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Introduction: Besides the traditional concept of atrial fibrillation (AF) perpetuating atrial structural remodeling, there is increasing evidence that atrial fibrosis might precede AF, highlighting the need for better characterization of the fibrotic substrate. We aimed to assess atrial fibrosis by use of late gadolinium enhancement magnetic resonance imaging (LGE-MRI) in non-AF individuals and to identify predisposing risk factors. A second aim was to establish a risk score for the prevalence of AF using atrial fibrosis in addition to established clinical variables.
Methods And Results: Non-AF individuals without structural heart disease (n = 91) and matched AF controls (n = 91) underwent MRI for assessment of LGE. According to the established UTAH classification, atrial LGE ≥20% was considered extensive. Mean left atrial (LA) fibrosis in non-AF and AF individuals were 8.8 ± 6.5% and 12.5 ± 5.8%, respectively. Body mass index (BMI) >30 kg/m and LA volume were predictors of atrial fibrosis. Diastolic function was not significantly different with respect to atrial fibrosis. A novel scoring system for the prevalence of AF (2 points for arterial hypertension and/or left ventricular ejection fraction <55%; 3 points for atrial fibrosis >6%) was derived demonstrating that patients in the intermediate/high-risk group had a significantly increased risk of AF.
Conclusion: This study reports unexpectedly high atrial fibrosis in non-AF patients without apparent heart disease, highlighting the concept that structural fibrotic alterations may precede AF onset in a significant proportion of individuals. BMI as a predictor of atrial fibrosis suggests that lifestyle and drug intervention, that is, weight reduction, could positively influence fibrosis development. The derived risk score for AF prevalence provides the basis for prospective studies on AF incidence.
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http://dx.doi.org/10.1111/jce.13846 | DOI Listing |
Circ Cardiovasc Imaging
September 2025
Department of Cardiology, Amsterdam UMC, The Netherlands. (L.H.G.A.H., N.v.P., M.J.B.K., P.B., C.A., M.J.W.G.).
Can J Cardiol
September 2025
Section of Cardiac Surgery, Department of Cardiac Sciences, Libin Cardiovascular Institute, Cumming School of Medicine, Calgary, Alberta, Canada.
There is evidence supporting the importance of local immune microenvironment with respect to physiological and pathological states. Cardiac fibrosis, post-operative atrial fibrillation, and post-surgical pericardial adhesions are the culmination of complex cascade of processes, many of which have immune-mediated etiologies. While extensive research has focused on describing the systemic markers, to date, little attention has been given to local pericardial factors that can impact fibrotic activity and/or lead to POAF and PSPA.
View Article and Find Full Text PDFWorld J Gastroenterol
August 2025
Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, United States.
Background: Cardiopulmonary changes in noncirrhotic portal hypertension (NCPH) are poorly understood.
Aim: To investigate cardiopulmonary changes using transthoracic echocardiography (TTE) in NCPH and their correlation with clinical features.
Methods: Prospective cohort including 10 preclinical NCPH [without portal hypertension (PH)] and 32 NCPH subjects who underwent TTE with agitated saline injection and comprehensive clinical evaluation were assessed.
Ann Med Surg (Lond)
September 2025
Department of Biomedical and Laboratory Science, Africa University, Mutare, Zimbabwe.
Cardiac arrhythmias, including atrial fibrillation and ventricular arrhythmias, are significant contributors to cardiovascular morbidity and mortality. Recent research has highlighted the critical role of inflammation in the pathogenesis of these arrhythmias, with inflammatory cytokines acting as key mediators. Cytokines such as interleukin-1, interleukin-6, tumor necrosis factor-alpha, and interleukin-17 are involved in promoting myocardial fibrosis, ion channel dysfunction, and autonomic dysregulation, which contribute to arrhythmic events.
View Article and Find Full Text PDFClin Res Cardiol
September 2025
Department for Internal Medicine and Cardiology, Heart Center Dresden, Faculty of Medicine and University Hospital Carl Gustav Carus, TUD Dresden University of Technology, Dresden, Germany.
Background And Aims: The pathophysiologic concept of atrial fibrillation (AF) has evolved towards defining atrial cardiomyopathy, recognizing inflammation-mediated remodeling of the left atrium (LA) as a source for arrhythmogenesis. One feature of atrial cardiomyopathy is the development of fibrosis, with low-voltage zones (LVZ) identified by invasive electroanatomic mapping as an accepted surrogate parameter. A mediator of pathological remodeling is epicardial adipose tissue (EAT).
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