Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia characterized by consistently irregular atrial and ventricular contractions. Heart rate variability (HRV) refers to the changes in the intervals between consecutive ventricular heartbeats. In sinus rhythm, HRV may be subtle and is quantitatively reflecting the dynamic interplay of the cardiac autonomic nervous system, which plays a crucial role in the onset, development, and maintenance of AF. HRV metrics, consisting of time-domain, frequency-domain, and nonlinear parameters, have been verified to vary significantly before and after AF episodes, and AF treatment-related procedures such as electrical cardioversion, ablation, and surgery of AF. Therefore, HRV may serve as a digital biomarker in predicting AF risk in long-term and acute risk period, identification of patients with AF risk in sinus rhythm and recurrence risk stratification after procedures. HRV in AF rhythm, predominantly influenced by dynamic atrioventricular node conduction under the onslaught of irregular atrial impulses, shows a huge disparity compared to that in sinus rhythm. Despite this, HRV in AF rhythm still provides valuable prognostic information, as reduced HRV may indicate a poor heart function and outcomes in patients with AF. Despite being influenced by lots of variables, HRV can still serve as an independent digital biomarker in the clinical management of AF throughout its entire lifecycle.

We suggest a new method for the detection of paroxysmal atrial fibrillation by analyzing surface-enhanced Raman scattering (SERS) spectra of blood serum of patients in question in comparison with SERS spectra of the serum of healthy donors. Spectral measurements were carried out on compact SERS substrates in dried blood serum droplets with immediate subsequent processing. To process the spectra, machine learning methods were used, in particular, the logistic regression method and the principal component method. Furthermore, thanks to the possibility of the physical-chemical interpretation of the coefficients of the method, the vibrational bands responsible for the signs of atrial fibrillation were identified and their correlation was carried out. Evaluation metrics were presented for the classification, among which the accuracy value was 0.82, that is a high indicator when analyzing samples directly from the blood serum of patients with the disease under study. It was shown that a small number of measured spectra for each sample (near 35 measurements) was sufficient to carry out the study. A comparative analysis of the logistic regression method and other commonly used machine learning methods was also carried out: support vector machines and random forest. Each method was evaluated and the advantages of logistic regression in solving the problem presented in this study were shown. The receiver operating characteristic curve (ROC) analysis was also used for graphical representation and comparison of methods. The presented study shows the prospects for using the described method for the analysis of diseases associated with cardiac risks.

Sepsis-induced atrial fibrillation (AF) is driven by systemic inflammation and macrophage-mediated atrial remodeling, with proinflammatory M1 macrophages playing a key role. This study investigates whether GTS-21, an α7nAChR agonist, can reduce AF susceptibility by promoting macrophage polarization towards the anti-inflammatory M2 phenotype.

A mouse model of lipopolysaccharide (LPS) (10 mg/kg)-induced sepsis was used to explore the relationship between atrial inflammation and AF. GTS-21 (20 mg/kg) was administered to assess its impact on 48-h survival and AF incidence. Cardiac function was evaluated using echocardiography. Markers of myocardial injury, including CK-MB, LDH, and cTnI, were measured. Macrophage polarization and atrial inflammation were assessed using immunofluorescence, flow cytometry, RT-qPCR, and western blotting. Oxidative stress and mitochondrial function were evaluated using reactive oxygen species (ROS) measurements, electron microscopy, and mitochondrial protein expression analysis. Calcium dynamics were studied using western blotting and confocal microscopy.

In LPS-induced septic mice, GTS-21 improved 48-h survival rates and reduced the induction rate and duration of AF (P < 0.05). Echocardiography showed a preserved left ventricular ejection fraction and enhanced diastolic function. Mechanistically, it promoted M2 macrophage polarization, inhibited the NF-κB P65/NLRP3/C-caspase 1 pathway to reduce IL-1β release, and alleviated oxidative stress. Additionally, mitochondrial structure was restored by reversing fission and promoting fusion, while calcium-handling proteins (NCX-1, RYR2, and SERCA2a) were regulated to prevent intracellular calcium overload, reducing AF susceptibility.

GTS-21 mitigated atrial inflammation and reduced the incidence of AF in mice with sepsis by regulating macrophage polarization, reducing oxidative stress, and preserving mitochondrial and calcium dynamics in cardiomyocytes. These findings highlight the therapeutic potential of GTS-21 in treating sepsis-induced AF.

Atrial fibrillation (AF) is a prevalent and chronic cardiovascular disorder associated with various pathophysiological alterations, including atrial electrical and structural remodeling, disrupted calcium handling, autonomic nervous system dysfunction, aberrant energy metabolism, and immune dysregulation. Emerging evidence suggests that long non-coding RNAs (lncRNAs) play a significant role in the pathogenesis of AF.

This discussion aims to elucidate the involvement of AF-related lncRNAs, with a specific focus on their role as miRNA sponges that modulate crucial signaling pathways, contributing to the progression of AF. We also address current limitations in AF-related lncRNA research and explore potential future directions in this field. Additionally, we summarize feasible strategies and promising delivery systems for targeting lncRNAs in AF therapy.

In conclusion, targeting AF-related lncRNAs holds substantial promise for future investigations and represents a potential therapeutic avenue for managing AF.

