Endomysial fibrosis, rather than overall connective tissue content, is the main determinant of conduction disturbances in human atrial fibrillation.

AF complexity AF substrate Atrial fibrillation Endomysial fibrosis Epicardial mapping Fibrosis

Journal

Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology
ISSN: 1532-2092
Titre abrégé: Europace
Pays: England
ID NLM: 100883649

Informations de publication

Date de publication:
15 07 2022
Historique:
received: 11 02 2022
accepted: 15 03 2022
pubmed: 30 3 2022
medline: 19 7 2022
entrez: 29 3 2022
Statut: ppublish

Résumé

Although in persistent atrial fibrillation (AF) a complex AF substrate characterized by a high incidence of conduction block has been reported, relatively little is known about AF complexity in paroxysmal AF (pAF). Also, the relative contribution of various aspects of structural alterations to conduction disturbances is not clear. In particular, the contribution of endomysial fibrosis to conduction disturbances during progression of AF has not been studied yet. During cardiac surgery, epicardial high-density mapping was performed in patients with acutely induced (aAF, n = 11), pAF (n = 12), and longstanding persistent AF (persAF, n = 9) on the right atrial (RA) wall, the posterior left atrial wall (pLA) and the LA appendage (LAA). In RA appendages, overall and endomysial (myocyte-to-myocyte distances) fibrosis and connexin 43 (Cx43) distribution were quantified. Unipolar AF electrogram analysis showed a more complex pattern with a larger number of narrower waves, more breakthroughs and a higher fractionation index (FI) in persAF compared with aAF and pAF, with no differences between aAF and pAF. The FI was consistently higher at the pLA compared with the RA. Structurally, Cx43 lateralization increased with AF progression (aAF = 7.5 ± 8.9%, pAF = 24.7 ± 11.1%, persAF = 35.1 ± 11.4%, P < 0.001). Endomysial but not overall fibrosis correlated with AF complexity (r = 0.57, P = 0.001; r = 0.23, P = 0.20; respectively). Atrial fibrillation complexity is highly variable in patients with pAF, but not significantly higher than in patients with acutely induced AF, while in patients with persistent AF complexity is higher. Among the structural alterations studied, endomysial fibrosis, but not overall fibrosis, is the strongest determinant of AF complexity.

Identifiants

pubmed: 35348667
pii: 6555065
doi: 10.1093/europace/euac026
pmc: PMC9282911
doi:

Substances chimiques

Connexin 43 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1015-1024

Informations de copyright

© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.

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Auteurs

Bart Maesen (B)

Department of Cardio-Thoracic Surgery, Maastricht University Medical Center, Maastricht, The Netherlands.
Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.

Sander Verheule (S)

Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
Department of Physiology, Maastricht University, Universiteitssingel 50, PO Box 616, 6200MD Maastricht, The Netherlands.

Stef Zeemering (S)

Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
Department of Physiology, Maastricht University, Universiteitssingel 50, PO Box 616, 6200MD Maastricht, The Netherlands.

Mark La Meir (M)

Department of Cardiac Surgery, UZ Brussels, Brussels, Belgium.

Jan Nijs (J)

Department of Cardiac Surgery, UZ Brussels, Brussels, Belgium.

Stijn Lumeij (S)

Department of Physiology, Maastricht University, Universiteitssingel 50, PO Box 616, 6200MD Maastricht, The Netherlands.

Dennis H Lau (DH)

Department of Physiology, Maastricht University, Universiteitssingel 50, PO Box 616, 6200MD Maastricht, The Netherlands.

Mathieu Granier (M)

Department of Physiology, Maastricht University, Universiteitssingel 50, PO Box 616, 6200MD Maastricht, The Netherlands.

Harry Jgm Crijns (HJ)

Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
Department of Cardiology, Maastricht University Medical Center, Maastricht, The Netherlands.

Jos G Maessen (JG)

Department of Cardio-Thoracic Surgery, Maastricht University Medical Center, Maastricht, The Netherlands.
Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.

Stefan Dhein (S)

Department of Cardiac Surgery, Clinic for Cardiac Surgery, Heart Centre Leipzig, Leipzig, Germany.

Ulrich Schotten (U)

Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
Department of Physiology, Maastricht University, Universiteitssingel 50, PO Box 616, 6200MD Maastricht, The Netherlands.

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