Characterization of the right ventricular substrate participating in postinfarction ventricular tachycardia.


Journal

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

Informations de publication

Date de publication:
10 2022
Historique:
received: 28 03 2021
revised: 24 02 2022
accepted: 27 02 2022
pubmed: 12 3 2022
medline: 5 10 2022
entrez: 11 3 2022
Statut: ppublish

Résumé

The right ventricle (RV) is uncommonly implicated in postinfarction ventricular tachycardia (VT). The prevalence and features of the RV substrate participating in postinfarction VT are undefined. The purpose of this study was to characterize critical right ventricular substrate (CRVS) involvement in patients with postinfarction VT. We retrospectively reviewed 1279 patients with postinfarction VT undergoing catheter ablation at our center from January 2000 through May 2020. Cases with CRVS defined by conclusive demonstration of participation in VT with activation, entrainment, and/or pacemapping during sinus rhythm were identified. CRVS was identified in 27 of 1279 patients (2.1%): age 65 ± 13 years, 96% male, median left ventricular (LV) ejection fraction 25%, and 93% with left bundle branch block (LBBB) morphology VT. CRVS was identified by RV activation and/or entrainment mapping (n = 19) or by the presence of low-voltage abnormal electrograms with excellent pacemap for the targeted VT and noninducibility after ablation (n = 8). VT termination during RV ablation occurred in 15 patients. After median follow-up of 20 months (interquartile range 9-53 months) and median of 2 procedures (interquartile range 1-3), 22 of 27 patients (80%) had no VT recurrence and 11 (41%) died. The RV contains critical substrate elements of postinfarction VT in at least 2.1% of cases. RV mapping should be considered in cases in which LV mapping fails to demonstrate adequate targets, particularly in patients with LBBB morphology VT.

Sections du résumé

BACKGROUND
The right ventricle (RV) is uncommonly implicated in postinfarction ventricular tachycardia (VT). The prevalence and features of the RV substrate participating in postinfarction VT are undefined.
OBJECTIVES
The purpose of this study was to characterize critical right ventricular substrate (CRVS) involvement in patients with postinfarction VT.
METHODS
We retrospectively reviewed 1279 patients with postinfarction VT undergoing catheter ablation at our center from January 2000 through May 2020. Cases with CRVS defined by conclusive demonstration of participation in VT with activation, entrainment, and/or pacemapping during sinus rhythm were identified.
RESULTS
CRVS was identified in 27 of 1279 patients (2.1%): age 65 ± 13 years, 96% male, median left ventricular (LV) ejection fraction 25%, and 93% with left bundle branch block (LBBB) morphology VT. CRVS was identified by RV activation and/or entrainment mapping (n = 19) or by the presence of low-voltage abnormal electrograms with excellent pacemap for the targeted VT and noninducibility after ablation (n = 8). VT termination during RV ablation occurred in 15 patients. After median follow-up of 20 months (interquartile range 9-53 months) and median of 2 procedures (interquartile range 1-3), 22 of 27 patients (80%) had no VT recurrence and 11 (41%) died.
CONCLUSION
The RV contains critical substrate elements of postinfarction VT in at least 2.1% of cases. RV mapping should be considered in cases in which LV mapping fails to demonstrate adequate targets, particularly in patients with LBBB morphology VT.

Identifiants

pubmed: 35276321
pii: S1547-5271(22)00213-2
doi: 10.1016/j.hrthm.2022.02.028
pii:
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1620-1628

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022. Published by Elsevier Inc.

Auteurs

Katie A Walsh (KA)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address: katie.walsh@pennmedicine.upenn.edu.

Jonathan M Daw (JM)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Aung Lin (A)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Gustavo Guandalini (G)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Matthew C Hyman (MC)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Ramanan Kumareswaran (R)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Jeffrey S Arkles (JS)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Robert D Schaller (RD)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Gregory E Supple (GE)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

David S Frankel (DS)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Saman Nazarian (S)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Michael P Riley (MP)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Fermin Garcia (F)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

David Lin (D)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Cory Tschabrunn (C)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Sanjay Dixit (S)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Andrew E Epstein (AE)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

David J Callans (DJ)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Francis E Marchlinski (FE)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Pasquale Santangeli (P)

Division of Cardiovascular Medicine, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

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