CPVT and Complete Atrio-Ventricular Block: The Flipside of the Same Coin

Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) is a rare electrical genetic disease characterized by ventricular polymorphic tachycardia and/or bidirectional ventricular tachycardia induced by the release of catecholamines caused by intense physical or emotional stress in structurally...

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Detalles Bibliográficos
Autores principales: Petrungaro, Mattia, Scarà, Antonio, Borrelli, Alessio, Sciarra, Luigi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Communication
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10054025/
https://www.ncbi.nlm.nih.gov/pubmed/36975861
http://dx.doi.org/10.3390/jcdd10030097
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author Petrungaro, Mattia
Scarà, Antonio
Borrelli, Alessio
Sciarra, Luigi
author_facet Petrungaro, Mattia
Scarà, Antonio
Borrelli, Alessio
Sciarra, Luigi
author_sort Petrungaro, Mattia
collection PubMed
description Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) is a rare electrical genetic disease characterized by ventricular polymorphic tachycardia and/or bidirectional ventricular tachycardia induced by the release of catecholamines caused by intense physical or emotional stress in structurally normal hearts. Mostly, it is caused by mutations in genes that are involved in calcium homeostasis, in particular in the gene encoding for cardiac ryanodine receptor (RyR2). Our observation is the first description of familial CPVT caused by mutation of the RyR2 gene, linked to the complete AV block.
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spelling pubmed-100540252023-03-30 CPVT and Complete Atrio-Ventricular Block: The Flipside of the Same Coin Petrungaro, Mattia Scarà, Antonio Borrelli, Alessio Sciarra, Luigi J Cardiovasc Dev Dis Communication Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) is a rare electrical genetic disease characterized by ventricular polymorphic tachycardia and/or bidirectional ventricular tachycardia induced by the release of catecholamines caused by intense physical or emotional stress in structurally normal hearts. Mostly, it is caused by mutations in genes that are involved in calcium homeostasis, in particular in the gene encoding for cardiac ryanodine receptor (RyR2). Our observation is the first description of familial CPVT caused by mutation of the RyR2 gene, linked to the complete AV block. MDPI 2023-02-23 /pmc/articles/PMC10054025/ /pubmed/36975861 http://dx.doi.org/10.3390/jcdd10030097 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Communication
Petrungaro, Mattia
Scarà, Antonio
Borrelli, Alessio
Sciarra, Luigi
CPVT and Complete Atrio-Ventricular Block: The Flipside of the Same Coin
title CPVT and Complete Atrio-Ventricular Block: The Flipside of the Same Coin
title_full CPVT and Complete Atrio-Ventricular Block: The Flipside of the Same Coin
title_fullStr CPVT and Complete Atrio-Ventricular Block: The Flipside of the Same Coin
title_full_unstemmed CPVT and Complete Atrio-Ventricular Block: The Flipside of the Same Coin
title_short CPVT and Complete Atrio-Ventricular Block: The Flipside of the Same Coin
title_sort cpvt and complete atrio-ventricular block: the flipside of the same coin
topic Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10054025/
https://www.ncbi.nlm.nih.gov/pubmed/36975861
http://dx.doi.org/10.3390/jcdd10030097
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