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Background Electrocardiogram (ECG) interpretation is an integral part of the clinical ECG workflow; however, this process is often time‐consuming and labor‐intensive. We aim to develop a rapid, inexpensive means to detect abnormal ECGs using artificial intelligence (AI) from scanned ECG printouts. Methods The study included 1172 12‐lead ECG scans performed in 1172 individuals from a community in Guangzhou, China; 878 (74.9%) were diagnosed with sinus rhythm, and the remaining 294 (25.1%) with abnormal rhythms. A deep learning model consisting of a convolutional neural network based on InceptionV3 and a fully connected layer followed by a GEV activation was trained to classify scanned tracings as either normal or abnormal. Results In a hold‐out testing set, the model achieved a area under curve (AUC), sensitivity, specificity, PPV, and NPV of 0.932 (95% confidence interval [CI]: 0.890, 0.976), 0.816 (95% CI: 0.657, 0.923), 0.993 (95% CI: 0.959, 1.0), 0.969 (95% CI: 0.838, 0.999), and 0.950 (95% CI: 0.90, 0.980) respectively, when using a probability threshold of 0.5. When compared with a physiological expert, these results show comparable performance with a statistically significant increase in specificity and a non‐significant decrease in sensitivity at the 95% level. Conclusions We have developed a rapid, inexpensive, accurate means to detect abnormal ECGs using AI. Easy and accurate identification of such “abnormal” ECGs could allow the mass automated review of ECGs in community settings where abnormal ones could be flagged using AI for detailed clinical review by healthcare professionals. We developed a deep learning algorithm that uses scanned ECG printouts to predict normal or abnormal rhythm. In addition, the method can produce saliency maps, showing which areas are relevant in the diagnosis to aid interpretability. The method has applications in low resource settings such as screening, where electrophysiological experts may not be available.

Background and objective Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the United States. However, current evidence on the association between muscle quality and CVD is limited. This study investigates the potential association between the muscle quality index (MQI) and the prevalence of CVD and CVD-related mortality. Methods Participants were selected from the National Health and Nutrition Examination Survey (NHANES) 2011–2014. Data on mortality and causes of death were obtained from the National Death Index (NDI) records through December 31, 2019. Statistical analysis used in this study, including weighted multivariable linear and logistic regression, cox regression and Kaplan-Meier (K-M) analysis, to estimate the association between MQI and all-cause mortality as well as CVD mortality. In addition, subgroup analysis was used to estimate the association between MQI and CVD subtypes, such as heart attack, coronary heart disease, angina, congestive heart failure, and stroke. Results A total of 5,053 participants were included in the final analysis. Weighted multivariable linear regression models revealed that a lower MQI.total level was independently associated with an increased risk of CVD development in model 3, with t value =-3.48, 95%CI: (-0.24, -0.06), P  = 0.002. During 5,053 person-years of 6.92 years of follow-up, there were 29 deaths from CVD. Still, the association between MQI.total and CVD mortality, as well as all-cause mortality did not reach statistical significance in the fully adjusted model (HR = 0.58, 95% CI: 0.21–1.62, P  = 0.30; HR = 0.91, 95% CI:0.65,1.28, P  = 0.59, respectively). Subgroup analysis confirmed that MQI.total was negatively associated with congestive heart failure (OR = 0.35, 95% CI = 0.18,0.68, P  = 0.01). Conclusion This study highlights the potential of MQI as a measure of muscle quality, its negative correlation with congestive heart failure (CHF). However, MQI was not very useful for predicting the health outcomes such as CVD and mortality. Therefore, more attention should be paid to the early recognition of muscle weakness progression in CHF. Further studies are needed to explore more effective indicator to evaluate the association between muscle quality and health outcomes.

Socioeconomic status (SES) has been linked to mortality rates, with family income being a quantifiable marker of SES. However, the precise association between the family income-to-poverty ratio (PIR) and all-cause mortality in adults aged 40 and older remains unclear. A cross-sectional study was conducted using data from NHANES III, including 20,497 individuals. The PIR was used to assess financial status, and various demographic, lifestyle, and clinical factors were considered. Mortality data were collected from the NHANES III linked mortality file. The study revealed a non-linear association between PIR and all-cause mortality. The piecewise Cox proportional hazards regression model showed an inflection point at PIR 3.5. Below this threshold, the hazard ratio (HR) for all-cause mortality was 0.85 (95% CI 0.79–0.91), while above 3.5, the HR decreased to 0.66 (95% CI 0.57–0.76). Participants with lower income had a higher probability of all-cause mortality, with middle-income and high-income groups showing lower multivariate-adjusted HRs compared to the low-income group. This study provides evidence of a non-linear association between PIR and all-cause mortality in adults aged 40 and older, with an inflection point at PIR 3.5. These findings emphasize the importance of considering the non-linear relationship between family income and mortality when addressing socioeconomic health disparities.

