BACKGROUND:Chronic fluid accumulation and malnutrition represent key pathophysiological mechanisms linked to adverse outcomes in chronic heart failure (CHF). We developed a composite index, the extracellular water (ECW) -to-lean body mass (LBM) ratio (ELR), which concurrently reflects these pathological processes, and assessed its prognostic utility in CHF patients. METHODS:A prospective cohort of 401 consecutive patients with CHF was enrolled between August 2019 and October 2021. The InBody S10 device measured ECW and LBM. The study evaluated long-term all-cause and cardiovascular mortality as primary endpoints. RESULTS:The mean age of this cohort was 69.51 years and 62.3 % were male. ELR showed superior predictive value for long-term all-cause mortality (AUC = 0.686) compared to ECW (0.502) and LBM (0.546), with similar patterns observed for cardiovascular mortality (0.649 vs. 0.525 and 0.564, respectively). The optimal ELR cutoff was 0.308 by Youden index analysis. Over a median of 1200-day follow-up, patients with ELR > 0.308 had markedly higher all-cause (40.1 % vs. 15.6 %, p < 0.001) and cardiovascular mortality rates (28.4 % vs. 11.2 %, p < 0.001). Kaplan-Meier curves revealed significantly divergent survival outcomes for both endpoints (log-rank p < 0.001). Multivariable analysis demonstrated ELR > 0.308 independently predicted all-cause (HR = 1.834, 95 %CI 1.134-2.968, p = 0.013) and cardiovascular mortality (HR = 2.026, 95 %CI 1.138-3.609, p = 0.017). These associations remained robust across all examined subgroups. CONCLUSION:The ELR represents a novel index that concurrently reflects both volume status and nutritional status in CHF patients, demonstrating potential as a long-term prognostic biomarker for this population.

OBJECTIVES:Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide, with metabolic risk factors (MRFs) playing a predominant role. This is of particular concern for adolescents and young adults (AYAs), as it can lead to lifelong cardiovascular risk. However, a comprehensive assessment of this burden is lacking. METHODS:Using data from the Global Burden of Disease Study 2021, we estimated the mortality and disability-adjusted life years (DALYs) caused by CVD-MRFs among individuals aged 15 to 39 years from 1990 to 2021. Analyses were stratified by age, sex, region, and Socio-demographic Index (SDI). Joinpoint regression analyzed trends, and a Bayesian age-period-cohort model projected future burden to 2050. RESULTS:In 2021, CVD-MRFs caused 213 000 deaths and 12.9 million DALYs globally among AYAs. While age-standardized rates declined modestly, absolute deaths and DALYs increased by 29.1% and 30.4% since 1990. The burden was highest in middle and low-middle SDI regions and was twice as high in males as in females. The 20 to 24-year age group was the only subgroup with a rising mortality trend. High body-mass index (BMI) and fasting plasma glucose (FPG) were the most rapidly growing MRFs, though high systolic blood pressure and low-density lipoprotein cholesterol remained the leading risks. Ischemic heart disease was the predominant condition. Projections indicate a persistent absolute burden through 2050. CONCLUSIONS:The AYAs face a growing absolute burden of CVD-MRFs, driven notably by high BMI and FPG. Urgent, targeted prevention strategies are essential, particularly for males, young adults aged 20 to 24 years, and populations in middle and low-middle SDI regions.

Background Atrial fibrillation and flutter (AF/AFL) impose a substantial and growing global burden, yet comprehensive assessments focusing on Asia, accounting for regional heterogeneity, demographic drivers, and future trajectories, remain limited. Objectives This study aims to systematically evaluate the burden of AF/AFL across Asia from 1990 to 2021, to quantify the contributions of demographic and epidemiological drivers, and to project future trends to inform region-specific prevention strategies. Methods Using Global Burden of Disease 2021 data, we analyzed prevalence, incidence, mortality, and disability-adjusted life years (DALYs) of AF/AFL across 48 Asian countries and territories. Joinpoint regression assessed temporal trends; decomposition analysis quantified contributions of population growth, aging, and epidemiological changes; and auto-regressive integrated moving average models projected burden to 2040. Results In 2021, Asia had 25,739,093 (95% uncertainty interval [UI]: 20,431,798-33,586,165) prevalent cases of AF/AFL, with age-standardized rate 529.04 (95% UI: 420.26-680.91) per 100,000. Southeast Asia exhibited the highest age-standardized burden, while only the high-income Asia-Pacific region showed declining trends. Although the burden on male was greater, older females were a group that could not be overlooked. Joinpoint analysis revealed a nonlinear trajectory with accelerated growth after 2014. Decomposition analysis identified population growth and aging as primary drivers. High systolic blood pressure was the leading risk factor, with high body mass index showing the most rapid increase. Projections indicate sustained rises through 2040, with particularly pronounced increases among females. Conclusions AF/AFL has become an increasingly severe public health challenge in Asia. Therefore, tailored prevention and control strategies should be developed according to regional characteristics to effectively alleviate its disease burden.

