Atrial fibrillation in the presence and absence of heart failure enhances expression of genes involved in cardiomyocyte structure, conduction properties, fibrosis, inflammation, and endothelial dysfunction
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Atrial fibrillation in the presence and absence of heart failure enhances expression of genes involved in cardiomyocyte structure, conduction properties, fibrosis, inflammation, and endothelial dysfunction. / Zeemering, Stef; Isaacs, Aaron; Winters, Joris; Maesen, Bart; Bidar, Elham; Dimopoulou, Christina; Guasch, Eduard; Batlle, Montserrat; Haase, Doreen; Hatem, Stéphane N; Kara, Mansour; Kääb, Stefan; Mont, Lluis; Sinner, Moritz F; Wakili, Reza; Maessen, Jos; Crijns, Harry J G M; Fabritz, Larissa; Kirchhof, Paulus; Stoll, Monika; Schotten, Ulrich.
in: HEART RHYTHM, Jahrgang 19, Nr. 12, 12.2022, S. 2115-2124.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Atrial fibrillation in the presence and absence of heart failure enhances expression of genes involved in cardiomyocyte structure, conduction properties, fibrosis, inflammation, and endothelial dysfunction
AU - Zeemering, Stef
AU - Isaacs, Aaron
AU - Winters, Joris
AU - Maesen, Bart
AU - Bidar, Elham
AU - Dimopoulou, Christina
AU - Guasch, Eduard
AU - Batlle, Montserrat
AU - Haase, Doreen
AU - Hatem, Stéphane N
AU - Kara, Mansour
AU - Kääb, Stefan
AU - Mont, Lluis
AU - Sinner, Moritz F
AU - Wakili, Reza
AU - Maessen, Jos
AU - Crijns, Harry J G M
AU - Fabritz, Larissa
AU - Kirchhof, Paulus
AU - Stoll, Monika
AU - Schotten, Ulrich
N1 - Crown Copyright © 2022. Published by Elsevier Inc. All rights reserved.
PY - 2022/12
Y1 - 2022/12
N2 - BACKGROUND: Little is known about genome-wide changes in the atrial transcriptome as a cause or consequence of atrial fibrillation (AF), and the effect of its common and clinically relevant comorbidity-heart failure (HF).OBJECTIVE: The purpose of this study was to explore candidate disease processes for AF by investigating gene expression changes in atrial tissue samples from patients with and without AF, stratified by HF.METHODS: RNA sequencing was performed in right and left atrial appendage tissue in 195 patients undergoing open heart surgery from centers participating in the CATCH-ME consortium (no history of AF, n = 91; paroxysmal AF, n = 53; persistent/permanent AF, n = 51). Analyses were stratified into patients with/without HF (n = 75/120) and adjusted for age, sex, atrial side, and a combination of clinical characteristics.RESULTS: We identified 35 genes associated with persistent AF compared to patients without a history of AF, both in the presence or absence of HF (false discovery rate <0.05). These were mostly novel associations, including 13 long noncoding RNAs. Genes were involved in regulation of cardiomyocyte structure, conduction properties, fibrosis, inflammation, and endothelial dysfunction. Gene set enrichment analysis identified mainly inflammatory gene sets to be enriched in AF patients without HF, and gene sets involved in cellular respiration in AF patients with HF.CONCLUSION: Analysis of atrial gene expression profiles identified numerous novel genes associated with persistent AF, in the presence or absence of HF. Interestingly, no consistent transcriptional changes were associated with paroxysmal AF, suggesting that AF-induced changes in gene expression predominate other changes.
AB - BACKGROUND: Little is known about genome-wide changes in the atrial transcriptome as a cause or consequence of atrial fibrillation (AF), and the effect of its common and clinically relevant comorbidity-heart failure (HF).OBJECTIVE: The purpose of this study was to explore candidate disease processes for AF by investigating gene expression changes in atrial tissue samples from patients with and without AF, stratified by HF.METHODS: RNA sequencing was performed in right and left atrial appendage tissue in 195 patients undergoing open heart surgery from centers participating in the CATCH-ME consortium (no history of AF, n = 91; paroxysmal AF, n = 53; persistent/permanent AF, n = 51). Analyses were stratified into patients with/without HF (n = 75/120) and adjusted for age, sex, atrial side, and a combination of clinical characteristics.RESULTS: We identified 35 genes associated with persistent AF compared to patients without a history of AF, both in the presence or absence of HF (false discovery rate <0.05). These were mostly novel associations, including 13 long noncoding RNAs. Genes were involved in regulation of cardiomyocyte structure, conduction properties, fibrosis, inflammation, and endothelial dysfunction. Gene set enrichment analysis identified mainly inflammatory gene sets to be enriched in AF patients without HF, and gene sets involved in cellular respiration in AF patients with HF.CONCLUSION: Analysis of atrial gene expression profiles identified numerous novel genes associated with persistent AF, in the presence or absence of HF. Interestingly, no consistent transcriptional changes were associated with paroxysmal AF, suggesting that AF-induced changes in gene expression predominate other changes.
KW - Humans
KW - Atrial Fibrillation
KW - Myocytes, Cardiac
KW - Heart Failure
KW - Fibrosis
KW - Inflammation/genetics
U2 - 10.1016/j.hrthm.2022.08.019
DO - 10.1016/j.hrthm.2022.08.019
M3 - SCORING: Journal article
C2 - 36007727
VL - 19
SP - 2115
EP - 2124
JO - HEART RHYTHM
JF - HEART RHYTHM
SN - 1547-5271
IS - 12
ER -