The prevalence and progression of cardiovascular disease (CVD) are significantly influenced by low-grade chronic inflammation. Our aim was to investigate the association of blood-count-based inflammatory markers with atrial fibrillation (AF), heart failure (HF), and cardiovascular mortality. We utilized prospective follow-up data from the UK Biobank, including 334,674 individuals (aged between 39 and 70 years) free of HF and AF at baseline. The exposures were blood-count-based inflammatory markers, including neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), systemic immune-inflammation index (SII), aggregate index of systemic inflammation (AISI), and systemic inflammatory response index (SIRI), which were computed using leukocyte counts (lymphocytes, monocytes, and neutrophils). The primary outcomes were the occurrence of AF, HF and cardiovascular-related deaths. Cox proportional hazards models were employed to determine hazard ratios (HRs) and their 95% confidence intervals (CIs) for assessing the longitudinal association between inflammatory markers and the development of cardiovascular events. Survival analysis was illustrated using Kaplan-Meier curves with the occurrence of AF, HF and CVD mortality as the endpoint. There were 16,994 incidences of AF and 7342 incidences of HF over a median follow-up of 10.4 years (range, 2.4-12.1). Additionally, there were 3434 deaths from CVD causes. A higher risk of cardiovascular mortality was significantly associated with NLR, MLR, SIRI, AISI, and SII in multivariable adjusted models (HR 1.44, 95% CI 1.30-1.58; HR 1.46, 95% CI 1.31-1.61; HR 1.57, 95% CI 1.41-1.75; HR 1.57, 95% CI 1.41-1.73; and HR 1.36, 95% CI 1.24-1.49, respectively). Furthermore, our analysis revealed positive associations between NLR, MLR, SIRI, and AISI and the risk for AF (HR 1.18, 95% CI 1.13-1.24; HR 1.19, 95% CI 1.14-1.25; HR 1.22, 95% CI 1.16-1.27; and HR 1.08, 95% CI 1.03-1.13, respectively), and HF (HR 1.42, 95% CI 1.33-1.52; HR 1.28, 95% CI 1.19-1.37; HR 1.45, 95% CI 1.35-1.56; and HR 1.32, 95% CI 1.23-1.41, respectively). Furthermore, the SII demonstrated a positive association with HF (HR 1.24, 95% CI 1.16-1.32). However, the association with AF was not statistically significant (HR 1.01, 95% CI 0.97-1.06). In summary, our research provides preliminary evidence that blood cell indices associated with the systemic inflammatory response, may serve as potential biomarkers for the risk of developing AF, HF and CVD mortality. Additionally, it is likely that a systemic inflammatory-immune response existed before the clinical diagnosis. Identifying high-risk populations based on the levels of inflammatory markers could help reduce the risk of death and prevent the onset of AF and HF. Further investigation is warranted to determine whether reducing inflammatory markers causally improves cardiovascular outcomes.

Clonal hematopoiesis of indeterminate potential (CHIP) has emerged as a novel risk factor for cardiovascular diseases. CHIP is characterized by the expansion of hematopoietic stem cell clones harboring somatic mutations in genes such as TET2, DNMT3A, and ASXL1, which are implicated in inflammation, atrial remodeling, and hypercoagulability. These mutations foster a pro-inflammatory and pro-thrombotic environment conducive to arrhythmogenesis, thereby linking CHIP to the development and progression of atrial fibrillation (AF). Mechanistic insights indicate that CHIP contributes to atrial fibrosis, disrupts calcium signaling, and exacerbates oxidative stress, all of which heighten susceptibility to AF. Clinical studies, including epidemiological and Mendelian randomization analyses, further support the association between CHIP and an increased risk of both incident and progressive AF, with specific mutations such as TET2 and ASXL1 identified as significant contributors. Additionally, CHIP has been linked to adverse outcomes in AF, including elevated rates of heart failure, thromboembolism, and mortality. Understanding CHIP's role in AF pathophysiology offers opportunities for the development of precision medicine approaches, providing novel avenues for early intervention and targeted AF treatment. This review synthesizes current mechanistic and clinical evidence on the role of CHIP in AF, emphasizes its potential as a biomarker for risk stratification, and explores emerging therapeutic strategies targeting CHIP-associated pathways.

Psoriasis is linked to an increased risk of atrial fibrillation (AF). However, data on the electrophysiological substrate and outcomes of AF ablation in patients with psoriasis are lacking.

We conducted a retrospective, multicenter study involving 48 patients with psoriasis (median age, 66 years [56-72]; 79% male) and paroxysmal (n=25.52%) or persistent AF (n=23.48%) who underwent ablation at 4 high-volume institutions between 2018 and 2023. Propensity score-matching identified 96 controls without psoriasis undergoing AF ablation at the same institutions. The primary end point was survival free from atrial tachyarrhythmia recurrence after an 8-week blanking period.

Baseline clinical characteristics were well balanced between groups. However, patients with psoriasis had higher CRP (C-reactive protein) than controls (0.85 mg/dL [0.45-1.2] versus 0.3 mg/dL [0.3-0.4], P<0.001) and a greater burden of left atrial low-voltage regions at electroanatomical mapping (20% [11%-20%] versus 5% [5%-10%]; P=0.013). Over a median follow-up of 20 (13-32) months, atrial tachyarrhythmia recurrence occurred in a higher proportion of patients with psoriasis (40% versus 24%, log-rank P=0.023). Patients with psoriasis also had a slightly higher risk of acute coronary syndrome (log-rank P=0.045), with similar risks of death (log-rank P=0.517) and procedural complications (2% versus 2%, P=1.000), whereas no stroke occurred. Multivariable analysis identified early recurrence within blanking period (adjusted hazard ratio [aHR], 5.9, P<0.001), preablation CRP levels (aHR, 1.2, P=0.016), and psoriasis history (aHR, 2.2, P=0.046) as predictors of atrial tachyarrhythmia recurrence. In the group with psoriasis, the optimal CRP cutoff associated with atrial tachyarrhythmia recurrence was found to be 1 mg/dL.

Psoriasis is associated with low-grade systemic inflammation, more severe electroanatomical markers of atrial cardiomyopathy, and worse postablation outcomes. The association between CRP levels and rhythm outcomes suggests that inflammation may drive recurrences among patients with psoriasis undergoing AF ablation.

Accumulative evidence has shown that systemic lupus erythematosus (SLE) increases the risk of various cardiovascular diseases including atrial fibrillation (AF). The study aimed to screen potential key genes underlying co-pathogenesis between SLE and AF, and to discover therapeutic targets for AF.

Differentially expressed genes (DEGs) were identified, and co-expressed gene modules were obtained through weighted gene co-expression network analysis (WGCNA) based on the AF and SLE expression profiles from the GEO database. Subsequently, machine learning algorithms including LASSO regression and support vector machine (SVM) method were employed to identify the candidate therapeutic target for SLE-related AF. Furthermore, the therapeutic role of TMEM45A was validated both in vivo and vitro.