BackgroundThe role of catheter ablation as an adjunct and alternative to ICD implantation is not known in patients at risk for recurrent ventricular tachycardia (VT) and sudden cardiac death (SCD) across Asia. Patients with nonischemic etiologies of cardiomyopathy, which are highly prevalent in Asia, have not been previously enrolled in randomized trials of VT ablation.ObjectiveTo evaluate whether preemptive catheter ablation in patients with monomorphic VT and an indication for ICD implantation results in improved clinical outcomes compared to ICD implantation with standard medical therapy alone. To examine the natural history of ablation outcomes in the absence of background ICD therapy in patients that refuse randomization.MethodsThe PAUSE-SCD study (NCT02848781) is a prospective, multi-center, randomized controlled trial enrolling patients with structural heart disease (EF < 50%) with an indication for ICD implantation. Patients are randomized in a 1:1 fashion to two treatment arms: ICD with ablation and ICD with standard medical therapy alone. A prospective registry cohort was designed to follow the outcomes of patients who refuse ICD and randomization but elect to receive catheter ablation as primary therapy. The primary endpoint is defined as a composite of recurrent VT, cardiovascular rehospitalization, and death. Pre-specified secondary endpoints include each of the individual components of the primary endpoint in addition to comparison between randomized and registry patients.ConclusionThe PAUSE-SCD study is a prospective, multi-center, randomized, and controlled trial examining the impact of preemptive catheter ablation on cardiovascular outcomes in patients with an indication for ICD at risk for recurrent VT and SCD. It represents the first multi-center VT ablation study in Asia, with a design intended to provide insights into the role of both ICD and ablation therapy in a predominantly nonischemic population.

Background Immune checkpoint inhibitor-related myocarditis (ICI-M) is increasingly recognized, but real-world data in thymic epithelial tumors (TET) remain limited. Objective To evaluate the clinical outcomes, focusing on ICI-M, in patients with TET receiving immune checkpoint inhibitors (ICI). Methods This retrospective study examined patients with TET at Guangdong Provincial People’s Hospital in China from January 2018 to March 2024. We assessed the biomarker changes by comparing the baseline values to peak levels during ICI therapy. Clinical characteristics, disease progression, and outcomes of patients with ICI-M were also analyzed. To investigate the relationships between clinical factors or biomarkers and all-cause mortality, we performed univariable Cox regression analysis. Results Among 31 patients, 7 developed ICI-M, all in the thymoma subgroup (7/12, 58.3%). During a median follow-up of 494 days (262–858), 13 patients died (13/31, 41.9%), including 6 cardiovascular deaths (46.2% of deaths). N-terminal pro B-type natriuretic peptide (NT-proBNP) and Creatine kinase (CK) increased significantly during ICI therapy. In univariable Cox analysis, each doubling of CK was associated with higher all-cause mortality (HR 1.22 per doubling, 95% CI 1.01–1.47; P  = 0.038). Conclusions In this cohort of TET patients receiving ICI therapy, myocarditis occurred frequently in thymoma patients. Overall mortality was substantial in TET patients, with nearly half of the deaths attributable to cardiovascular causes. These findings highlight the need for vigilant cardiovascular monitoring in all TET patients undergoing ICI therapy and warrant confirmation in larger multicenter studies.

