Left-axis deviation in patients with nonischemic heart failure and left bundle branch block is a purely electrical phenomenon.


Journal

Heart rhythm
ISSN: 1556-3871
Titre abrégé: Heart Rhythm
Pays: United States
ID NLM: 101200317

Informations de publication

Date de publication:
08 2021
Historique:
received: 18 12 2020
revised: 19 03 2021
accepted: 30 03 2021
pubmed: 9 4 2021
medline: 12 2 2022
entrez: 8 4 2021
Statut: ppublish

Résumé

Possible mechanisms of left-axis deviation (LAD) in the setting of left bundle branch block (LBBB) include differences in cardiac electrophysiology, structure, or anatomic axis. The purpose of this study was to clarify the mechanism(s) responsible for LAD in patients with LBBB. Twenty-nine patients with nonischemic cardiomyopathies and LBBB underwent noninvasive electrocardiographic imaging (ECGi), cardiac computed tomography, and magnetic resonance imaging in order to define ventricular electrical activation, characterize cardiac structure, and determine the cardiac anatomic axis. Sixteen patients had a normal QRS axis (NA) (mean axis 8° ± 23°), whereas 13 patients had LAD (mean axis -48° ± 13°; P <.001). Total activation times were longer in the LAD group (112 ± 25 ms vs 91 ± 14 ms; P = .01) due to delayed activation of the basal anterolateral region (107 ± 10 ms vs 81 ± 17 ms; P <.001). Left ventricular (LV) activation in patients with LAD was from apex to base, in contrast to a circumferential pattern of activation in patients with NA. Apex-to-base delay was longer in the LA group (95 ± 13 ms vs 64 ± 21 ms; P <.001) and correlated with QRS frontal axis (R LAD in LBBB appears to be due to electrophysiological abnormalities rather than structural factors or cardiac anatomic axis.

Sections du résumé

BACKGROUND
Possible mechanisms of left-axis deviation (LAD) in the setting of left bundle branch block (LBBB) include differences in cardiac electrophysiology, structure, or anatomic axis.
OBJECTIVE
The purpose of this study was to clarify the mechanism(s) responsible for LAD in patients with LBBB.
METHODS
Twenty-nine patients with nonischemic cardiomyopathies and LBBB underwent noninvasive electrocardiographic imaging (ECGi), cardiac computed tomography, and magnetic resonance imaging in order to define ventricular electrical activation, characterize cardiac structure, and determine the cardiac anatomic axis.
RESULTS
Sixteen patients had a normal QRS axis (NA) (mean axis 8° ± 23°), whereas 13 patients had LAD (mean axis -48° ± 13°; P <.001). Total activation times were longer in the LAD group (112 ± 25 ms vs 91 ± 14 ms; P = .01) due to delayed activation of the basal anterolateral region (107 ± 10 ms vs 81 ± 17 ms; P <.001). Left ventricular (LV) activation in patients with LAD was from apex to base, in contrast to a circumferential pattern of activation in patients with NA. Apex-to-base delay was longer in the LA group (95 ± 13 ms vs 64 ± 21 ms; P <.001) and correlated with QRS frontal axis (R
CONCLUSION
LAD in LBBB appears to be due to electrophysiological abnormalities rather than structural factors or cardiac anatomic axis.

Identifiants

pubmed: 33831543
pii: S1547-5271(21)00316-7
doi: 10.1016/j.hrthm.2021.03.042
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1352-1360

Informations de copyright

Copyright © 2021 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.

Auteurs

Saer Abu-Alrub (S)

Cardio-Thoracic Unit, Bordeaux University Hospital (CHU), Pessac-Bordeaux, France; Cardiology Department, CHU Clermont-Ferrand, Clermont-Ferrand, France. Electronic address: saer0330@gmail.com.

Marc Strik (M)

Cardio-Thoracic Unit, Bordeaux University Hospital (CHU), Pessac-Bordeaux, France; IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, Pessac-Bordeaux, France.

Peter Huntjens (P)

Division of Cardiology, Washington University, St. Louis, Missouri.

F Daniel Ramirez (FD)

Cardio-Thoracic Unit, Bordeaux University Hospital (CHU), Pessac-Bordeaux, France; IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, Pessac-Bordeaux, France.

Mark Potse (M)

IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, Pessac-Bordeaux, France.

Hubert Cochet (H)

Cardio-Thoracic Unit, Bordeaux University Hospital (CHU), Pessac-Bordeaux, France; IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, Pessac-Bordeaux, France.

Hugo Marchand (H)

Cardio-Thoracic Unit, Bordeaux University Hospital (CHU), Pessac-Bordeaux, France.

Samuel Buliard (S)

Cardio-Thoracic Unit, Bordeaux University Hospital (CHU), Pessac-Bordeaux, France.

Romain Eschalier (R)

Cardiology Department, CHU Clermont-Ferrand, Clermont-Ferrand, France.

Michel Haïssaguerre (M)

Cardio-Thoracic Unit, Bordeaux University Hospital (CHU), Pessac-Bordeaux, France; IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, Pessac-Bordeaux, France.

Pierre Bordachar (P)

Cardio-Thoracic Unit, Bordeaux University Hospital (CHU), Pessac-Bordeaux, France; IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, Pessac-Bordeaux, France.

Sylvain Ploux (S)

Cardio-Thoracic Unit, Bordeaux University Hospital (CHU), Pessac-Bordeaux, France; IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, Pessac-Bordeaux, France.

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