Totally, 26 DEGs were identified in SLE and AF. The PPI network combined with WGCNA identified 51 key genes in SLE and AF. Ultimately, Machine learning-based methods screened three hub genes in SLE combined with AF, including TMEM45A, ITGB2 and NFKBIA. The cMAP analysis exposed KI-8751 and YM-155 as potential drugs for AF treatment. Regarding TMEM45A, the aberrant expression was validated in blood of SLE patients. Additionally, TMEM45A expression was up-regulated in the atrial tissue of patients with AF. Furthermore, TMEM45A knockdown alleviated AF occurrence and atrial fibrosis in vivo and Ang II-induced NRCFs fibrosis in vitro.

The crosstalk genes underlying co-pathogenesis between SLE and AF were unraveled. Furthermore, the pro-fibrotic role of TMEM45A was validated in vivo and vitro, highlighting its potential as a therapeutic target for AF.

The pathophysiology of arrhythmias is complex, involving changes in cardiac contractile and conduction systems, electrical conduction heterogeneity, and structural alterations. Recent studies indicate that cardiac macrophages can induce arrhythmias by interacting with cardiomyocytes or altering tissue composition. Due to the heterogeneity and diversity, macrophages develop different cellular functions during pathological processes. This review identifies various macrophage subpopulations and focuses on their pathological mechanisms in arrhythmogenesis. Furthermore, we explore the interactions of macrophages with other immune cells and summarize the promising approaches for targeting macrophages in arrhythmias treatment. Macrophages directly or indirectly influence arrhythmogenesis through multiple systemic effects. Preclinical studies suggest that modifying macrophages' phenotype or regulating their activity may directly affect cardiac conduction. This review provides a theoretical basis for developing immunotherapies for patients with cardiac arrhythmias.

Atrial fibrillation (AF) is a prevalent cardiac arrhythmia with a multifactorial pathophysiology involving electrical, structural, and autonomic remodeling of the atria. AF is closely associated with elevated interleukin-6 (IL-6) levels, which contribute to atrial remodeling and the progression of AF. This review summarizes the mechanisms by which IL-6 promotes AF through inflammatory pathways, atrial fibrosis, electrical remodeling, and calcium mishandling. Experimental models have demonstrated that IL-6 neutralization reduces the incidence of AF, highlighting its potential as a therapeutic target. Future studies should focus on IL-6 blockade strategies to manage AF, aiming to improve patient outcomes.

Atrial fibrillation (AF), a common cardiac arrhythmia, is associated with severe complications such as stroke and heart failure. Although the precise mechanisms underlying AF remain elusive, inflammation is acknowledged as a pivotal factor in its progression. Angiotensin II (AngII) is implicated in promoting atrial remodeling and inflammation. However, the exact pathways through which AngII exacerbates AF are still not fully defined. This study explores the key molecular mechanisms involved, including dysregulation of calcium ions, altered connexin expression, and activation of signaling pathways such as TGF-β, PI3K/AKT, MAPK, NF-κB/NLRP3, and Rac1/JAK/STAT3. These pathways are instrumental in contributing to atrial fibrosis, electrical remodeling, and increased susceptibility to AF. Ang II-induced inflammation disrupts ion channel function, resulting in structural and electrical remodeling of the atria and significantly elevating the risk of AF. Anti-inflammatory treatments such as RAAS inhibitors, colchicine, and statins have demonstrated potential in reducing the incidence of AF, although clinical outcomes are inconsistent. This manuscript underscores the link between AngII-induced inflammation and the development of AF, proposing the importance of targeting inflammation in the management of AF.

Atrial fibrillation (AF) has become the pre-dominant arrhythmia worldwide and is associated with high morbidity and mortality. Its pathogenesis is intricately linked to the deleterious impact of cardiovascular risk factors, emphasizing the pivotal imperative for early detection and mitigation strategies targeting these factors for the prevention of primary AF. While traditional risk factors are well recognized, an increasing number of novel risk factors have been identified in recent decades. This review explores the emerging non-traditional risk factors for the primary prevention of AF, including unhealthy lifestyle factors in current society (sleep, night shift work, and diet), biomarkers (gut microbiota, hyperuricaemia, and homocysteine), adverse conditions or diseases (depression, epilepsy, clonal haematopoiesis of indeterminate potential, infections, and asthma), and environmental factors (acoustic pollution and other environmental factors). Unlike traditional risk factors, individuals have limited control over many of these non-traditional risk factors, posing challenges to conventional prevention strategies. The purpose of this review is to outline the current evidence on the associations of non-traditional risk factors with new-onset AF and the potential mechanisms related to these risk factors. Furthermore, this review aims to explore potential interventions targeting these risk factors at both the individual and societal levels to mitigate the growing burden of AF, suggesting guideline updates for primary AF prevention.

Background: Significant sex differences exist in atrial fibrillation (AF). Better understanding of its underlying mechanism would help AF management. This study aimed to investigate the contribution of circulating metabolites to sex differences in AF and the association between them. Methods: A total of 108 patients with AF were enrolled. Untargeted metabolomics were performed in plasma samples of male and female patients. Correlation analysis with clinical characteristics and Mendelian randomization were used to identify sex-specific metabolites associated with AF, which was further validated in additional patients. Transcriptomics data of the left atrium were used to investigate the molecular alteration of the left atrium responding to identified sex-specific circulating metabolites. The effect of selected sex-specific metabolites on cardiomyocytes was further investigated. Results: A total of 60 annotated metabolites were found with different levels between male and female patients. Among these sex-specific metabolites, three metabolites, 7-Methylguanosine, succinic acid, and N-Undecylbenzenesulfonic acid, were positively related to the left atrial remodeling. Additionally, succinic acid was significantly associated with increased risk of AF (OR = 1.26; 95% CI: 1.13 to 1.40; p < 0.001). And, SUCLA2, the gene of succinic acid metabolism, was significantly increased in the left atrium of male patients (fold change = 1.53; p = 0.008). Treatment with succinic acid led to cardiomyocyte hypertrophy and mitochondrial dysfunction. Conclusions: This study highlights sex differences in circulating metabolites in patients with AF and identifies the associations between sex-specific metabolites and AF. succinic acid, which is much higher in male patients, contributes to the process of AF.