Background: Evidence is needed to determine the benefits and harms of screening for atrial fibrillation (AF) in stroke prevention. This meta-analysis aimed to evaluate the benefits and issues of AF screening among older adults. Methods: This systematic review and meta-analysis were conducted and reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. We systematically searched several databases from inception through 28 March 2025, selecting randomized controlled trials (RCTs) comparing AF screening, including systematic and opportunistic screening, versus routine practice or no screening. Two reviewers independently extracted the data and appraised the risks of bias of the studies. Results: Thirteen articles covering 12 RCTs were included in the meta-analysis. For routine screening, systematic screening, rather than opportunistic screening, was more effective in detecting new AF cases (relative risk (RR), 2.07; 95% CI, 1.41 to 3.04; p = 0.0002). However, no difference was observed in the effectiveness of systematic and opportunistic screening in detecting AF (RR, 1.39; 95% CI, 0.59 to 3.30; p = 0.45). Compared with no screening, single-time-point screening did not improve the AF detection rate, whereas intermittent/continuous screening was associated with a greater likelihood of detecting AF (RR, 2.40; 95% CI, 1.59 to 3.64; p < 0.0001). There were no significant differences in the anticoagulation prescription rate between patients who underwent screening and routine care (RR, 1.16; 95% CI, 0.94 to 1.44; p = 0.16). Systematic screening was associated with a lower risk for the composite endpoint (combination of thrombosis-related events and mortality; RR, 0.96; 95% CI, 0.93 to 0.99; p = 0.02) but not for the individual endpoints. Compared with routine care, systematic screening did not increase the risk of major bleeding (RR, 0.88; 95% CI, 0.72 to 1.06; p = 0.18), whereas a positive screening result could promote anxiety. Conclusions: Systematic screening outperformed routine care but was comparable to opportunistic screening in detecting undiagnosed AF. Systematic screening was related to a reduction in the composite endpoints of stroke and all-cause mortality without increasing the risk of bleeding. PROSPERO Registration: This systematic review was prospectively registered in PROSPERO, registration number: CRD42024558614, https://www.crd.york.ac.uk/PROSPERO/view/CRD42024558614.

Objective To investigate the therapeutic effects of liraglutide, a glucagon‐like peptide‐1 receptor agonist, on clinical progression and splenic T‐cell subsets in experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis. Methods EAE was induced in C57BL/6 mice via myelin oligodendrocyte glycoprotein immunization. The mice were divided into three groups: healthy controls (n = 8), EAE (n = 10), and EAE + liraglutide (n = 10). The EAE + liraglutide treatment group received subcutaneous liraglutide (10 µg/kg every other day) starting at 8 days postimmunization. Body weight and disease score were monitored for 30 days, and part of the animals (n = 4 for each group) were sacrificed 20 days postimmunization for flow cytometry of splenocytes, and splenic T helper 1 (Th1) and regulatory T (Treg) cell proportions were analyzed. Results Liraglutide significantly reduced maximum clinical scores (EAE 2.50 ± 0.41 versus EAE + liraglutide 1.75 ± 0.59, p = 0.005), but no significant differences in body weight were observed between the EAE and EAE + liraglutide groups. EAE induction decreased the proportion of splenic Treg cells (6.38% ± 0.72% versus control 10.55% ± 0.87%, p = 0.013), with liraglutide treatment showing no significant effect on Treg proportion relative to EAE alone (7.53% ± 1.54% versus 6.38% ± 0.72%, p = 0.975). However, the proportion of Th1 cells significantly increased after EAE induction (11.95% ± 1.58% versus control 6.05% ± 3.23%, p = 0.025), which was reduced by liraglutide (5.94% ± 2.53% versus EAE, p = 0.025). Conclusions The present preliminary findings demonstrate that liraglutide alleviates EAE severity, probably through peripheral immunomodulatory effects of splenic T helper cells. The glucagon‐like peptide‐1 receptor agonist (GLP‐1RA) liraglutide alleviates disease severity of experimental autoimmune encephalomyelitis (EAE) mice by reducing splenic T helper 1 cell expansion. These findings suggest GLP‐1RA might exert disease‐modifying effects in the EAE model through peripheral immunomodulatory effects of splenic T helper cells.

Background Biomarkers have been related to the arrhythmia recurrence following catheter ablation (CA) of atrial fibrillation (AF). We hypothesized that concurrent measurement of several biomarkers would additively improve their predictive value. Methods One thousand four hundred and ten consecutive AF patients (68% male; 57.2 ± 11.6 years) undergoing CA were enrolled. Baseline characteristics, serum B type brain natriuretic peptide (BNP) and high sensitivity C reactive protein (hsCRP), estimated glomerular filtration rate (eGFR), ablation parameters, arrhythmia data at discharge, 1, 3, 6, and then every 6 months post CA were collected. Follow‐up ended when arrhythmia recurred or until 31st December 2016. Results Three hundred and sixty‐five (25.9%) patients had arrhythmia recurrence post‐CA during a mean follow‐up of 20.7 ± 8.8 months. BNP, hsCRP, and eGFR levels and their cut‐off values of 237.45 pg/mL, 1.6 mg/dL, and 82.5 mL/min/1.73 m2 were good predictors for AF recurrence (all P < 0.01). On multivariate analysis, increasing BNP and hsCRP, decreasing eGFR, gender, and early recurrence (ER) were independent predictors of AF recurrence (all P < 0.01). Compared to BNP alone, BNP plus eGFR or both eGFR and CRP showed incrementally better predictive values (ROC comparisons, all P < 0.01). Similar findings were evident in the subgroups of patients with paroxysmal or nonparoxysmal AF. Conclusion Measurement of BNP, CRP, and eGFR were incrementally additive to clinical risk factors in a cumulative manner to improve prediction of arrhythmia recurrence post‐CA of AF. The implications of poor arrhythmia outcome in AF patients with multiple abnormal biomarkers pre‐CA procedure may help with patient selection and inform the likelihood of success or the need of more complicated CA procedure(s).

