Electro-mechanical (dys-)function in long QT syndrome type 1.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
01 Jan 2019
Historique:
received: 13 03 2018
revised: 18 05 2018
accepted: 06 07 2018
pubmed: 19 7 2018
medline: 25 7 2019
entrez: 19 7 2018
Statut: ppublish

Résumé

Prolonged repolarization is the hallmark of long QT syndrome (LQTS), which is associated with subclinical mechanical dysfunction. We aimed at elucidating mechanical cardiac function in LQTS type 1 (loss of I Transgenic LQT1 and wild type (WT) rabbits (n = 12/10) were subjected to tissue phase mapping MRI, ECG, and epicardial AP recording. Protein and mRNA levels of ion channels and Ca At baseline, QT intervals were longer in LQT1 compared to WT rabbits, but baseline systolic and diastolic myocardial peak velocities were similar in LQT1 and WT. E-4031 prolonged QT more pronouncedly in LQT1. Additionally, E-4031 increased systolic and decreased diastolic peak velocities more markedly in LQT1 - unmasking systolic and diastolic LQT1-specific mechanical alterations. E-4031-induced alterations of diastolic peak velocities correlated with the extent of QT prolongation. While baseline mechanical function is normal in LQT1 despite a distinct QT prolongation, further prolongation of repolarization by I

Sections du résumé

BACKGROUND BACKGROUND
Prolonged repolarization is the hallmark of long QT syndrome (LQTS), which is associated with subclinical mechanical dysfunction. We aimed at elucidating mechanical cardiac function in LQTS type 1 (loss of I
METHODS METHODS
Transgenic LQT1 and wild type (WT) rabbits (n = 12/10) were subjected to tissue phase mapping MRI, ECG, and epicardial AP recording. Protein and mRNA levels of ion channels and Ca
RESULTS RESULTS
At baseline, QT intervals were longer in LQT1 compared to WT rabbits, but baseline systolic and diastolic myocardial peak velocities were similar in LQT1 and WT. E-4031 prolonged QT more pronouncedly in LQT1. Additionally, E-4031 increased systolic and decreased diastolic peak velocities more markedly in LQT1 - unmasking systolic and diastolic LQT1-specific mechanical alterations. E-4031-induced alterations of diastolic peak velocities correlated with the extent of QT prolongation.
CONCLUSION CONCLUSIONS
While baseline mechanical function is normal in LQT1 despite a distinct QT prolongation, further prolongation of repolarization by I

Identifiants

pubmed: 30017522
pii: S0167-5273(18)31662-0
doi: 10.1016/j.ijcard.2018.07.050
pii:
doi:

Substances chimiques

Anti-Arrhythmia Agents 0
Piperidines 0
Pyridines 0
E 4031 113558-89-7

Types de publication

Journal Article

Langues

eng

Pagination

144-151

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2018 Elsevier B.V. All rights reserved.

Auteurs

David Ziupa (D)

Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany; Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Marius Menza (M)

Faculty of Medicine, University of Freiburg, Freiburg, Germany; Department of Radiology, Medical Physics, University Medical Center Freiburg, Freiburg, Germany.

Susanne Koppermann (S)

Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany; Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Robin Moss (R)

Faculty of Medicine, University of Freiburg, Freiburg, Germany; Institute of Experimental Cardiovascular Medicine, Heart Center, University of Freiburg, Freiburg, Germany.

Julia Beck (J)

Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany; Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Gerlind Franke (G)

Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany; Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Stefanie Perez Feliz (S)

Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany; Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Michael Brunner (M)

Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Sonja Mayer (S)

Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany; Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Heiko Bugger (H)

Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany; Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Gideon Koren (G)

Cardiovascular Research Center, Division of Cardiology, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, RI, USA.

Manfred Zehender (M)

Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany; Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Bernd A Jung (BA)

Faculty of Medicine, University of Freiburg, Freiburg, Germany; Department of Radiology, Medical Physics, University Medical Center Freiburg, Freiburg, Germany.

Gunnar Seemann (G)

Faculty of Medicine, University of Freiburg, Freiburg, Germany; Institute of Experimental Cardiovascular Medicine, Heart Center, University of Freiburg, Freiburg, Germany.

Daniela Foell (D)

Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany; Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Christoph Bode (C)

Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany; Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Katja E Odening (KE)

Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany; Faculty of Medicine, University of Freiburg, Freiburg, Germany. Electronic address: katja.odening@universitaets-herzzentrum.de.

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Classifications MeSH