Atrial fibrillation (AF) recurrence after cardioversion is common, and inflammation plays a critical role in its pathophysiology. We aimed to elucidate the predictive role of the ratio of high-density lipoprotein cholesterol to c-reactive protein (HDL-C/CRP) as an inflammatory marker in AF recurrence after electrical cardioversion (ECV). We analyzed patients who underwent elective ECV for atrial fibrillation between June 2020 and December 2023. Baseline levels of HDL-C and CRP were obtained. Ninety-six patients were included. The median age was 59 years, and 48% were female. Atrial fibrillation recurred after ECV in 56 patients (58%). In the AF recurrence group, CHA2DS2-VASc score was higher (2 [1-3] vs. 1[0-2]; p = 0.013), left atrial diameter was larger (43 ± 5 vs. 40 ± 6 mm; p = 0.015), and HDL-C/CRP ratio was lower (5.6 [2.7-13.0] vs. 14.0 [4.8-38.0]; p = 0.003) compared with the sinus rhythm group. Cox regression analysis showed that HDL-C/CRP was a predictor of AF recurrence at follow-up (unadjusted HR = 0.97; CI 95%: 0.95-0.99; p = 0.004; adjusted HR = 0.98; CI 95%: 0.96-0.99; p = 0.030). ROC curve showed that HDL-C/CRP ratio was able to predict AF recurrence after ECV (AUC = 0.68; p = 0.003). Kaplan-Meier analysis showed that patients with baseline HDL-C/CRP <7.4 had higher AF recurrence (log-rank test p = 0.013). Our research demonstrated that the lower HDL-C/CRP ratio predicted AF recurrence after ECV during follow-up.

Retained blood syndrome (RBS) is defined as the postoperative retention of blood within the thoracic cavity. In addition to the mechanical impacts on cardiac and pulmonary function, RBS triggers inflammatory processes. It is associated with increased morbidity following cardiac surgery. The goal of this non-systematic review was to summarize the current understanding of the pathophysiology, consequences and both prophylactic and therapeutic measures related to RBS.

The subjects to be covered were defined in advance. A literature search was conducted in PubMed and Google Scholar using relevant search terms and MeSH terms.

RBS is a significant complication following cardiac surgical procedures. It is associated with a poorer prognosis due to mechanical suppression of haemodynamics and the amplification of inflammatory processes. Therefore, preventing pericardial and pleural effusions should be a priority in cardiac surgical care. If RBS occurs, aggressive anti-inflammatory therapy should be initiated to prevent the development of long-term complications.

Dyslipidemia is a metabolic disorder characterized by quantitative and/or qualitative abnormalities in serum lipid levels. Elevated serum cholesterol levels can modify the turnover and recruitment of ionic channels in myocytes and cellular homeostasis, including those of inflammatory cells. Experimental and clinical data indicate that inflammation is implicated in the pathophysiology of atrial remodeling, which is the substrate of atrial fibrillation (AF). Data about the association between increased lipid serum levels and AF are few and contrasting. Lipoprotein (a), adiposity, and inflammation seem to be the main drivers of AF; in contrast, low-density lipoproteins, high-density lipoproteins and triglycerides are not directly involved in AF onset. The present review aimed to describe the pathophysiological link between dyslipidemia and AF, the efficacy of lipid-lowering therapies in atherosclerotic cardiovascular disease (ASCVD) patients with and without AF, and the impact of lipid-lowering therapies on AF incidence.

Atrial fibrillation (AF) is a predominant cardiac arrhythmia with unclear etiology. This study used bioinformatics and machine learning to explore the relationship between mitochondrial energy metabolism-related genes (MEMRGs) and immune infiltration in AF. The datasets GSE31821, GSE41177, and GSE79768 were retrieved from the Gene Expression Omnibus (GEO) database, and differential expression analysis identified 59 mitochondrial energy metabolism-related differentially expressed genes (MEMRDEGs) associated with AF. Key MEMRDEGs were selected using the least absolute shrinkage and selection operator (LASSO) and support vector machine (SVM) methods, and a diagnostic model was developed. Immune infiltration was assessed using single-sample gene set enrichment analysis (ssGSEA) and the microenvironment cell population counter (MCPcounter). The diagnostic model, based on the key genes ACAT1, ALDH1L2, HTT, OGDH, and SLC25A3, achieved an area under the curve (AUC) of 0.903. Significant differences in immune cell composition were observed between the AF and control groups. ALDH1L2 was positively correlated with most immune cells, while SLC25A3 showed a negatively correlated with the monocytic lineage. The findings indicate that MEMRGs interact with immune responses in AF, offering insights into the potential molecular mechanisms and therapeutic targets for AF.

This study aims to examine the possible causal link between periodontal diseases and atrial fibrillation (AF), with a focus on the modifiable risk factors that facilitate this connection.

Firstly, bidirectional and multivariable Mendelian Randomisation (MR) analyses were conducted using genome-wide association studies (GWAS) data on periodontal disease (87,497 cases/259,234 controls) from FinnGen and AF (55,114 cases/482,295 controls) from AFGen. Then, a 2-step MR approach was employed to evaluate the mediating role and proportions of 25 candidate factors among the direct causality between periodontal disease and AF.

Periodontal disease was found to be associated with an increased risk of AF (odds ratio 1.16, 95% CI 1.027-1.314, p = .017), independent of other covariates such as dental caries, pulp, and periapical diseases. Conversely, no causal relationship was detected indicating that AF leads to periodontal disease condition. Furthermore, in the 2-step MR analysis, 5 out of 25 candidate mediators were screened as statistically significant. Ranked by partial mediation proportion, these modifiable mediators included weight (30.3%), IL-17 (17.2%), TNF (14.08%), coronary atherosclerosis (13.4%), and hypertension (11.6%).

