our findings highlight the urgent need for public health strategies focusing on risk factor management and effective treatment to mitigate the ICCVD burden among women.

Background: Cardiovascular disease (CVD) is a leading cause of mortality among cancer survivors, yet the contributions of socioeconomic, lifestyle, and clinical factors to CVD remain unexplored. Objective: This study was aimed at examining associations between these factors and prevalent CVD in adults with prior cancer and comparing them with those in a matched non-cancer cohort. Methods: We analyzed 97,648 adults from the National Health and Nutrition Examination Survey. Associations of socioeconomic, lifestyle, and clinical factors with a composite endpoint of five self-reported cardiovascular events were assessed with multivariable logistic regression. Interaction analyses assessed differences by cancer status, and sensitivity analyses examined individual cardiovascular outcomes. Results: We included 5584 cancer survivors and 9933 matched participants without cancer. Age, sex, unemployment, low income, current smoking, obesity, diabetes, hypertension, and hypercholesterolemia were associated with elevated odds of CVD prevalence in both groups. Among only cancer survivors, an absence of private insurance, or the presence of food insecurity or low educational attainment, was also independently associated with CVD prevalence. Sensitivity analyses indicated broadly consistent results across individual outcomes. Conclusions: Socioeconomic, lifestyle, and clinical factors were associated with prevalent CVD among cancer survivors, with socioeconomic disadvantage contributing to disparities in CVD burden. Because the outcomes were self-reported, and the study was cross-sectional, the findings should be interpreted as associative rather than causal or predictive.

Background: The long-term effects of sustained weight gain and loss on atrial fibrillation (AF) risk remain unclear. Herein, we examined associations between long-term weight change and incident AF. Methods: We analyzed 64,119 AF-free participants from the Kailuan cohort whose height and weight were measured in 2006-2007 and 2010-2011. Weight change was assessed as changes in body mass index (BMI), body weight, and percentage weight changes. Incident AF was ascertained according to International Classification of Diseases codes and biennial electrocardiograms. Multivariable Cox models estimated hazard ratios (HRs) and 95% confidence intervals (CIs). Results: Over a median 10.0 years’ follow-up, 583 participants developed AF. Compared with stable BMI (−3 to 3 kg/m²), BMI loss ≥3 kg/m² was associated with diminished AF risk (HR 0.61, 95% CI 0.41-0.91), whereas BMI gain ≥3 kg/m² was associated with elevated risk (HR 1.41, 95% CI 1.01-1.97). Similarly, weight loss ≥10 kg was associated with diminished AF risk (HR 0.54, 95% CI 0.31-0.92), whereas weight gain ≥10 kg was associated with elevated AF risk (HR 1.66, 95% CI 1.12-2.36). The findings were consistent across percentage-change definitions. Conclusions: Long-term weight gain was associated with elevated incident AF risk, whereas sustained weight loss was associated with diminished risk, thus supporting the importance of long-term weight management for AF prevention.

Cardiovascular disease develops through gradual accumulation of risk factors and progressive vascular damage. Longitudinal studies are well suited to determine when and how these changes occur, but they introduce several analytic challenges, including repeated measurements on the same individuals, irregular or sparse follow-up schedules, missing data, and non-linear trajectories. We conducted a narrative, application-focused review categorizing methods into five major classes: traditional or marginal models, mixed-effect models, joint models, trajectory and mixture models, and functional or machine-learning approaches. For each class, we provide intuitive descriptions, typical cardiovascular applications, and a balanced discussion of assumptions, strengths, limitations, and recommended sensitivity analyses. We emphasize practical guidance for method selection, model validation, and transparent reporting. In summary, no single method addresses every research goal. The analytic strategy should fit both the clinical question and data characteristics, with clear definition of objectives, careful assessment of assumptions, appropriate handling of missing data, and validation on independent samples whenever possible. Future methodological development should focus on making hybrid models more accessible, improving integration of sparse and dense data sources, and advancing reporting standards for longitudinal cardiovascular research.