BACKGROUND:Heart failure attributable to atrial fibrillation/flutter (HF-AF/AFL) represents a growing global public health challenge. However, comprehensive analyses of its long-term trends, the independent effects of age, period, and cohort, and future projections remain scarce. This study aimed to address these gaps by characterizing transitions in HF-AF/AFL burden from 1990 to 2021. METHODS:Based on the Global Burden of Disease Study (GBD) 2021, we estimated the global prevalence and years lived with disability (YLDs) for HF-AF/AFL. Joinpoint regression was used to analyze temporal trends from 1990 to 2021. An age-period-cohort model assessed independent effects of age, period, and birth cohort, and a Bayesian age-period-cohort (BAPC) approach projected disease burden to 2050. All estimates were stratified by age, sex, and sociodemographic index (SDI). RESULTS:The global burden of HF-AF/AFL increased significantly from 1990 to 2021, demonstrating a distinct socioeconomic gradient, with the highest burden observed in high-SDI regions. Although the absolute burden remained greater among females, the increase was more pronounced in males. Joinpoint regression identified a recent inflection point, marked by modest global declines in age-standardized prevalence (ASPR) and years lived with disability (ASYR) rates from 2018 to 2021; this downturn was particularly evident among females and in high-SDI regions. Age-period-cohort analysis confirmed an exponential increase in risk with age, a persistent rise in risk across successive periods, and elevated susceptibility in more recent birth cohorts. Projections indicate a continued rise in burden, with the number of prevalent cases forecast to reach approximately 1.44 million globally by 2050, corresponding to an ASPR of 15.04 per 100,000, and YLDs projected to rise to around 0.13 million, with an ASYR of 1.35 per 100,000. This upward trajectory was consistent across SDI strata, although future burdens exhibited regional heterogeneity. CONCLUSIONS:The global burden of HF-AF/AFL is substantial and increasing. Our analysis projects a continued rise in this burden over the coming decades and identifies distinct risk patterns driven by age, period, and birth cohort. These findings underscore the necessity for targeted public health strategies to address this growing challenge.

The complex interplay between chronic metabolic disorders and acute cardiovascular decompensation represents a critical frontier in cardiology. This integrative research program conducted at Chongqing Medical University systematically examines the gut-liver-heart axis across the cardiovascular disease spectrum through three interconnected studies. First, a case-control investigation of coronary artery disease (CAD) patients with and without nonalcoholic fatty liver disease (NAFLD) revealed distinct intestinal dysbiosis patterns characterized by increased Coprococcus and Veillonella alongside decreased Parabacteroides, Bacteroides fragilis, and Bifidobacterium longum, with these microbial alterations correlating significantly with body mass index, triglyceride levels, and hepatic transaminases. Second, a retrospective cohort study of acute myocardial infarction complicated by cardiogenic shock demonstrated that elevated admission bilirubin (HR = 1.020, P = 0.003) and alanine aminotransferase independently predicted 30-day mortality, while serum albumin exerted protective effects (HR = 0.955, P < 0.001). Third, analysis of a comprehensive clinical registry illuminated the systemic clustering of metabolic, renal, and inflammatory abnormalities that underpin both chronic cardiometabolic disease and acute cardiovascular collapse. Collectively, these findings establish a pathogenic continuum wherein chronic intestinal dysbiosis and subclinical hepatic dysfunction create a vulnerable substrate that amplifies injury during acute ischemic events. This research framework provides mechanistic insights into the gut-liver-heart axis and proposes integrated biomarker panels for risk stratification across cardiovascular disease stages.