Our findings demonstrated the genetic causality between periodontal disease and AF. Maintaining oral hygiene, adopting standardised periodontal therapy, and restricting body weight are critical goals for patients with periodontal disease to mitigate disease progression to AF.

Atrial fibrillation (AF), the most common type of heart arrhythmia, is recognized as an independent risk factor for stroke. Fortunately, catheter ablation (CA) offers an effective treatment option for AF patients. However, numerous studies have reported suboptimal outcomes, as AF recurrence rates often remain elevated even after CA. Consequently, there exists a need for early identification of patients prone to recurrence, necessitating anti-inflammatory and/or antiarrhythmic treatment post-CA. The discovery and application of markers associated with AF recurrence could significantly aid in this early identification process. In this review, we present an overview of AF recurrence markers from three distinct perspectives (biochemical, imaging, and electrocardiographic markers).

We present a case series of patients with granulomatous myocarditis presenting as atrial arrhythmias accompanied by lymphadenopathy.

Atrial myocarditis (AM) may be the cause of atrial fibrillation (AF) in patients without risk factors.

Patients with atrial fibrillation without risk factors underwent 18F-Fluorodeoxyglucose positron emission tomography (18F-FDG-PET). We performed biopsy of lymph nodes or myocardium in patients with atrial uptake of 18F-FDG-PET.

AM was observed in 15 patients. The median age of the patients was 42 years and left ventricular ejection fraction (LVEF) at presentation was 45%. All patients had AF, atrial flutter was noted in 4 patients (26.7%) and 2 patients (13.3%) had atrioventricular nodal reentrant tachycardia (AVNRT). 18F-FDG-PET uptake was noted in the atria in all patients and in the ventricles in 3 patients (20%). Cardiac sarcoidosis was the diagnosis in 12 patients (80%) while 3 patients (20%) had tuberculosis. The median CHA2DS2 VASc score was 1. Four patients (26.7%) presented with ischemic stroke. All patients were treated with disease-specific therapy in addition to antiarrhythmic medications. Over a median follow up of 26 months, a significant improvement in clinical status commensurate with a decline in atrial uptake was noted. A non-significant improvement in LVEF to 56% with disease-specific therapy was observed. (p = 0.09).

Atrial fibrillation with granulomatous lymphadenopathy may be a presenting feature of AM. The risk of stroke is high in these individuals. AM should be suspected in young individuals presenting with atrial fibrillation and stroke without conventional risk factors.

Decreased left atrial appendage emptying velocity (LAAV) is a marker for thrombus formation. This study evaluates the association between LAAV and inflammatory indices in non-valvular atrial fibrillation (AF) patients.

The study population was 1428 patients with AF, 875 of whom enrolled. Based on the LAAV, patients were divided into three groups of 262 patients with a velocity of <25 cm/s, 360 patients with a velocity of 25 to 55 cm/s, and 253 patients with a velocity of >55 cm/s to assess and compare in terms of inflammatory indices, including the platelet-to-lymphocyte ratio, neutrophil-to-lymphocyte ratio, systemic immune inflammation index, neutrophil - to - platelet ratio and white blood cell-to-platelet ratio (WPR).

There was no statistical difference in the level of inflammatory indices between the three groups, and none of them were related to LAAV (p > .05) except WPR with a weak negative correlation (p = 0.01, r = -0.10). Patients with lower LAAV were found to have a higher age (p = 0.001), decreased left ventricular ejection fraction (p = 0.001) and greater left atrial volume index (p = 0.001).

This study did not show any association between inflammatory indices and LAAV in non-valvular AF patients except for the WPR.

Sepsis is a life-threatening form of organ dysfunction resulting from a dysregulated response to infection. The complex pathogenesis of sepsis poses challenges because of the lack of reliable biomarkers for early identification and effective treatments. As sepsis progresses to severe forms, cardiac dysfunction becomes a major concern, often manifesting as ventricular dilation, a reduced ejection fraction, and a diminished contractile capacity, known as sepsis-induced cardiomyopathy (SIC). The absence of standardized diagnostic and treatment protocols for SIC leads to varied criteria being used across medical institutions and studies, resulting in significant outcome disparities. Despite the high prevalence of SIC, accurate statistical data are lacking. To understand how SIC affects sepsis prognosis, a thorough exploration of its pathophysiological mechanisms, including systemic factors and complex signalling within myocardial and immune cells, is required. Identifying the factors influencing SIC occurrence and progression is crucial and must be conducted within specific clinical contexts. In this review, the clinical manifestations, pathophysiological mechanisms, and treatment strategies for SIC are discussed, along with the clinical background. We aim to connect current practices with future research challenges, providing clear guidance for clinicians and researchers.

A relationship may exist between the gut microbiota, inflammatory factors and atrial fibrillation (AF); however, the precise biological mechanisms linking these components remain uncertain.In this study, 211 single-nucleotide polymorphisms associated with the gut microbiota were collected from the MiBioGen consortium. Summary data for AF were sourced from large-scale genome-wide association studies. Two-step Mendelian randomization (MR) was applied to estimate the possible mediating effect of inflammatory cytokines on the causality between the gut microbiota and AF. MR confirmed the effects of class Lentisphaeria, family Bifidobacteriaceae, family XIII, genus Anaerostipes, genus Howardella, genus Intestinibacter, genus Lachnospiraceae (NK4A136 group), genus Odoribacter, genus Ruminococcus gnavus, order Bifidobacteriales, order Victivallales and phylum Lentisphaerae on AF prevention. Moreover, MR revealed the role of Fms-related tyrosine kinase 3 ligand, interleukin-6, interleukin-7, leukaemia inhibitory factor receptor, sulfotransferase 1A1 and tumour necrosis factor ligand superfamily member 12 in protecting against AF. Fibroblast growth factor 5, interleukin-2 receptor subunit β, and tumour necrosis factor had a causal effect, increasing AF risk. The mediation exploration indicated that the indirect effect of genus Rikenellaceae (RC9 gut group) (id.11191) on AF mediated by interleukin-6 was OR 1.011 (95% confidence interval 1.002–1.024; mediation proportion=23.913%). This study supplies genetic insights into the potential causal association between the gut microbiota and AF. These causal associations and mediating effects are useful for managing AF through manipulation of the gut microbiota.