Background: Stroke survivors often experience physical dysfunction, fatigue, and cognitive impairment, and may also spend prolonged periods engaged in sedentary behavior because of daily living demands. However, the specific effects of sedentary behavior on stroke prognosis remain unclear. Methods: A comprehensive search of PubMed, Embase, the Cochrane Library, and Web of Science, covering all records from database inception to March 2026, was conducted through both computer-based and manual methods. Results: A random-effects model was applied for the meta-analysis. Seven studies involving 1874 participants, with a median follow-up duration of 2.17 years, were included. During the post-stroke period characterized by sedentary behavior, changes in the fatigue severity scale (FSS; 95% CI: 2.99-3.42, P = 0.02) and physical function (SIS, BMI, and BAPAS) were observed in 202 participants. In addition, the incidence of various diseases during follow-up was increased in 1374 participants, and changes in blood glucose levels were reported in 178 participants. However, owing to the heterogeneity of assessment scales used across studies, the forest plots showed substantial heterogeneity (I² > 80%). Therefore, our findings have limited clinical interpretability and should be considered to indicate overall trends. Conclusions: The overall trends from this meta-analysis suggest that higher sedentary behavior may be associated with adverse effects on physical function, fatigue, cardiovascular events, and blood glucose levels during stroke prognosis. Such behavior might decrease quality of life during survival, and increase the risks of stroke recurrence and other diseases. The specific mechanisms underlying the association between sedentary behavior and stroke prognosis require further investigation and confirmation.

Objective: Heart disease remains a leading cause of global mortality; consequently, accurate, reliable, and interpretable predictive models are needed for early diagnosis. This study was aimed at developing a robust hybrid ensemble learning framework that improves heart disease predictive accuracy while preserving clinical interpretability. Methods: The Cardio-Sense Ensemble Framework (CSEF) for heart disease prediction was developed by using the publicly available Behavioral Risk Factor Surveillance System dataset. Laplacian binary optimization was used for optimized feature selection, to eliminate redundancy and enhance discriminative information. The refined feature set was used to train multiple baseline classifiers, including logistic regression, random forest, K-nearest neighbors, and XGBoost. Their outputs were combined with Light Gradient Boosting Machine as a meta-classifier. Model performance was assessed with accuracy, sensitivity, specificity, and the area under the receiver operating characteristic curve (AUC). Results: The CSEF achieved an accuracy of 0.98 and an AUC of 0.98, thus outperforming conventional machine learning models while demonstrating improved sensitivity and specificity. Conclusion: Our hybrid ensemble framework offers superior predictive performance and interpretability; therefore, it is suitable for early cardiovascular risk screening and clinical decision-support integration.

Acute coronary syndrome (ACS), a primary manifestation of coronary artery disease (CAD), remains a leading cause of global mortality, particularly in low-and middle-income countries. Despite advances in diagnostics and therapy, accurate early risk stratification of ACS remains challenging. Traditional biomarkers such as cardiac troponins and CK-MB are essential for diagnosis but do not capture the full complexity of disease severity, particularly in cases involving inflammation, endothelial dysfunction and plaque instability. This review highlights emerging evidence regarding the roles of inflammatory cytokines and novel biomarkers in ACS pathophysiology, diagnosis and prognostication. Pro-inflammatory cytokines such as IL-6, IL-18 and TNF-α play key roles in atherogenesis and plaque destabilization, whereas anti-inflammatory mediators such as IL-10 and TGF-β decrease vascular injury. Novel biomarkers including Copeptin, GDF-15, microRNAs, sST2, Galectin-3, Endocan and MMP-9 offer enhanced prognostic capabilities and, in contrast to traditional biomarkers, often provide additional prognostic information in specific scenarios. Integrating these biomarkers with advanced risk models such as the GRACE score and digital health technologies, including AI, is transforming ACS management. However, challenges persist in standardization, cost-effectiveness, real-time implementation and interpretation in comorbid populations. This review emphasizes the potential of these biomarkers in improving personalized care and treatment for patients with ACS, while addressing evidence levels, clinical bottlenecks and integration strategies.

