The precordial R' wave: A novel discriminator between cardiac sarcoidosis and arrhythmogenic right ventricular cardiomyopathy in patients presenting with ventricular tachycardia.


Journal

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

Informations de publication

Date de publication:
09 2021
Historique:
received: 16 02 2021
revised: 16 04 2021
accepted: 28 04 2021
pubmed: 7 5 2021
medline: 19 2 2022
entrez: 6 5 2021
Statut: ppublish

Résumé

Cardiac sarcoidosis (CS) with right ventricular (RV) involvement can mimic arrhythmogenic right ventricular cardiomyopathy (ARVC). Histopathological differences may result in disease-specific RV activation patterns detectable on the 12-lead electrocardiogram. Dominant subepicardial scar in ARVC leads to delayed activation of areas with reduced voltages, translating into terminal activation delay and occasionally (epsilon) waves with a small amplitude. Conversely, patchy transmural RV scar in CS may lead to conduction block and therefore late activated areas with preserved voltages reflected as preserved R' waves. The purpose of this study was to evaluate the distinct terminal activation patterns in precordial leads V Thirteen patients with CS affecting the RV and 23 patients with gene-positive ARVC referred for ventricular tachycardia ablation were retrospectively included in a multicenter approach. A non-ventricular-paced 12-lead surface electrocardiogram was analyzed for the presence and the surface area of the R' wave (any positive deflection from baseline after an S wave) in leads V An R' wave in leads V An easily applicable algorithm including PR prolongation and the surface area of the maximum R' wave in leads V

Sections du résumé

BACKGROUND
Cardiac sarcoidosis (CS) with right ventricular (RV) involvement can mimic arrhythmogenic right ventricular cardiomyopathy (ARVC). Histopathological differences may result in disease-specific RV activation patterns detectable on the 12-lead electrocardiogram. Dominant subepicardial scar in ARVC leads to delayed activation of areas with reduced voltages, translating into terminal activation delay and occasionally (epsilon) waves with a small amplitude. Conversely, patchy transmural RV scar in CS may lead to conduction block and therefore late activated areas with preserved voltages reflected as preserved R' waves.
OBJECTIVE
The purpose of this study was to evaluate the distinct terminal activation patterns in precordial leads V
METHODS
Thirteen patients with CS affecting the RV and 23 patients with gene-positive ARVC referred for ventricular tachycardia ablation were retrospectively included in a multicenter approach. A non-ventricular-paced 12-lead surface electrocardiogram was analyzed for the presence and the surface area of the R' wave (any positive deflection from baseline after an S wave) in leads V
RESULTS
An R' wave in leads V
CONCLUSION
An easily applicable algorithm including PR prolongation and the surface area of the maximum R' wave in leads V

Identifiants

pubmed: 33957319
pii: S1547-5271(21)00411-2
doi: 10.1016/j.hrthm.2021.04.032
pii:
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1539-1547

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

Copyright © 2021 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.

Auteurs

Jarieke C Hoogendoorn (JC)

Department of Cardiology, Willem Einthoven Center of Arrhythmia Research and Management, Leiden University Medical Center, Leiden, The Netherlands.

Jeroen Venlet (J)

Department of Cardiology, Willem Einthoven Center of Arrhythmia Research and Management, Leiden University Medical Center, Leiden, The Netherlands.

Yannick N J Out (YNJ)

Department of Cardiology, Willem Einthoven Center of Arrhythmia Research and Management, Leiden University Medical Center, Leiden, The Netherlands.

Sumche Man (S)

Department of Cardiology, Willem Einthoven Center of Arrhythmia Research and Management, Leiden University Medical Center, Leiden, The Netherlands.

Saurabh Kumar (S)

Department of Cardiology, Brigham and Women's Hospital, Boston, Massachusetts.

Marek Sramko (M)

Department of Cardiology, Institute of Clinical and Experimental Medicine, Prague, The Czech Republic.

Dirk G Dechering (DG)

Department of Cardiology II (Electrophysiology), University Hospital Münster, Münster, Germany.

Ikutaro Nakajima (I)

Department of Cardiology, Vanderbilt University Medical Center, Nashville, Tennessee.

Konstantinos C Siontis (KC)

Department of Cardiology, University of Michigan, Ann Arbor, Michigan; Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota.

Masaya Watanabe (M)

Department of Cardiology, Hokkaido University Hospital, Hokkaido, Japan.

Yoshinori Nakamura (Y)

Department of Cardiology, Willem Einthoven Center of Arrhythmia Research and Management, Leiden University Medical Center, Leiden, The Netherlands.

Usha B Tedrow (UB)

Department of Cardiology, Brigham and Women's Hospital, Boston, Massachusetts.

Frank Bogun (F)

Department of Cardiology, University of Michigan, Ann Arbor, Michigan.

Lars Eckardt (L)

Department of Cardiology II (Electrophysiology), University Hospital Münster, Münster, Germany.

Petr Peichl (P)

Department of Cardiology, Institute of Clinical and Experimental Medicine, Prague, The Czech Republic.

William G Stevenson (WG)

Department of Cardiology, Vanderbilt University Medical Center, Nashville, Tennessee.

Katja Zeppenfeld (K)

Department of Cardiology, Willem Einthoven Center of Arrhythmia Research and Management, Leiden University Medical Center, Leiden, The Netherlands. Electronic address: k.zeppenfeld@lumc.nl.

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