Inflammation has been widely recognized as one of the major pathophysiological drivers of the development of atrial fibrillation (AF), which works in tandem with other risk factors of AF including obesity, diabetes, hypertension, and heart failure (HF). Our current understanding of the role of inflammation in the natural history of AF remains elusive; however, several key players, including the NLRP3 (NLR family pyrin domain containing 3) inflammasome, have been acknowledged to be heavily influential on chronic inflammation in the atrial myocardium, which leads to fibrosis and eventual degradation of its electrical function. Nevertheless, our current methods of pharmacological modalities with reported immunomodulatory properties, including well-established classes of drugs e.g., drugs targeting the renin-angiotensin-aldosterone system (RAAS), statins, and vitamin D, have proven effective in reducing the overall risk of developing AF, the onset of postoperative atrial fibrillation (POAF), and reducing overall mortality among patients with AF. This might bring hope for further progress in developing new treatment modalities targeting cellular checkpoints of the NLRP3 inflammasome pathway, or revisiting other well-known anti-inflammatory drugs e.g., colchicine, vitamin C, nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticosteroids, and antimalarial drugs. In our review, we aim to find relevant upstream anti-inflammatory treatment methods for the management of AF and present the most current real-world evidence of their clinical utility.

The aim of this study was to explore the correlation between blood test indicators and Atrial Fibrillation (AF) in Individuals Aged 65 and Older in Yangzhou, Jiangsu.

From January 1, 2019, to August 31, 2023, an epidemiological cross-sectional survey was conducted among the elderly population undergoing health check-ups at Northern Jiangsu People's Hospital in Jiangsu Province. Patients diagnosed with AF after a 12-lead electrocardiogram were included in the case group, and non-AF individuals matched by age and gender in a 1:4 frequency ratio were included in the control group. Least Absolute Shrinkage and Selection Operator (LASSO) regression was used to select important variables from routine blood tests and biochemical indicators and their derived indicators (such as TyG, TyG-BMI, TG/HDL-c, RAR, NLR, MHR). Based on the selected variables, participants were divided into four groups (Q1 ~ Q4), and multifactorial Logistic regression analysis, restricted cubic spline regression, gender subgroup analysis and Receiver Operating Characteristic (ROC) curve were used to explore the relationship between the relevant variables and AF.

A total of 5,879 elderly individuals over the age of 65 were included in the study, with a prevalence of AF of 2.96% (174/5,879). The prevalence of AF in the overall population, as well as in male and female populations, showed a continuous increasing trend with age (P for trend < 0.001). A total of 696 individuals without AF after matching served as the control group, and LASSO regression identified albumin, direct bilirubin, and uric acid as three significant indicators. After adjusting for relevant confounding factors, lower levels of albumin, and higher levels of direct bilirubin and uric acid were significantly associated with the occurrence of AF (P < 0.05). Gender subgroup analysis revealed that in the elderly female population, albumin was not significantly associated with AF (P > 0.05), while direct bilirubin and uric acid were significantly associated with AF (P < 0.05). In the male population, albumin, direct bilirubin, and uric acid were significantly associated with AF (P < 0.05). Restricted cubic spline regression analysis showed a significant nonlinear relationship between direct bilirubin and AF (P for nonlinear < 0.001). The ROC curve analysis indicates that albumin, direct bilirubin, and uric acid all have good association strength with AF in elderly patients, with direct bilirubin showing the strongest association effect (AUC (95% CI) = 0.728 (0.686, 0.769)).

Low levels of albumin, high levels of direct bilirubin, and uric acid are all significantly associated with AF in the elderly population of the Central Jiangsu region. The conclusions of this study need further validation with a larger sample size.

The common occurrence of atrial fibrillation (AF) as a cardiac arrhythmia, along with its link to sleep deprivation (SD), is gaining more acknowledgment. Even with progress in comprehending the development of AF, the molecular connections between SD and AF are still not well-defined. The objective of this research was to pinpoint the shared molecular routes responsible for SD-induced AF and investigate possible treatment targets.

Utilizing bioinformatics, we examined two transcriptome datasets from the Gene Expression Omnibus (GEO) database to pinpoint genes with differential expression (DEGs) common to SD and AF. Analyses focusing on functional enrichment, such as Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), were conducted to pinpoint crucial biological mechanisms and pathways. Furthermore, we utilized immunofluorescence and Western blot techniques to evaluate YBX1 expression and its role in activating NLRP3 inflammasomes in a rat model induced by SD.

A total of 540 common DEGs were precisely identified between the AF and SD data collections. Studies emphasizing functional enrichment have highlighted the significance of inflammation pathways, particularly the NOD-like receptor signaling route. The application of machine learning uncovered four crucial genes-CDC5L, MAPK14, RAB5A, and YBX1-with YBX1 becoming the predominant gene in diagnostic processes. Investigating immune penetration revealed significant connections between YBX1 expression and specific immune cell types, notably CD8+ T cells and M1 macrophages. Live studies have demonstrated that SD amplifies the atrial electrical rearrangement, structural changes, the infiltration of inflammatory cells, and the heightened presence of YBX1 along with inflammasome elements.

The research pinpoints YBX1 as a crucial gene in SD-related AF, possibly influencing its impact via the NOD-like receptor signaling route and the invasion of immune cells. The results offer crucial understanding of the molecular processes behind AF and propose YBX1 as a possible treatment focus to reduce the risk of AF caused by SD.