Tricuspid regurgitation (TR) is common and associated with substantial morbidity and mortality. Although optimized medical therapy (OMT) can alleviate symptoms, it may be insufficient in severe cases, and surgical interventions carry considerable procedural risk, limiting their use; consequently, tricuspid transcatheter valve interventions (TTVIs) have emerged as a less invasive alternative. We conducted a systematic search of PubMed, Scopus, and Web of Science to identify randomized clinical trials and observational studies comparing TTVI plus OMT versus OMT alone. The primary outcome was all-cause mortality, and secondary outcomes included heart failure (HF) hospitalization and a combined outcome of all-cause mortality and HF hospitalization. Eight studies (five observational and three randomized trials) comprising 4836 patients were included. Compared with OMT alone, TTVI plus OMT was associated with a significant reduction in all-cause mortality (HR = 0.59, 95% CI: 0.44-0.78, P < 0.001) and HF hospitalization (HR = 0.69, 95% CI: 0.49-0.96, P = 0.03), and it significantly reduced the combined outcome (HR = 0.59, 95% CI: 0.47-0.74, P < 0.001). However, subgroup analysis showed that the mortality benefit was driven primarily by observational studies (HR = 0.48, 95% CI: 0.37-0.61), whereas randomized trials demonstrated no significant difference (HR = 0.88, 95% CI: 0.75-1.03). Overall, TTVI combined with OMT may be associated with lower mortality and HF hospitalization compared with OMT alone, although the apparent benefit is largely derived from non-randomized evidence.

Background: Hypertensive disorders of pregnancy (HDP), the third leading cause of maternal mortality worldwide, account for approximately 16% of all maternal deaths. The incidence and mortality rates of HDP vary across regions. Objective: This study was aimed at examining global trends in HDP prevalence from 1990 to 2021, identifying major risk factors associated with HDP-related mortality, and assessing the influence of dietary habits on HDP risk. Methods: Using data from the 2021 global burden of disease (GBD) study, we conducted a cross-sectional analysis across 204 countries and 21 regions. The estimated annual percentage change was used to evaluate trends in incidence, disability-adjusted life years (DALYs), and mortality associated with HDP. Mendelian randomization analysis was applied to investigate the causal relationships between dietary habits and HDP risk. In addition, projections of HDP prevalence were made through 2035 according to GBD data. Results: Although the absolute number of HDP cases has risen, HDP incidence, DALYs, and mortality rates have declined globally. Regional, age-related, and socioeconomic disparities persist, and low-income countries are disproportionately affected because of limited healthcare resources. Behavioral risks, maternal and child malnutrition, and iron deficiency were identified as risk factors for HDP-related mortality. Conclusions: Despite the overall decline in HDP incidence, DALYs, and mortality rates over the past 3 decades, the persistent high burden in low socio-demographic index regions highlights the urgent need for targeted health interventions. Addressing broader socioeconomic determinants is essential to sustainably decrease the global effects of HDP.

In normal cardiac energy metabolism, 95% of the heart’s energy is provided by mitochondria, and preferences for energy-providing substrates vary at different times (Nguyen BY, Ruiz-Velasco A, Bui T, Collins L, Wang X, Liu W. Mitochondrial function in the heart: the insight into mechanisms and therapeutic potentials. Br J Pharmacol 2019;176(22):4302-4318). However, prolonged metabolic alterations impair cardiac function (Hu L, Tang D, Qi B, Guo D, Wang Y, Geng J, et al. Mfn2/Hsc70 complex mediates the formation of mitochondria-lipid droplets membrane contact and regulates myocardial lipid metabolism. Adv Sci (Weinh) 2024;11(14):e2307749). Therefore, this study primarily focuses on the relationship between amino acid metabolism and diabetic cardiomyopathy and atherosclerosis. Changes in metabolic processes also promote the development and worsening of these two diseases. Lipid and glucose metabolism in such diseases have been extensively studied, and emerging evidence suggests that amino acid metabolism also plays major roles in diabetic cardiomyopathy and atherosclerosis. Specific amino acid intake or catabolism might influence oxidative stress, inflammation, and fibrosis, among related processes, thus indirectly highlighting their potential as novel targets for metabolic interventions. However, the mechanisms and clinical relevance of amino acid metabolism in these diseases remain incompletely understood and warrant further investigation.