Mitral regurgitation (MR) is a significant risk factor for heart failure, yet existing rodent models face limitations in invasiveness and reproducibility. This study established a novel percutaneous, ultrasound-guided rat model of MR to overcome these constraints. Thirty male Sprague–Dawley rats underwent echocardiography-guided mitral valve injury, allocated to severe MR (40–70

Introduction: Heart failure (HF) persists as a critical public health priority globally, and comprehensive epidemiological assessments of the rising number of young HF patients remain limited. This study aimed to quantify the global burden of HF among individuals aged 15-44 from 1990 to 2021 and predict until 2050. Methods: Using data from the Global Burden of Disease Study (GBD) 2021, we quantified HF burden among adolescents and young adults (AYA) aged 15-44 years from 1990 to 2021 globally, with stratified by six 5-year age subgroups, sex, sociodemographic index (SDI). Results: In 2021, HF affected 5.45 million cases (age-standardized prevalence rate [ASPR]: 156.43/100,000), with 525,221 YLDs (age-standardized YLD rate [ASYR]: 15.07/100,000) from 1990 to 2021, representing a substantial increase. High SDI regions bore the highest burden. Analyses revealed a consistent male predominance, with the highest burden observed in the 40-44 year age group. Etiologically, cardiomyopathy dominated globally (25.84%). Projections to 2050 forecast continued increase. Conclusion: This study shows HF burden in AYA aged 15-44 years is substantial and continuously growing, characterized by significant gender, age, socio-economic, and geographic differences; cardiomyopathy dominates, highlighting the need for early screening and targeted global health actions.

Background:Malnutrition and sodium water retention are some of the most common complications of chronic heart failure (CHF). To date, several parameters or risk stratification tools have been established to predict one's volume or nutritional status. Unfortunately, there is no biomarker that may reflect both conditions, thus, in this study, we established a novel biomarker known as total body water (TBW) to lean body mass ratio (LBM) ratio (TLR). Accordingly, we also assessed the prognostic value of TLR in CHF patients. Methods:A total of 401 consecutive patients with CHF from August 2019 to October 2021 were prospectively enrolled. TBW and LBM were obtained by InBody S10. The primary endpoint was long-term all-cause and cardiovascular mortality. The cut-off and prognostic value of TLR was determined by receiver operating characteristic curves and Cox regression analysis. Patients were then divided into two groups according to the cut-off value of TLR. Results:During a median follow-up of 1,200 days, the high-TLR group (TLR ≥ 0.783) was presented with a higher all-cause mortality (41.27% vs. 18.40%, p < 0.001) and cardiovascular mortality (28.57% vs. 13.68%, p < 0.001) compared to the low-TLR group (TLR < 0.783). Furthermore, patients in the high-TLR group tended to be older, presented with atrial fibrillation, had higher NYHA class, had a history of chronic kidney disease, had a higher level of N-terminal prohormone of brain natriuretic peptide, worse nutritional status, and a lower level of albumin (all p < 0.05). The Kaplan-Meier curves of the two group patients revealed that the cumulative all-cause and cardiovascular mortality were lower in patients with lower TLR (all log-rank p < 0.001). In the multivariate Cox proportional hazard analysis, TLR ≥ 0.783 was an independent predictor for both all-cause mortality (HR = 2.108, 95%CI 1.400, 3.173, p < 0.001) and cardiovascular mortality (HR = 2.044, 95%CI 1.264, 3.305, p = 0.004). Conclusion:The TLR may serve as a novel composite biomarker that reflects both volume and nutritional status in CHF patients and is associated with long-term prognosis. Its prognostic performance appears comparable to several established biomarkers, though further validation is warranted.

In the era of non-vitamin K antagonist oral anticoagulants (NOACs), it remains unclear whether rate control versus rhythm control as an initial treatment strategy affects the prognosis of patients with new-onset atrial fibrillation (AF). This is a post hoc analysis of the prospective global GLORIA-AF registry aimed to compare the impact of rate control versus rhythm control as an initial treatment strategy on the prognosis in AF patients. The primary endpoint was a composite of all-cause mortality and thromboembolism during a 24 month follow-up. A total of 20,571 patients were included in this study, including 8391 with rhythm control and 12,180 with rate control as an initial treatment strategy. Compared with rate control strategy, rhythm control strategy was associated with decreased risk of the primary endpoint (HR = 0.96, 95