This review aims to explore the clinical significance of atrial fluorodeoxyglucose (FDG) uptake observed in positron emission tomography (PET) scans, focusing on its association with atrial fibrillation (AF), cardiac sarcoidosis, and myocarditis. We discuss the implications of atrial uptake for patient management and prognosis.

Recent studies have demonstrated that atrial FDG uptake is frequently present in patients with AF, particularly those with persistent AF, and is linked to increased risks of stroke and poorer outcomes after ablation. In cardiac sarcoidosis, atrial uptake correlates with inflammation and an elevated risk of AF. Additionally, non-granulomatous myocarditis has been associated with localized atrial FDG uptake, necessitating careful differentiation from other causes. : Atrial FDG uptake reflects underlying pathological processes such as inflammation, which can significantly impact patient management and outcomes across various cardiovascular diseases. Recognizing these findings can facilitate early intervention, improve prognosis, and support the development of clear guidelines for clinical practice, emphasizing the need for continued research in this area.

Atrial fibrillation and heart failure have both been suggested to increase stroke and dementia risk. However, in observational studies, reversed causation and unmeasured confounding may occur. To mitigate these issues, this study aims to investigate if higher genetic risk for atrial fibrillation and heart failure increases dementia and stroke risk. Data were obtained from the population-based Gothenburg H70 Birth Cohort Studies in Sweden. Participants (N = 984) were born in 1930 with baseline examinations at age 70, 75, 79 or 85 and follow-ups until age 88-89. Polygenic risk scores at the 5 × 10-8, 1 × 10-5, 1 × 10-3 and 1 × 10-1 thresholds were generated for atrial fibrillation and heart failure. Stroke was diagnosed based on self-reports, close-informant interviews, and the National Patient Register. Dementia was diagnosed based on neuropsychiatric examinations, close-informant interviews, and the National Patient Register. Cox regression analyses were performed, adjusted for sex, age at baseline and the first five principal components to correct for population stratification. Those within the highest atrial fibrillation-polygenic risk score tertile had a 1.5 (95% CI 1.09-2.03) increased risk of dementia (at the 1 × 10-5 threshold) and a 1.5 (95% CI 1.07-2.03) increased risk of stroke (at the 1 × 10-3 threshold) compared to the lowest tertile. Those within the highest heart failure-polygenic risk score tertile had a 1.6 (95% CI 1.19-2.27) increased risk of dementia (at the 5 × 10-8 threshold), but no increased risk of stroke (HR 1.2; 95% CI 0.83-1.60 at the 1 × 10-5 threshold), compared to the lowest tertile. When analysing the polygenic risk scores as a continuous variable, the associations were in the same direction, although weaker. This study, investigating genetic risk of atrial fibrillation and heart failure in relation to stroke and dementia, supports the increasing body of evidence suggesting that atrial fibrillation is associated with both stroke and dementia risk. Whether heart failure increases dementia risk is less established, but the present study found that genetic risk of heart failure increased dementia risk. The finding that genetic risk for heart failure did not increase stroke risk needs to be interpreted with caution, as it may be due to a lack of statistical power. There are guidelines on how to best treat atrial fibrillation to prevent stroke, but more knowledge is needed on how to treat atrial fibrillation and heart failure to prevent dementia.

Atrial fibrillation (AF) is the most prevalent form of sustained cardiac arrhythmia, with vascular endothelial growth factor (VEGF) increasingly recognized for its potential role in the pathogenesis of AF through mechanisms involving atrial remodeling, inflammation, and fibrosis. This systematic review aims to synthesize available evidence on the association between VEGF and AF, exploring the implications of VEGF as a biomarker and therapeutic target.

We conducted a comprehensive search across PubMed, Embase, and Web of Science until November 10 2024, selecting studies based on pre-defined criteria that involve adults with AF and measurements of VEGF levels. The selected studies included observational and experimental designs, excluding non-English and methodologically insufficient publications. Narrative synthesis was used for summarising the results.

Eight studies met the inclusion criteria. The studies show a general trend of elevated VEGF levels in AF patients compared to controls, with significant heterogeneity in findings across studies. VEGF subtypes such as VEGF-A and VEGF-D demonstrated stronger associations with AF risk compared to VEGF-C. These variations point to the complex role of VEGF in AF, influencing factors like angiogenesis, endothelial function, and inflammatory responses.

VEGF is potentially a significant contributor to AF pathophysiology, with its levels reflecting disease activity. The variability observed across studies suggests a need for standardized measurement approaches and further investigation into VEGF subtypes. Future research should focus on longitudinal studies to better understand the causal relationships and the potential of VEGF as a therapeutic target and biomarker in AF management.

Not applicable.

New-onset atrial fibrillation (NOAF) is associated with increased morbidity and mortality. Despite identifying numerous factors contributing to NOAF, the underlying mechanisms remain uncertain. This study introduces the triglyceride-glucose index (TyG index) as a predictive indicator and establishes a clinical predictive model. We included 551 patients with acute myocardial infarction (AMI) without a history of atrial fibrillation (AF). These patients were divided into two groups based on the occurrence of postoperative NOAF during hospitalization: the NOAF group (n = 94) and the sinus rhythm (SR) group (n = 457). We utilized a regression model to analyze the risk factors of NOAF and to establish a predictive model. The predictive performance, calibration, and clinical effectiveness were evaluated using the receiver operational characteristics (ROC), calibration curve, decision curve analysis, and clinical impact curve. 94 patients developed NOAF during hospitalization. TyG was identified as an independent predictor of NOAF and was significantly higher in the NOAF group. Left atrial (LA) diameter, age, the systemic inflammatory response index (SIRI), and creatinine were also identified as risk factors for NOAF. Combining these with the TyG to build a clinical prediction model resulted in an area under the curve (AUC) of 0.780 (95% CI 0.358-0.888). The ROC, calibration curve, decision curve analysis, and clinical impact curve demonstrated that the performance of the new nomogram was satisfactory. By incorporating the TyG index into the predictive model, NOAF after AMI during hospitalization can be effectively predicted. Early detection of NOAF can significantly improve the prognosis of AMI patients.