Osteoprotegerin (OPG), a glycoprotein in the tumor necrosis factor superfamily, regulates bone metabolism by suppressing the formation and activation of osteoclasts. Nonetheless, increasing evidence underscores its physiological importance, particularly in cardiovascular diseases (CVDs). Elevated OPG levels are associated with atherosclerosis, arterial calcification, and heart failure, thus indicating their involvement in cardiac remodeling and vascular pathology. OPG regulates calcification and vascular homeostasis by restricting the transdifferentiation of vascular smooth muscle cells into osteogenic phenotypes. OPG expression is aberrant in illnesses posing cardiovascular risk, such as aortic valve stenosis, chronic renal disease, and diabetes. Beyond structural regulation, OPG interacts with inflammatory and apoptotic mediators, including RANKL and TRAIL, in signaling pathways linking bone metabolism, inflammation, and vascular dysfunction. Myocardial infarction, left ventricular remodeling, and mortality are associated with elevated circulating OPG and altered OPG/TRAIL ratios. This review discusses molecular and clinical insights regarding OPG’s multifaceted role in CVDs, highlighting its potential as a regulator of disease etiology and a predictive biomarker. In cardiovascular medicine, understanding the OPG/RANKL/TRAIL axis has potential to facilitate targeted therapy and risk stratification.

Cardiovascular diseases (CVDs), a leading global cause of mortality, are characterized by complex pathogenesis involving multifactorial molecular and cellular processes. Pannexin-1 (Panx1), a transmembrane channel protein, facilitates intercellular signaling through regulated release of small molecules such as adenosine triphosphate (ATP), thereby modulating diverse physiological and pathological pathways. This review explores the structural and functional landscape of Panx1, including its physiological roles, post-translational modifications and activation mechanisms. Its contributions to the pathophysiology of myocardial ischemia-reperfusion injury, cardiac remodeling, electrophysiological abnormalities, and diabetic cardiomyopathy are emphasized. Current evidence highlights the dual pathophysiological roles of Panx1 channels in CVDs: whereas ATP-mediated activation initiates cytoprotective signaling cascades, channel hyperactivation exacerbates pathological progression. Future research should prioritize mechanistic elucidation of Panx1’s molecular biology, and the development of targeted inhibitors with enhanced specificity and therapeutic efficacy, to advance novel therapeutic strategies for cardiovascular disorders.

Background: Transglutaminase 2 (TGM2) has been implicated in various health conditions, yet its role in acute coronary syndrome (ACS) remains poorly characterized in clinical settings. This study investigated the association between circulating TGM2 levels and the severity of coronary stenosis in ACS. Methods: A total of 242 individuals with ACS were included in this study. Clinical data were collected, and the severity of coronary stenosis was evaluated with the Gensini and Syntax scoring systems. Kaplan-Meier analysis, logistic regression, and receiver operating characteristic (ROC) curve analysis were performed. Results: Circulating TGM2 levels were significantly higher in the STEMI group (176.3 pg/mL) and the non-STEMI group (181 pg/mL) than the UA group (64 pg/mL) and the stable CAD group (50.95 pg/mL) (P < 0.001). Multivariate analysis, after adjustment for confounding factors, identified TGM2 as an independent risk factor for acute myocardial infarction (odds ratio: 44.292 per 100 pg/mL increase in TGM2; 95% CI: 2.491-7.398; P < 0.001). During a median follow-up of 477 days, Kaplan-Meier survival analysis demonstrated that patients with higher TGM2 levels (≥91.9 pg/mL) exhibited a significantly lower MACE-free survival rate (P = 0.0142). ROC curve analysis further revealed that combining TGM2 and Gensini scores yielded superior predictive performance for MACE to that of either parameter alone. Conclusion: Circulating TGM2 is elevated in ACS and is strongly associated with the presence of AMI. Furthermore, it provides prognostic information for MACE, particularly when it is used in combination with established anatomical risk scores.

Objective: This study investigated the association between serum uric acid (UA) levels and atrial fibrillation (AF) burden in Chinese patients with AF. Methods: In this cross-sectional study, AF burden was defined as the proportion of AF duration to total monitoring time, recorded by a patch device over ≥24 hours. Serum UA levels were measured at the start of monitoring. Multivariate logistic regression was used to assess associations. Results: A total of 952 patients with AF (66.4% women; median age 64 years) were included. A 1-SD increase in UA (91.4 μmol/L) was associated with elevated risk of persistent AF (adjusted OR: 1.32; 95% CI: 1.12-1.55; P < 0.001). The highest UA quintile had a greater risk of persistent AF than the lowest quintile of patients (adjusted OR: 2.43; 95% CI: 1.49-3.98; P for trend < 0.001). Conclusion: Serum UA levels are positively associated with AF burden in a dose-dependent manner. UA might serve as an accessible biomarker and potential therapeutic target for AF burden assessment.