Predictors of New-Onset Atrial Tachyarrhythmias After Transcatheter Atrial Septal Defect Closure in Adults.


Journal

Heart, lung & circulation
ISSN: 1444-2892
Titre abrégé: Heart Lung Circ
Pays: Australia
ID NLM: 100963739

Informations de publication

Date de publication:
Sep 2021
Historique:
received: 27 11 2020
revised: 03 02 2021
accepted: 27 02 2021
pubmed: 18 4 2021
medline: 30 9 2021
entrez: 17 4 2021
Statut: ppublish

Résumé

New-onset atrial tachyarrhythmia (ATA) often develops after atrial septal defect (ASD) closure. Its development raises some potential concerns such as stroke and bleeding complications caused by anticoagulant therapy and limited access to the left atrium for catheter ablation. Although it is essential to identify the risk factors of new-onset ATA, few studies have examined these factors. This study investigated unknown risk factors for the development of new-onset ATA after transcatheter ASD closure in patients without a history of ATA. A total of 238 patients without a history of ATA, aged ≥18 years and who underwent transcatheter ASD closure at the current hospital were reviewed. Patient characteristics were compared between the groups with and without new-onset ATA. The factors associated with new-onset ATA were examined using univariate and multivariable analyses. Thirteen (13) (5.5%) patients experienced ATA during follow-up (mean, 21±14 months). Compared with patients without new-onset ATA, patients with new-onset ATA were older (48±18 vs 66±11 years; p<0.001) and had high brain natriuretic peptide (BNP) levels (36±36 vs 177±306 pg/mL; p<0.001). On multivariable analysis, BNP ≥40 pg/mL before ASD closure was associated with new-onset ATA after adjusting for age (OR, 4.91; 95% CI, 1.22-19.8; p=0.025). Patients with BNP levels >40 pg/mL before transcatheter ASD closure may have a higher risk of developing new-onset ATA.

Sections du résumé

BACKGROUND BACKGROUND
New-onset atrial tachyarrhythmia (ATA) often develops after atrial septal defect (ASD) closure. Its development raises some potential concerns such as stroke and bleeding complications caused by anticoagulant therapy and limited access to the left atrium for catheter ablation. Although it is essential to identify the risk factors of new-onset ATA, few studies have examined these factors. This study investigated unknown risk factors for the development of new-onset ATA after transcatheter ASD closure in patients without a history of ATA.
METHODS METHODS
A total of 238 patients without a history of ATA, aged ≥18 years and who underwent transcatheter ASD closure at the current hospital were reviewed. Patient characteristics were compared between the groups with and without new-onset ATA. The factors associated with new-onset ATA were examined using univariate and multivariable analyses.
RESULTS RESULTS
Thirteen (13) (5.5%) patients experienced ATA during follow-up (mean, 21±14 months). Compared with patients without new-onset ATA, patients with new-onset ATA were older (48±18 vs 66±11 years; p<0.001) and had high brain natriuretic peptide (BNP) levels (36±36 vs 177±306 pg/mL; p<0.001). On multivariable analysis, BNP ≥40 pg/mL before ASD closure was associated with new-onset ATA after adjusting for age (OR, 4.91; 95% CI, 1.22-19.8; p=0.025).
CONCLUSION CONCLUSIONS
Patients with BNP levels >40 pg/mL before transcatheter ASD closure may have a higher risk of developing new-onset ATA.

Identifiants

pubmed: 33863668
pii: S1443-9506(21)00106-2
doi: 10.1016/j.hlc.2021.02.018
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1406-1413

Informations de copyright

Copyright © 2021 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.

Auteurs

Kotaro Miura (K)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Mai Kimura (M)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Atsushi Anzai (A)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Takahide Arai (T)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Takashi Kawakami (T)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Shinsuke Yuasa (S)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Kentaro Hayashida (K)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Jin Endo (J)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Hikaru Tsuruta (H)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Yuji Itabashi (Y)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Akio Kawamura (A)

Department of Cardiovascular Medicine, International University of Health and Welfare, Narita, Japan.

Keiichi Fukuda (K)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Hideaki Kanazawa (H)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan. Electronic address: kanazawa@a5.keio.jp.

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