Background:Fabry disease is a cardiomyopathy with multisystemic manifestations that is easily to be misdiagnosed as another type of cardiomyopathy. Fabry cardiomyopathy may present with left ventricular outflow tract obstruction (LVOTO), mimicking obstructive hypertrophic cardiomyopathy (oHCM). We present three cases of genetically confirmed Fabry disease that were initially misdiagnosed as oHCM, highlighting the importance of early recognition and tailored management. Methods:We performed Fabry disease screening on patients diagnosed with oHCM and ultimately identified three individuals who have received oHCM-specific treatments including mavacamten and alcohol septal ablation. Results:Three patients (2 females, 1 male; aged 48-66 years) who were initially diagnosed with and managed for oHCM based on septal hypertrophy and elevated left ventricular outflow tract gradients (LVOTG), was found to have GLA gene mutations. Enzyme replacement therapy with agalsidase alfa in two patients was associated with stabilization or improvement in wall thickness and LVOTO. Conclusion:Fabry cardiomyopathy can present with a hypertrophic phenotype and significant LVOTO, and is often misdiagnosed as oHCM. This further underscores the importance of genetic testing in the etiological diagnosis of hypertrophic cardiomyopathies. Enzyme replacement therapy may ameliorate obstruction, while mavacamten and septal reduction therapies require caution without definitive genotype-phenotype correlation.

BACKGROUND:Estimated glucose disposal rate (eGDR) and frailty index (FI) captures insulin resistance and multisystem decline, respectively. However, the combined prognostic value of eGDR and FI for cardiovascular diseases (CVD) and mortality remains underexplored. METHODS:This prospective cohort study included 6,684 participants from the CHARLS. The composite index eGDRFI was calculated as FI/eGDR. The study endpoints were incident CVD, stroke, heart disease, and all-cause mortality. RESULTS:After adjustment, each 1-unit increase in eGDRFI was significantly associated with higher risks of CVD (HR = 1.098, 95% CI 1.061-1.136) and all-cause mortality (HR = 1.080, 95% CI 1.048-1.113) (both P < 0.001). Compared to the lowest quartile (Q1), participants in the highest eGDRFI quartile (Q4) had markedly increased risks of CVD (HR = 1.833, 95% CI 1.494-2.249) and mortality (HR = 1.511, 95% CI 1.212-1.884) (both P < 0.001). ROC curve analysis demonstrated that eGDRFI achieved higher discriminative ability for predicting incident CVD (AUC = 0.600) compared to eGDR (AUC = 0.590) and FI (AUC = 0.563), as well as for predicting all-cause mortality (eGDRFI AUC = 0.606 vs. eGDR 0.547 and FI 0.601). CONCLUSION:The combined eGDRFI is a robust predictor of cardiovascular events and mortality in middle-aged and older adults, and may serve as a practical tool for risk stratification.

Abstract Background Stressful life events (SLEs) in adulthood are potential risk factors for cardiovascular disease (CVD), yet evidence remains inconsistent. This study examined the association between adulthood SLEs and incident CVD and evaluated mediation by depression, physical inactivity, and smoking. Methods We analyzed harmonized data from two nationally representative aging cohorts: the US Health and Retirement Study and the English Longitudinal Study of Ageing. SLEs were assessed at baseline, and incident CVD was physician-diagnosed. We used Cox and restricted mean survival time (RMST) regression to estimate hazard ratios (HRs) and RMST differences, set at the time point when 90% of incident CVD events had accrued (7.8 years). Population attributable fractions (PAFs) based on RMST and mediation analyses via RMST pseudo-value regression quantified contributions of SLEs and behavioral pathways. Results Among 18,898 participants without baseline cardiovascular disease (mean age 64.5 years; 39.8% male), 2,782 incident CVD cases were documented (incidence rate: 2.51 per 100 person-years). RMST analysis showed that any SLE exposure was related to significant reductions in event-free survival, including a 2.22-month decrease for CVD (95% CI: -2.90 to -1.53), a 1.57-month decrease for heart disease (95% CI: -2.16 to -0.99), and a 0.79-month decrease for stroke (95% CI: -1.16 to -0.41), with a clear dose-response relationship. Corresponding Cox proportional hazards models showed adjusted HRs of 1.20 (95% CI: 1.11–1.30) for CVD, 1.16 (95% CI: 1.07–1.27) for heart disease, and 1.26 (95% CI: 1.09–1.46) for stroke. Each additional SLE increased CVD, heart disease, and stroke risks by 11%, 10%, and 11%. PAFs attributable to SLEs exposure were 2.6% for CVD, 1.7% for heart disease, and 0.8% for stroke. Mediation analyses revealed that depression, physical inactivity, and current smoking accounted for 7.2%, 4.5%, and 4.5% of the total effect of SLEs on CVD, respectively. Conclusions Adulthood SLEs are independently associated with increased CVD risk, with depression, physical inactivity, and smoking explaining a modest proportion of this association.

