Atrial Fibrillation Substrate and Catheter Ablation Outcomes in MYBPC3- and MYH7-Mediated Hypertrophic Cardiomyopathy.

HCM ablation atrial fibrillation

Journal

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

Informations de publication

Date de publication:
07 May 2024
Historique:
received: 01 09 2023
revised: 26 02 2024
accepted: 16 03 2024
medline: 31 5 2024
pubmed: 31 5 2024
entrez: 31 5 2024
Statut: aheadofprint

Résumé

The effects of disease-causing MYBPC3 or MYH7 genetic variants on atrial myopathy, atrial fibrillation (AF) clinical course, and catheter ablation efficacy remain unclear. The aim of this study was to characterize the atrial substrate of patients with MYBPC3- or MYH7-mediated hypertrophic cardiomyopathy (HCM) and its impact on catheter ablation outcomes. A retrospective single-center study of patients with HCM who underwent genetic testing and catheter ablation for AF was performed. Patients with MYBPC3- or MYH7-mediated HCM formed the gene-positive cohort; those without disease-causative genetic variants formed the control cohort. High-density electroanatomical mapping was performed using a 3-dimensional mapping system, followed by radiofrequency ablation. Twelve patients were included in the gene-positive cohort (mean age 55.6 ± 9.9 years, 83% men, 50% MYBPC3, 50% MYH7, mean ejection fraction 59.3% ± 13.7%, mean left atrial [LA] volume index 51.7 ± 13.1 mL/m Patients with MYBPC3- or MYH7-mediated HCM undergoing AF ablation have appreciably more low-amplitude LA signals, suggestive of fibrosis. However, catheter ablation remains an effective rhythm-control strategy.

Sections du résumé

BACKGROUND BACKGROUND
The effects of disease-causing MYBPC3 or MYH7 genetic variants on atrial myopathy, atrial fibrillation (AF) clinical course, and catheter ablation efficacy remain unclear.
OBJECTIVES OBJECTIVE
The aim of this study was to characterize the atrial substrate of patients with MYBPC3- or MYH7-mediated hypertrophic cardiomyopathy (HCM) and its impact on catheter ablation outcomes.
METHODS METHODS
A retrospective single-center study of patients with HCM who underwent genetic testing and catheter ablation for AF was performed. Patients with MYBPC3- or MYH7-mediated HCM formed the gene-positive cohort; those without disease-causative genetic variants formed the control cohort. High-density electroanatomical mapping was performed using a 3-dimensional mapping system, followed by radiofrequency ablation.
RESULTS RESULTS
Twelve patients were included in the gene-positive cohort (mean age 55.6 ± 9.9 years, 83% men, 50% MYBPC3, 50% MYH7, mean ejection fraction 59.3% ± 13.7%, mean left atrial [LA] volume index 51.7 ± 13.1 mL/m
CONCLUSIONS CONCLUSIONS
Patients with MYBPC3- or MYH7-mediated HCM undergoing AF ablation have appreciably more low-amplitude LA signals, suggestive of fibrosis. However, catheter ablation remains an effective rhythm-control strategy.

Identifiants

pubmed: 38819352
pii: S2405-500X(24)00261-5
doi: 10.1016/j.jacep.2024.03.026
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Ikram U Haq (IU)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA. Electronic address: https://twitter.com/IkramHaqMD.

Nadia Akhiyat (N)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.

Nader Al-Shakarchi (N)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.

Konstantinos C Siontis (KC)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.

Siva K Mulpuru (SK)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.

Alan Sugrue (A)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.

John Giudicessi (J)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.

Paul A Friedman (PA)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.

Samuel J Asirvatham (SJ)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.

Ammar M Killu (AM)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA. Electronic address: killu.ammar@mayo.edu.

Classifications MeSH