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Altered fibrin clot properties and elevated von Willebrand factor are associated with progression to permanent atrial fibrillation: A cohort study.
Eur J Clin Invest
January 2025
Department of Thromboembolic Disorders, Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland.
Background: The role of a prothrombotic state in atrial fibrillation (AF) progression to permanent arrythmia (PerAF) is unclear. Formation of denser and poorly lysable fibrin clots has been observed in AF patients also with sinus rhythm in association with higher stroke risk. We investigated whether altered fibrin clot properties and other prothrombotic state markers may contribute to AF transition to PerAF.
View Article and Find Full Text PDFReduced PI3K(p110α) induces atrial myopathy, and PI3K-related lipids are dysregulated in athletes with atrial fibrillation.
J Sport Health Sci
January 2025
Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia; Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora, VIC 3086, Australia; Department of Diabetes, Central Clinical School, Monash University, Clayton, VIC 3800, Australia; Department of Cardiometabolic Health, University of Melbourne, Melbourne, VIC 3010, Australia; Department of Cardiovascular Research, Translation and Implementation, La Trobe University, Bundoora, VIC 3086, Australia; Department of Physiology and Department of Medicine Alfred Hospital, Monash University, Clayton, VIC 3800, Australia; Heart Research Institute, Newtown, NSW 2042, Australia. Electronic address:
Background: Elucidating mechanisms underlying atrial myopathy, which predisposes individuals to atrial fibrillation (AF), will be critical for preventing/treating AF. In a serendipitous discovery, we identified atrial enlargement, fibrosis, and thrombi in mice with reduced phosphoinositide 3-kinase (PI3K) in cardiomyocytes. PI3K(p110α) is elevated in the heart with exercise and is critical for exercise-induced ventricular enlargement and protection, but the role in the atria was unknown.
View Article and Find Full Text PDFLactobacillus gasseri prevents ibrutinib-associated atrial fibrillation through butyrate.
Europace
January 2025
Department of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Ibrutinib, a widely used anti-cancer drug, is known to significantly increase the susceptibility to atrial fibrillation (AF). While it is recognized that drugs can reshape the gut microbiota, influencing both therapeutic effectiveness and adverse events, the role of gut microbiota in ibrutinib-induced AF remains largely unexplored. Utilizing 16S rRNA gene sequencing, fecal microbiota transplantation, metabonomics, electrophysiological examination, and molecular biology methodologies, we sought to validate the hypothesis that gut microbiota dysbiosis promotes ibrutinib-associated AF and to elucidate the underlying mechanisms.
View Article and Find Full Text PDFRoutine use of genetic data in healthcare is much-discussed, yet little is known about its performance in epidemiological models including traditional risk factors. Using severe COVID-19 as an exemplar, we explore the integration of polygenic risk scores (PRS) into disease models alongside sociodemographic and clinical variables. PRS were optimized for 23 clinical variables and related traits previously-associated with severe COVID-19 in up to 450,449 UK Biobank participants, and tested in 9,560 individuals diagnosed in the pre-vaccination era.
View Article and Find Full Text PDFConstitutive deletion of the obscurin-Ig58/59 domains induces atrial remodeling and Ca2+-based arrhythmogenesis.
JCI Insight
January 2025
Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, United States of America.
Obscurin is a giant protein that coordinates diverse aspects of striated muscle physiology. Obscurin immunoglobulin domains 58/59 (Ig58/59) associate with essential sarcomeric and Ca2+ cycling proteins. To explore the pathophysiological significance of Ig58/59, we generated the Obscn-ΔIg58/59 mouse model, expressing obscurin constitutively lacking Ig58/59.
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