AimsLeft atrial reservoir strain (LASr) and global work efficiency (GWE) have individually demonstrated prognostic value in secondary mitral regurgitation (SMR), but their interrelationship and combined utility remain unclear. We aimed to investigate the independent prognostic value of LASr and GWE, and to explore whether GWE plays a role in the LASr–mortality association in medically managed SMR patients.Methods and resultsThis retrospective study included 399 patients with SMR (median age 70.0 years, 66.4% male) who were medically managed without valve intervention. LASr and GWE were measured using speckle-tracking echocardiography. Cox regression and mediation analyses were performed. During a median follow-up of 35.0 months, 103 deaths (25.8%) occurred. Both LASr (adjusted HR 0.891 per 1% increase, 95% CI 0.850–0.933, P < 0.001) and GWE (adjusted HR 0.920 per 1% increase, 95% CI 0.891–0.951, P < 0.001) independently predicted all-cause mortality. Exploratory mediation analysis showed that GWE statistically accounted for a portion of the LASr–mortality association, with an indirect effect of −0.183 (95% CI −0.305 to −0.112, P < 0.001) and a mediation proportion of 16.3%.ConclusionIn medically managed SMR patients, both LASr and GWE independently predict all-cause mortality, and GWE statistically accounts for the relationship between LASr and mortality. These findings generate the hypothesis that left atrial dysfunction is statistically associated with impaired myocardial work efficiency, supporting the integrated assessment of both parameters for risk stratification across different SMR severity and phenotypes.

Background Aspirin remains the cornerstone of antiplatelet therapy for acute myocardial infarction (AMI); however, its use is limited in patients with aspirin intolerance, hypersensitivity, or high bleeding risk. Indobufen, a reversible cyclooxygenase-1 inhibitor, has emerged as a potential alternative, yet its cardioprotective effects beyond platelet inhibition and the underlying mechanisms remain incompletely understood. Methods Clinical serum samples were collected from patients with ST-segment elevation myocardial infarction (STEMI) receiving aspirin or indobufen therapy. In parallel, myocardial infarction was induced in mice by left anterior descending coronary artery ligation, and neonatal rat cardiac fibroblasts (NRCFs) were subjected to hypoxia in vitro. Cardiac function, fibrosis, autophagy, apoptosis, and oxidative stress were evaluated using echocardiography, histology, immunostaining, western blotting, and transmission electron microscopy. Publicly available single-cell RNA sequencing data were analyzed to explore relevant cellular pathways. Results In STEMI patients, indobufen treatment was associated with lower circulating levels of cardiac troponin I, thromboxane B₂, IL-1β, and IL-12, along with increased IL-10 levels than aspirin treatment, and these associations remained significant after multivariable adjustment for baseline clinical characteristics. In vivo, indobufen improved cardiac function and attenuated myocardial fibrosis, accompanied by modulation of autophagy-related signaling, reduced apoptosis, and alleviation of oxidative stress. In vitro, indobufen attenuated hypoxia-induced cardiac fibroblast activation, apoptosis, and mitochondrial dysfunction, whereas aspirin exerted limited effects under the same conditions. Mechanistically, indobufen was associated with increased activation of AKT and AMPK signaling pathways and coordinated modulation of autophagy-related proteins. Further pharmacological inhibition of AMPK partially attenuated the autophagy-related effects of indobufen, suggesting that AMPK signaling contributes, at least in part, to the cytoprotective effects of indobufen. Conclusions These findings suggest that indobufen may exert myocardial protective effects beyond platelet inhibition, potentially through AKT/AMPK-associated regulation of autophagy, apoptosis, and fibroblast activation. These findings provide a rationale for further investigation of indobufen as a potential alternative antiplatelet strategy in myocardial infarction.

