High liver fibrosis scores in metabolic dysfunction-associated fatty liver disease patients are associated with adverse atrial remodeling and atrial fibrillation recurrence following catheter ablation.

MAFLD (metabolic associated fatty liver disease) atrial fibrillation atrial remodeling catheter ablation liver fibrosis

Journal

Frontiers in endocrinology
ISSN: 1664-2392
Titre abrégé: Front Endocrinol (Lausanne)
Pays: Switzerland
ID NLM: 101555782

Informations de publication

Date de publication:
2022
Historique:
received: 30 05 2022
accepted: 01 08 2022
entrez: 19 9 2022
pubmed: 20 9 2022
medline: 21 9 2022
Statut: epublish

Résumé

A number of epidemiological studies have suggested an association between metabolic dysfunction-associated fatty liver disease (MAFLD) and the incidence of atrial fibrillation (AF). However, the pathogenesis leading to AF in the context of MAFLD remains unclear. We therefore aimed at assessing the impact of MAFLD and liver fibrosis status on left atrium (LA) structure and function. Patients with a Fatty Liver Index (FLI) >60 and the presence of metabolic comorbidities were classified as MAFLD+. In MAFLD+ patients, liver fibrosis severity was defined using the non-alcoholic fatty liver disease (NAFLD) Fibrosis Score (NFS), as follows: MAFLD w/o fibrosis (NFS ≦ -1.455), MAFLD w/indeterminate fibrosis (-1.455 < NFS < 0.675), and MAFLD w/fibrosis (NFS ≧ 0.675). In the first cohort of patients undergoing AF ablation, the structural and functional impact on LA of MAFLD was assessed by LA strain analysis and endocardial voltage mapping. Histopathological assessment of atrial fibrosis was performed in the second cohort of patients undergoing cardiac surgery. Finally, the impact of MAFLD on AF recurrence following catheter ablation was assessed. In the AF ablation cohort (NoMAFLD n = 123; MAFLD w/o fibrosis n = 37; MAFLD indeterm. fibrosis n = 75; MAFLD w/severe fibrosis n = 10), MAFLD patients with high risk of F3-F4 liver fibrosis presented more LA low-voltage areas as compared to patients without MAFLD (16.5 [10.25; 28] vs 5.0 [1; 11] low-voltage areas p = 0.0115), impaired LA reservoir function assessed by peak left atrial longitudinal strain (19.7% ± 8% vs 8.9% ± 0.89% p = 0.0268), and increased LA volume (52.9 ± 11.7 vs 43.5 ± 18.0 ml/m In conclusion, we found that liver fibrosis scoring in MAFLD patients is associated with adverse atrial remodeling and AF recurrences following catheter ablation. The impact of the management of MAFLD on LA remodeling and AF ablation outcomes should be assessed in dedicated studies.

Sections du résumé

Background
A number of epidemiological studies have suggested an association between metabolic dysfunction-associated fatty liver disease (MAFLD) and the incidence of atrial fibrillation (AF). However, the pathogenesis leading to AF in the context of MAFLD remains unclear. We therefore aimed at assessing the impact of MAFLD and liver fibrosis status on left atrium (LA) structure and function.
Methods
Patients with a Fatty Liver Index (FLI) >60 and the presence of metabolic comorbidities were classified as MAFLD+. In MAFLD+ patients, liver fibrosis severity was defined using the non-alcoholic fatty liver disease (NAFLD) Fibrosis Score (NFS), as follows: MAFLD w/o fibrosis (NFS ≦ -1.455), MAFLD w/indeterminate fibrosis (-1.455 < NFS < 0.675), and MAFLD w/fibrosis (NFS ≧ 0.675). In the first cohort of patients undergoing AF ablation, the structural and functional impact on LA of MAFLD was assessed by LA strain analysis and endocardial voltage mapping. Histopathological assessment of atrial fibrosis was performed in the second cohort of patients undergoing cardiac surgery. Finally, the impact of MAFLD on AF recurrence following catheter ablation was assessed.
Results
In the AF ablation cohort (NoMAFLD n = 123; MAFLD w/o fibrosis n = 37; MAFLD indeterm. fibrosis n = 75; MAFLD w/severe fibrosis n = 10), MAFLD patients with high risk of F3-F4 liver fibrosis presented more LA low-voltage areas as compared to patients without MAFLD (16.5 [10.25; 28] vs 5.0 [1; 11] low-voltage areas p = 0.0115), impaired LA reservoir function assessed by peak left atrial longitudinal strain (19.7% ± 8% vs 8.9% ± 0.89% p = 0.0268), and increased LA volume (52.9 ± 11.7 vs 43.5 ± 18.0 ml/m
Conclusion
In conclusion, we found that liver fibrosis scoring in MAFLD patients is associated with adverse atrial remodeling and AF recurrences following catheter ablation. The impact of the management of MAFLD on LA remodeling and AF ablation outcomes should be assessed in dedicated studies.

Identifiants

pubmed: 36120456
doi: 10.3389/fendo.2022.957245
pmc: PMC9471263
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

957245

Informations de copyright

Copyright © 2022 Decoin, Butruille, Defrancq, Robert, Destrait, Coisne, Aghezzaf, Woitrain, Gouda, Schino, Klein, Maboudou, Brigadeau, Klug, Vincentelli, Dombrowicz, Staels, Montaigne and Ninni.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Raphaël Decoin (R)

Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011 - EGID, Lille, France.

Laura Butruille (L)

Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011 - EGID, Lille, France.

Thomas Defrancq (T)

CHU Lille, Institut Coeur-Poumon, Lille, France.

Jordan Robert (J)

CHU Lille, Institut Coeur-Poumon, Lille, France.

Nicolas Destrait (N)

CHU Lille, Institut Coeur-Poumon, Lille, France.

Augustin Coisne (A)

Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011 - EGID, Lille, France.
CHU Lille, Institut Coeur-Poumon, Lille, France.

Samy Aghezzaf (S)

CHU Lille, Institut Coeur-Poumon, Lille, France.

Eloise Woitrain (E)

Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011 - EGID, Lille, France.

Zouriatou Gouda (Z)

Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011 - EGID, Lille, France.

Sofia Schino (S)

CHU Lille, Institut Coeur-Poumon, Lille, France.

Cédric Klein (C)

CHU Lille, Institut Coeur-Poumon, Lille, France.

Patrice Maboudou (P)

CHU Lille, Biochemistry Emergency, Lille, France.
CHU Lille, Service de Biochimie Automatisée Protéines, Lille, France.

François Brigadeau (F)

CHU Lille, Institut Coeur-Poumon, Lille, France.

Didier Klug (D)

CHU Lille, Institut Coeur-Poumon, Lille, France.

Andre Vincentelli (A)

Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011 - EGID, Lille, France.
CHU Lille, Institut Coeur-Poumon, Lille, France.

David Dombrowicz (D)

Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011 - EGID, Lille, France.

Bart Staels (B)

Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011 - EGID, Lille, France.

David Montaigne (D)

Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011 - EGID, Lille, France.
CHU Lille, Institut Coeur-Poumon, Lille, France.

Sandro Ninni (S)

Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011 - EGID, Lille, France.
CHU Lille, Institut Coeur-Poumon, Lille, France.

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