Ischemic ventricular tachycardia from below the posteromedial papillary muscle, a particular entity: Substrate characterization and challenges for catheter ablation.


Journal

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

Informations de publication

Date de publication:
08 2019
Historique:
received: 04 01 2019
pubmed: 16 5 2019
medline: 26 11 2020
entrez: 16 5 2019
Statut: ppublish

Résumé

In patients with ischemic ventricular tachycardia (VT), substrate may be "protected" by the posteromedial papillary muscle (PMPM), explaining failure of endocardial-only ablation. We sought to characterize the arrhythmogenic substrate and ablation approach in patients with ischemic VT mapped to the inferior left ventricle in which endocardial ablation failed because of inaccessible substrate underlying the PMPM. We included 10 patients with recurrent ischemic VT, evidence of inferior scar, and failed endocardial ablation. In all patients, epicardial mapping was performed via a percutaneous (n = 9) or surgical (n = 1) approach, and VT elimination was achieved by ablation opposite to the PMPM. Clinical characteristics, electrocardiographic characteristics, and procedural data were analyzed. In all patients, intracardiac echocardiography showed hyperechoic scar below the PMPM, and 5 exhibited a pattern characterized by subendocardial basal scar that became intramural and epicardial at distal segments. In 4 patients, VT remained inducible despite endocardial scar isolation, manifested by the absence of electrograms, dissociated potentials, and/or exit block. Eleven inducible VTs were mapped to the epicardium underlying the PMPM: 8 had a right bundle branch block configuration with variable transition, while 3 exhibited left bundle branch block with negative concordance. An inferior QS pattern was present in 10 of 11 VTs. Noninducibility was achieved in 8 patients, and 7 patients remained arrhythmia-free after a mean follow-up of 27 ± 23 months. In patients with inferior ischemic scar, VT may arise from the area underneath the PMPM, limiting endocardial ablation. Intracardiac echocardiography accurately defines the substrate distribution, and an epicardial approach may eliminate VT. A pattern of "basal-endocardial/apical-epicardial" ischemic involvement is described.

Sections du résumé

BACKGROUND
In patients with ischemic ventricular tachycardia (VT), substrate may be "protected" by the posteromedial papillary muscle (PMPM), explaining failure of endocardial-only ablation.
OBJECTIVE
We sought to characterize the arrhythmogenic substrate and ablation approach in patients with ischemic VT mapped to the inferior left ventricle in which endocardial ablation failed because of inaccessible substrate underlying the PMPM.
METHODS
We included 10 patients with recurrent ischemic VT, evidence of inferior scar, and failed endocardial ablation. In all patients, epicardial mapping was performed via a percutaneous (n = 9) or surgical (n = 1) approach, and VT elimination was achieved by ablation opposite to the PMPM. Clinical characteristics, electrocardiographic characteristics, and procedural data were analyzed.
RESULTS
In all patients, intracardiac echocardiography showed hyperechoic scar below the PMPM, and 5 exhibited a pattern characterized by subendocardial basal scar that became intramural and epicardial at distal segments. In 4 patients, VT remained inducible despite endocardial scar isolation, manifested by the absence of electrograms, dissociated potentials, and/or exit block. Eleven inducible VTs were mapped to the epicardium underlying the PMPM: 8 had a right bundle branch block configuration with variable transition, while 3 exhibited left bundle branch block with negative concordance. An inferior QS pattern was present in 10 of 11 VTs. Noninducibility was achieved in 8 patients, and 7 patients remained arrhythmia-free after a mean follow-up of 27 ± 23 months.
CONCLUSION
In patients with inferior ischemic scar, VT may arise from the area underneath the PMPM, limiting endocardial ablation. Intracardiac echocardiography accurately defines the substrate distribution, and an epicardial approach may eliminate VT. A pattern of "basal-endocardial/apical-epicardial" ischemic involvement is described.

Identifiants

pubmed: 31085181
pii: S1547-5271(19)30138-9
doi: 10.1016/j.hrthm.2019.02.016
pii:
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1174-1181

Informations de copyright

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

Auteurs

Andres Enriquez (A)

Division of Cardiology, Queen's University, Kingston, Ontario, Canada; Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

David Briceno (D)

Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Carlos Tapias (C)

Cardioinfantil Foundation, Bogota, Colombia.

Yasuhiro Shirai (Y)

Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Daniele Muser (D)

Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Jackson Liang (J)

Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Tatsuya Hayashi (T)

Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Pasquale Santangeli (P)

Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

David S Frankel (DS)

Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Gregory E Supple (GE)

Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Robert D Schaller (RD)

Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Jeffrey Arkles (J)

Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Diego Rodriguez (D)

Cardioinfantil Foundation, Bogota, Colombia.

David J Callans (DJ)

Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Francis E Marchlinski (FE)

Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

Luis Saenz (L)

Cardioinfantil Foundation, Bogota, Colombia.

Fermin C Garcia (FC)

Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address: Fermin.Garcia@uphs.upenn.edu.

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Classifications MeSH