Sleep apnoea has a dose-dependent effect on atrial remodelling in paroxysmal but not persistent atrial fibrillation: a high-density mapping study.


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:
21 05 2021
Historique:
received: 12 05 2020
accepted: 06 01 2021
pubmed: 16 1 2021
medline: 10 8 2021
entrez: 15 1 2021
Statut: ppublish

Résumé

Obstructive sleep apnoea (OSA) associates with atrial fibrillation (AF), but the relationship of OSA severity and AF phenotype with the atrial substrate remains poorly defined. We sought to define the atrial substrate across the spectrum of OSA severity utilizing high-density mapping. Sixty-six consecutive patients (male 71%, age 61 ± 9) having AF ablation (paroxysmal AF 36, persistent AF 30) were recruited. All patents underwent formal overnight polysomnography and high-density left atrial (LA) mapping (mean 2351 ± 1244 points) in paced rhythm. Apnoea-hypopnoea index (AHI) (mean 21 ± 18) associated with lower voltage (-0.34, P = 0.005), increased complex points (r = 0.43, P < 0.001), more low-voltage areas (r = 0.42, P < 0.001), and greater voltage heterogeneity (r = 0.39, P = 0.001), and persisted after multivariable adjustment. Atrial conduction heterogeneity (r = 0.24, P = 0.025) but not conduction velocity (r = -0.09, P = 0.50) associated with AHI. Patchy regions of low voltage that co-localized with slowed conduction defined the atrial substrate in paroxysmal AF, while a diffuse atrial substrate predominated in persistent AF. The association of AHI with remodelling was most apparent among paroxysmal AF [LA voltage: paroxysmal AF -0.015 (-0.025, -0.005), P = 0.004 vs. persistent AF -0.006 (-0.017, 0.005), P = 0.30]. Furthermore, in paroxysmal AF an AHI ≥ 30 defined a threshold at which atrial remodelling became most evident (nil-mild vs. moderate vs. severe: 1.92 ± 0.42 mV vs. 1.84 ± 0.28 mV vs. 1.34 ± 0.41 mV, P = 0.006). In contrast, significant remodelling was observed across all OSA categories in persistent AF (1.67 ± 0.55 mV vs. 1.50 ± 0.66 mV vs. 1.55 ± 0.67 mV, P = 0.82). High-density mapping observed that OSA associates with marked atrial remodelling, predominantly among paroxysmal AF cohorts with severe OSA. This may facilitate the identification of AF patients that stand to derive the greatest benefit from OSA management.

Identifiants

pubmed: 33447844
pii: 6099039
doi: 10.1093/europace/euaa275
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

691-700

Informations de copyright

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.

Auteurs

Chrishan Joseph Nalliah (CJ)

Department of Cardiology, Royal Melbourne Hospital, Melbourne 3050, Australia.
Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.

Geoffrey R Wong (GR)

Department of Cardiology, Royal Melbourne Hospital, Melbourne 3050, Australia.
Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.

Geoffrey Lee (G)

Department of Cardiology, Royal Melbourne Hospital, Melbourne 3050, Australia.
Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.

Aleksandr Voskoboinik (A)

Department of Respiratory and Sleep Medicine, Royal Melbourne Hospital, Melbourne, Australia.
Department of Cardiology, The Alfred Hospital, Melbourne, Australia.

Kirk Kee (K)

Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.
Department of Respiratory and Sleep Medicine, Royal Melbourne Hospital, Melbourne, Australia.

Jeremy Goldin (J)

Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.
Department of Respiratory and Sleep Medicine, Royal Melbourne Hospital, Melbourne, Australia.

Troy Watts (T)

Department of Cardiology, Royal Melbourne Hospital, Melbourne 3050, Australia.

Dominik Linz (D)

Centre for Heart Rhythm Disorders (CHRD), South Australian Health and Medical Research Institute (SAHMRI), University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia.

Daniel Wirth (D)

Department of Cardiology, Royal Melbourne Hospital, Melbourne 3050, Australia.

Ramanathan Parameswaran (R)

Department of Cardiology, Royal Melbourne Hospital, Melbourne 3050, Australia.
Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.

Hariharan Sugumar (H)

Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.
Department of Cardiology, The Alfred Hospital, Melbourne, Australia.

Sandeep Prabhu (S)

Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.
Department of Cardiology, The Alfred Hospital, Melbourne, Australia.

Alex McLellan (A)

Department of Cardiology, Royal Melbourne Hospital, Melbourne 3050, Australia.
Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.

Han Ling (H)

Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.
Department of Cardiology, The Alfred Hospital, Melbourne, Australia.

Stephen Joseph (S)

Department of Cardiology, Royal Melbourne Hospital, Melbourne 3050, Australia.
Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.

Joseph B Morton (JB)

Department of Cardiology, Royal Melbourne Hospital, Melbourne 3050, Australia.
Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.

Peter Kistler (P)

Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.
Department of Cardiology, The Alfred Hospital, Melbourne, Australia.

Prashanthan Sanders (P)

Centre for Heart Rhythm Disorders (CHRD), South Australian Health and Medical Research Institute (SAHMRI), University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia.

Jonathan M Kalman (JM)

Department of Cardiology, Royal Melbourne Hospital, Melbourne 3050, Australia.
Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.

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