It has been proposed that colchicine may have the potential to prevent cardiovascular and cerebrovascular dysfunctions.

This study evaluated the impact of colchicine on preventing recurrent stroke in patients with both ischemic stroke (IS) and atrial fibrillation (AF).

A randomized, double-blinded, placebo-controlled trial was conducted at Golestan Hospital (Ahvaz, Iran) over one year, involving IS patients with AF. Demographic and clinical data were collected from the participants, who were then assigned to either the intervention or placebo groups. The experimental group was administered colchicine at a dosage of 0.05 mg twice daily for one year, while the control group received a placebo at a comparable dosage over the same timeframe.

In one year, 108 patients completed the study. There were 55 patients in the intervention group and 53 patients in the placebo group. During the second trimester of the trial, three patients in the colchicine group and 10 patients in the placebo group experienced recurrent strokes. Gastrointestinal issues were the most commonly reported complications (33 cases) among the two groups, followed by myalgia (8 patients). There were significant differences in the frequency of recurrent stroke and serum levels of C-reactive protein (CRP) between the colchicine and placebo groups (p < 0.05) after intervention.

In this study, colchicine was effective in reducing recurrent stroke and CRP levels in IS patients with AF compared to the control group. Further randomized controlled trials with larger sample sizes and extended durations are recommended to validate the results of this trial.

In patients with atrial fibrillation (AF), recurrent AF and sinus rhythm during follow-up are determined by interactions between cardiovascular disease processes and rhythm control therapy. Predictors of attaining sinus rhythm at follow-up are not well known.

To quantify the interaction between cardiovascular disease processes and rhythm outcomes, 14 biomarkers reflecting AF-related cardiovascular disease processes in 1586 patients in the EAST-AFNET 4 biomolecule study (71 years old, 45% women) were quantified at baseline. Mixed logistic regression models including clinical features were constructed for each biomarker. Biomarkers were interrogated for interaction with early rhythm control. Outcome was sinus rhythm at 12 months. Results were validated at 24 months and in external datasets.

Higher baseline concentrations of three biomarkers were independently associated with a lower chance of sinus rhythm at 12 months: angiopoietin 2 (ANGPT2) (odds ratio [OR] .76 [95% confidence interval .65-.89], P < .001), bone morphogenetic protein 10 (BMP10) (OR .83 [.71-.97], P = .017), and N-terminal pro-B-type natriuretic peptide (NT-proBNP) (OR .73 [.60-.88], P < .001). Analysis of rhythm at 24 months confirmed the results. Early rhythm control interacted with the predictive potential of NT-proBNP (Pinteraction = .033). The predictive effect of NT-proBNP was reduced in patients randomized to early rhythm control (usual care: OR .64 [.51-.80], P < .001; early rhythm control: OR .90 [.69-1.18], P = .453). External validation confirmed that low concentrations of ANGPT2, BMP10, and NT-proBNP predict sinus rhythm during follow-up.

Low concentrations of ANGPT2, BMP10, and NT-proBNP identify patients with AF who are likely to attain sinus rhythm during follow-up. The predictive ability of NT-proBNP is attenuated in patients receiving rhythm control.

To determine cell-free mitochondrial DNA (mt-cfDNA) levels in tachycardia-induced cardiomyopathy (TIC) and non-TIC among atrial fibrillation (AF) cases.

TIC is a reversible cardiomyopathy resulting from tachyarrhythmias, such as AF. The exact cause of TIC is not fully understood, but mitochondrial dysfunction has been reported in a variety of cardiomyopathies and may be involved in TIC as well. AF is recognized to be associated with systemic inflammation, and studies have shown that in patients with AF have elevated levels of mt-cfDNA increased, and this increase is linked to systemic inflammation.

We enrolled 67 patients with TIC (TIC group) and 671 patients without TIC (non-TIC group), who underwent catheter ablation for AF at our hospital between November 2009 and September 2016 and did not meet the exclusion criteria. We performed quantitative PCR analysis of plasma mt-cfDNA and nuclear-cfDNA and compared clinical factors and these measurements between the two groups.

Levels of mt-cfDNA were significantly lower in the TIC group than in the non-TIC group (1110.01 vs. 1918.71 copies/μg plasma, P = 0.027), while levels of nuclear-cfDNA were comparable between these two groups. In particular, mt-cfDNA (P = 0.0003, odds ratio [OR] 2.54), non-paroxysmal AF (P < 0.0001, OR 3.07), and diabetes mellitus (P = 0.006, OR 2.36) were identified as independent factors associated with TIC.

There are lower mt-cfDNA in TIC, and decreased plasma levels of circulating mt-cfDNA may be a new biomarker and involve in related mechanisms for AF associated TIC.

Tachycardia-induced cardiomyopathy (TIC) is a reversible cardiomyopathy caused by tachyarrhythmias, such as atrial fibrillation (AF) tachycardia. The pathogenesis of TIC remains incompletely understood, and there is currently no method to predict its development in patients. In this study, we show that cell-free mitochondrial DNA (mt-cfDNA) levels were significantly lower in the TIC group than in the non-TIC group. Persistent AF, coexisting diabetes mellitus, and decreased mt-cfDNA levels were independently associated with TIC. Decreased mt-cfDNA levels may serve as a novel biomarker for predicting TIC in patients with AF.

Honeysuckle is a conventional Chinese medicine with several therapeutic applications. With the advancement of modern scientific technologies, Honeysuckle's pharmacological effects and medicinal properties have been investigated more thoroughly. Studies demonstrate that the bioactive compounds in Honeysuckle possess anti-inflammatory effects via several mechanisms, protecting the cardiovascular system. This article provides a reference for the clinical use of Honeysuckle by reviewing research on the therapeutic impact of Honeysuckle and its active constituents on cardiovascular diseases, such as coronary atherosclerotic heart disease (CHD), myocardial ischemia-reperfusion (MI/R), acute myocardial infarction (AMI), hypertension, arrhythmia, and heart failure, through the inhibition of inflammatory responses.