BackgroundHereditary transthyretin cardiac amyloidosis (ATTR-CA) is a rare autosomal dominant systemic disorder characterized by amyloid deposition in the peripheral nerves, myocardium, kidneys, and gastrointestinal tract. The clinical manifestations of ATTR-CA are nonspecific, resulting in high rates of misdiagnosis and underdiagnosis.Case presentationWe report the case of a 58-year-old woman who presented with recurrent severe abdominal pain and echocardiographic evidence of ventricular hypertrophy. Initial cardiac magnetic resonance imaging at an outside institution suggested left ventricular non-compaction (LVNC). Prior to receiving the correct diagnosis, she was incorrectly diagnosed with chronic cholecystitis, somatic symptom disorder, or LVNC at multiple institutions. A multidisciplinary team evaluation integrating cardiac imaging, technetium-99m phosphate scintigraphy, and genetic testing confirmed the diagnosis of ATTR-CA associated with the Ser23Asn (TTR c.128G>A p.Ser43Asn) variant. She was treated with tafamidis but died suddenly only two months after diagnosis. This case illustrates the multisystem involvement of ATTR-CA, in which atypical presentations frequently result in diagnostic delays. It represents a rarely reported instance of ATTR-CA presenting primarily with severe recurrent abdominal pain.ConclusionIn patients with ventricular hypertrophy, ATTR-CA may manifest with atypical symptoms such as severe, recurrent abdominal pain, which can result from autonomic neuropathy or gastrointestinal amyloid deposition. When the clinical diagnosis remains uncertain, multidisciplinary team consultation is essential to synthesize all available findings.

Background Catecholamine-induced cardiomyopathy (CICMP) is myocardial injury from excessive catecholamine secretion by pheochromocytoma/paraganglioma (PPGL), with reversible cardiac dysfunction post-tumor resection. Case Summary A 29-year-old female initially hospitalized for severe myocarditis recovered but presented 3 years later with marked blood pressure fluctuations. She was diagnosed with CICMP secondary to pheochromocytoma and managed with aggressive blood pressure control and successful tumor resection, achieving favorable outcomes with stable blood pressure off medications. Discussion Literature review shows CICMP is occult. The reminder for clinicians from this case is that for atypical myocarditis, especially in patients experiencing blood pressure fluctuations, PPGL should be considered, and relevant examinations should be promptly completed. Take-Home Message Blood pressure lability in a young patient with suspected myocarditis should immediately raise suspicion for PPGL and prompt biochemical screening.

AIMS:Early recurrence of atrial tachyarrhythmia (ERAT) after catheter ablation for atrial fibrillation (AF) is common, yet its prognostic significance and implications for the duration of the blanking period remain uncertain. We aimed to evaluate the association between ERAT and post-ablation clinical outcomes, late arrhythmia recurrence, and AF burden, and to explore the optimal duration of the blanking period. METHODS AND RESULTS:This post hoc analysis included 811 patients from the CABANA trial who underwent catheter ablation and had trial-specific electrocardiographic monitoring data available. ERAT was defined as any episode of AF, atrial flutter, or atrial tachycardia lasting >30 s within the 90-day blanking period. The primary outcome was a composite of all-cause mortality, disabling stroke, serious bleeding, or cardiac arrest. Secondary outcomes included cardiovascular hospitalization and late atrial tachyarrhythmia recurrence. During a median 4 years (IQR 2.5-5.2) follow-up, ERAT occurred in 567 patients (69.9%). Patients with ERAT had higher risks of cardiovascular hospitalization [adjusted hazard ratio (aHR) 1.35, 95% confidence interval (CI) 1.07-1.71] and of the composite outcome of all-cause mortality or cardiovascular hospitalization (aHR 1.33, 95% CI 1.07-1.66), but no increased risk of the primary composite outcome. ERAT was independently associated with late atrial tachyarrhythmia recurrence (aHR 1.35, 95% CI 1.07-1.71). Prognostic relevance varied by timing, with the strongest association observed for ERAT occurring between 60 and 90 days after ablation (aHR 1.80, 95% CI 1.16-2.79). Receiver operating characteristic analysis identified 58 days as the optimal threshold for predicting late arrhythmia recurrence (AUC 0.727). CONCLUSION:ERAT was associated with higher risks of cardiovascular hospitalization and late atrial tachyarrhythmia recurrence in a time-dependent manner, supporting a shorter blanking period to better identify patients at risk of adverse rhythm outcomes.