The propagation of information risk in complex public opinion environments not only leads to severe direct reputational losses for companies but also results in significant economic damages. Therefore, during the nascent stage of information risk, identifying potential propagation pathways, determining key dissemination channels, and taking timely measures become crucial. To address this issue, this paper proposes a multi-criteria decision-making method for evaluating information risk propagation in complex public opinion environments. In this method, this paper utilizes probabilistic hesitant fuzzy sets to express the evaluation information, and provide several distance and similarity measurement methods for probabilistic hesitant fuzzy elements. To ensure the rationality of the evaluation indicator weights, this study first applies these distance measurement methods to improve the Grey Relational Analysis—Decision Making Trial and Evaluation Laboratory (GRA-DEMATEL) method for determining the objective weights of evaluation indicators. Next, this paper uses the Delphi method to establish the subjective weights of each evaluation indicator. Finally, by employing a weight synthesis operator, this paper combines the subjective and objective weights to obtain the final indicator weights. Additionally, this paper utilizes the similarity measurement methods for probabilistic hesitant fuzzy elements to improve the combined compromise solution (CoCoSo) method in evaluating and ranking potential information risk propagation pathways. Furthermore, this paper incorporates the “Probability Splitting Algorithm” to handle probabilistic hesitant fuzzy elements, enabling their application in these methodologies. Finally, based on a case study of information risk propagation in the catering industry, we conducted a sensitivity analysis and effectiveness verification of the proposed approach. The results demonstrate the effectiveness of the method and its ability to address real-world issues.

Background: The nucleotide-binding oligomerization domain [NOD-], leucine-rich repeats [LRR-], and Pyrin domain-containing protein 3 (NLRP3) inflammasome plays an essential role in hypertension-related atrial fibrillation (AF). p300 is involved in cardiovascular inflammation. In this study, we aimed to investigate the role of p300 in NLRP3 inflammasome activation and its subsequent impact on the Ikur current in angiotensin II (Ang II)-induced HL-1 cells and Ang II-infused mice. Methods: Expression levels of p300, Kv1.5, and NLRP3 in left atrial appendage (LAA) tissues from AF and participants with sinus rhythm (SR) were detected by Western blot. A hypertension mouse model was established in p300 knockout (p300-KO) mice via Ang II infusion, and AF incidence was assessed by electrocardiogram (ECG) after rapid atrial pacing. In vitro, the expression level of p300 in HL-1 cells was modulated by adenoviral overexpression, curcumin (an inhibitor of p300) treatment, and small interfering RNA (siRNA) knockdown. NLRP3 inflammasome activation was evaluated by Western blot and enzyme-linked immunosorbent assay, and electrophysiological properties of HL-1 cells were analyzed using whole-cell patch-clamp recordings. Co-immunoprecipitation assays were performed to investigate the interaction between p300 and nuclear factor kappa B (NF-κB). Results: The expression levels of p300, Kv1.5, and NLRP3 were found to be significantly higher in the LAA tissue of AF patients compared to SR patients. p300-KO decreased AF incidence in Ang II-infused mice by impairing NLRP3 inflammasome activation. p300-OE facilitated NLRP3 inflammasome activation, which subsequently increased the Ikur density and shortened the action potential duration of HL-1 cells. Both curcumin and p300-siRNA treatments reversed Ang II-induced atrial electrical remodeling and NLRP3 inflammasome activation. Moreover, co-immunoprecipitation showed that p300 interacts with NF-κB to promote NLRP3 inflammasome activation. Conclusions: p300 participates in hypertension-induced AF susceptibility by interacting with NF-κB to activate the NLRP3 inflammasome, which subsequently upregulates the transmembrane current of Ikur in atrial cardiomyocytes.