Dynamic Atrial Substrate During High-Density Mapping of Paroxysmal and Persistent AF: Implications for Substrate Ablation.


Journal

JACC. Clinical electrophysiology
ISSN: 2405-5018
Titre abrégé: JACC Clin Electrophysiol
Pays: United States
ID NLM: 101656995

Informations de publication

Date de publication:
11 2019
Historique:
received: 26 03 2019
revised: 16 05 2019
accepted: 05 06 2019
entrez: 23 11 2019
pubmed: 23 11 2019
medline: 21 10 2020
Statut: ppublish

Résumé

This study sought to determine the impact of rate and direction on left atrial (LA) substrate. The extent to which substrate mapped in sinus rhythm varies according to cycle length and direction of wave front propagation is unknown. A total of 73 consecutive patients with atrial fibrillation (AF) underwent electroanatomic LA mapping before pulmonary vein isolation using multipolar catheter during distal coronary sinus (CS) pacing at 600 ms and 300 ms. Additional maps were created during left superior pulmonary vein pacing at 300 ms. Bipolar voltage, conduction velocity (CV), and complex signals were determined. Mean age was 61 ± 9 years, 67% were men, and 53% had persistent AF. Global mean voltage was lower with CS pacing at 300 ms compared with 600 ms (1.56 ± 0.47 mV vs. 1.74 ± 0.48 mV; p < 0.001). This was seen in all LA segments. Global CV was reduced (30.4 ± 13.0 cm/s vs. 38.6 ± 14.0 cm/s; p < 0.001) with greater complex signals at 300 ms (8.9% vs. 5.3%; p < 0.005). Compared with CS pacing, left superior pulmonary vein pacing demonstrated highly regional changes with decreased voltage (1.04 ± 0.43 mV vs. 1.47 ± 0.53 mV; p = 0.01) and CV (24.4 ± 13.0 cm/s vs. 39.9 ± 16.6 cm/s; p = 0.008), and greater complex signals posteriorly. Longer AF duration in paroxysmal AF (p = 0.02) and shorter duration in persistent AF (p = 0.015) and left ventricular ejection fraction (p = 0.016) were independent predictors of voltage change. In patients with AF, variation in cycle length and direction of wave front activation produce both generalized and regional changes in voltage, CV, and complex fractionation, resulting in significant changes in substrate maps. This study highlights the potential limitations of static low-voltage maps to identify the AF ablation target zone.

Sections du résumé

OBJECTIVES
This study sought to determine the impact of rate and direction on left atrial (LA) substrate.
BACKGROUND
The extent to which substrate mapped in sinus rhythm varies according to cycle length and direction of wave front propagation is unknown.
METHODS
A total of 73 consecutive patients with atrial fibrillation (AF) underwent electroanatomic LA mapping before pulmonary vein isolation using multipolar catheter during distal coronary sinus (CS) pacing at 600 ms and 300 ms. Additional maps were created during left superior pulmonary vein pacing at 300 ms. Bipolar voltage, conduction velocity (CV), and complex signals were determined.
RESULTS
Mean age was 61 ± 9 years, 67% were men, and 53% had persistent AF. Global mean voltage was lower with CS pacing at 300 ms compared with 600 ms (1.56 ± 0.47 mV vs. 1.74 ± 0.48 mV; p < 0.001). This was seen in all LA segments. Global CV was reduced (30.4 ± 13.0 cm/s vs. 38.6 ± 14.0 cm/s; p < 0.001) with greater complex signals at 300 ms (8.9% vs. 5.3%; p < 0.005). Compared with CS pacing, left superior pulmonary vein pacing demonstrated highly regional changes with decreased voltage (1.04 ± 0.43 mV vs. 1.47 ± 0.53 mV; p = 0.01) and CV (24.4 ± 13.0 cm/s vs. 39.9 ± 16.6 cm/s; p = 0.008), and greater complex signals posteriorly. Longer AF duration in paroxysmal AF (p = 0.02) and shorter duration in persistent AF (p = 0.015) and left ventricular ejection fraction (p = 0.016) were independent predictors of voltage change.
CONCLUSIONS
In patients with AF, variation in cycle length and direction of wave front activation produce both generalized and regional changes in voltage, CV, and complex fractionation, resulting in significant changes in substrate maps. This study highlights the potential limitations of static low-voltage maps to identify the AF ablation target zone.

Identifiants

pubmed: 31753431
pii: S2405-500X(19)30409-8
doi: 10.1016/j.jacep.2019.06.002
pii:
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1265-1277

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2019. Published by Elsevier Inc.

Auteurs

Geoffrey R Wong (GR)

Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia; Department of Medicine, University of Melbourne, Melbourne, Australia.

Chrishan J Nalliah (CJ)

Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia; Department of Medicine, University of Melbourne, Melbourne, Australia.

Geoffrey Lee (G)

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

Aleksandr Voskoboinik (A)

Baker IDI Heart and Diabetes Institute, Melbourne, Australia; Heart Centre, Alfred Hospital, Melbourne, Australia.

Sandeep Prabhu (S)

Baker IDI Heart and Diabetes Institute, Melbourne, Australia; Heart Centre, Alfred Hospital, Melbourne, Australia.

Ramanathan Parameswaran (R)

Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia; Department of Medicine, University of Melbourne, Melbourne, Australia.

Hariharan Sugumar (H)

Baker IDI Heart and Diabetes Institute, Melbourne, Australia; Heart Centre, Alfred Hospital, Melbourne, Australia.

Robert D Anderson (RD)

Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia; Department of Medicine, University of Melbourne, Melbourne, Australia.

Alex McLellan (A)

Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia; Baker IDI Heart and Diabetes Institute, Melbourne, Australia.

Liang-Han Ling (LH)

Baker IDI Heart and Diabetes Institute, Melbourne, Australia; Heart Centre, Alfred Hospital, Melbourne, Australia.

Joseph B Morton (JB)

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

Prashanthan Sanders (P)

Centre for Heart Rhythm Disorders, Royal Adelaide Hospital, Adelaide, Australia.

Peter M Kistler (PM)

Baker IDI Heart and Diabetes Institute, Melbourne, Australia; Heart Centre, Alfred Hospital, Melbourne, Australia.

Jonathan M Kalman (JM)

Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia; Department of Medicine, University of Melbourne, Melbourne, Australia. Electronic address: jon.kalman@mh.org.au.

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