Clinical and electrophysiological characteristics of idiopathic ventricular arrhythmias originating from the slow pathway region.


Journal

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

Informations de publication

Date de publication:
09 2019
Historique:
received: 21 04 2019
pubmed: 22 6 2019
medline: 18 11 2020
entrez: 22 6 2019
Statut: ppublish

Résumé

The slow pathway region (SPR) is commonly targeted during ablation of atrioventricular nodal reentrant tachycardia. However, its role in idiopathic ventricular arrhythmias (IVAs) remains unknown. The purpose of this study was to describe the electrocardiographic and electrophysiological characteristics of IVAs that were successfully ablated from the SPR. Medical records of consecutive patients undergoing ablation of IVAs in the para-Hisian region between 2010 and 2018 were reviewed to identify subjects whose ventricular arrhythmias were targeted from the SPR. Among 63 patients with para-Hisian IVAs undergoing ablation, the SPR was targeted in 12 (20%; mean age 64 ± 7 years; 9 men). All patients presented with ventricular premature depolarizations manifesting left bundle branch block morphology with variable precordial transition (leads V The SPR can be a source of IVAs, which can be safely and successfully ablated in most cases using radiofrequency energy. IVAs arising from this location manifest unique electrocardiographic features.

Sections du résumé

BACKGROUND
The slow pathway region (SPR) is commonly targeted during ablation of atrioventricular nodal reentrant tachycardia. However, its role in idiopathic ventricular arrhythmias (IVAs) remains unknown.
OBJECTIVE
The purpose of this study was to describe the electrocardiographic and electrophysiological characteristics of IVAs that were successfully ablated from the SPR.
METHODS
Medical records of consecutive patients undergoing ablation of IVAs in the para-Hisian region between 2010 and 2018 were reviewed to identify subjects whose ventricular arrhythmias were targeted from the SPR.
RESULTS
Among 63 patients with para-Hisian IVAs undergoing ablation, the SPR was targeted in 12 (20%; mean age 64 ± 7 years; 9 men). All patients presented with ventricular premature depolarizations manifesting left bundle branch block morphology with variable precordial transition (leads V
CONCLUSION
The SPR can be a source of IVAs, which can be safely and successfully ablated in most cases using radiofrequency energy. IVAs arising from this location manifest unique electrocardiographic features.

Identifiants

pubmed: 31226487
pii: S1547-5271(19)30570-3
doi: 10.1016/j.hrthm.2019.06.013
pii:
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1421-1428

Informations de copyright

Copyright © 2019 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.

Auteurs

David F Briceño (DF)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Jackson J Liang (JJ)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Yasuhiro Shirai (Y)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Timothy M Markman (TM)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Andres Enriquez (A)

Heart Rhythm Service, Queen's University, Kingston, Ontario, Canada.

Aung Lin (A)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Pasquale Santangeli (P)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Michael P Riley (MP)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Robert D Schaller (RD)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Saman Nazarian (S)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

David Lin (D)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Ramanan Kumareswaram (R)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Jeffery S Arkles (JS)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Mathew C Hyman (MC)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Gregory E Supple (GE)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

David S Frankel (DS)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Fermin C Garcia (FC)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

David J Callans (DJ)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Francis E Marchlinski (FE)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Sanjay Dixit (S)

Division of Cardiology, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address: sanjay.dixit@pennmedicine.upenn.edu.

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