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SCN5A gene mutations and the risk of ventricular fibrillation and syncope in Brugada syndrome patients: A meta‐analysis

Mutations in the gene encoding the main cardiac sodium channel (SCN5A) are the commonest genetic cause of Brugada syndrome (BrS). However, the effect of SCN5A mutations on the outcomes of ventricular fibrillation (VF) and syncope remains uncertain. To clarify this relationship, a meta‐analysis was p...

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Autores principales: Raharjo, Sunu Budhi, Maulana, Rido, Maghfirah, Irma, Alzahra, Fatimah, Putrinarita, Agnes Dinar, Hanafy, Dicky A., Yuniadi, Yoga
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6174414/
https://www.ncbi.nlm.nih.gov/pubmed/30327691
http://dx.doi.org/10.1002/joa3.12097
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author Raharjo, Sunu Budhi
Maulana, Rido
Maghfirah, Irma
Alzahra, Fatimah
Putrinarita, Agnes Dinar
Hanafy, Dicky A.
Yuniadi, Yoga
author_facet Raharjo, Sunu Budhi
Maulana, Rido
Maghfirah, Irma
Alzahra, Fatimah
Putrinarita, Agnes Dinar
Hanafy, Dicky A.
Yuniadi, Yoga
author_sort Raharjo, Sunu Budhi
collection PubMed
description Mutations in the gene encoding the main cardiac sodium channel (SCN5A) are the commonest genetic cause of Brugada syndrome (BrS). However, the effect of SCN5A mutations on the outcomes of ventricular fibrillation (VF) and syncope remains uncertain. To clarify this relationship, a meta‐analysis was performed. A comprehensive search was conducted to identify all eligible studies from PubMed, MEDLINE, EBSCO, ProQuest, Science Direct, Clinical Key, and Cochrane database for cohort studies of BrS populations that had been systematically tested for SCN5A mutations. We did meta‐analysis to see the relationship between SCN5A mutations and the occurrence of VF and/or syncope using RevMan 5.3. Five clinical studies met our criteria and included a total of 665 BrS patients. These studies included 45 patients with VF and 178 patients with syncope. We found that in BrS patients with SCN5A mutations the rate of VF event was 30.7% while in patients without mutations was 28.5% (Risk Ratio [RR] = 1.11, [95% CI: 0.61, 2.00], P = 0.73, I (2) = 0%). The occurrence of syncope events was 35.9% in patients with SCN5A mutations and 34.5% in patients without mutations (RR = 1.12, [95% CI: 0.87, 1.45], P = 0.37, I (2) = 39%). Furthermore, the occurrence of combined VF and syncope events were similar between the 2 groups (RR = 1.12, [95% CI: 0.89, 1.42], P = 0.34, I (2) = 11%). BrS patients with SCN5A mutations exhibit a similar risk of future occurence of VF and/or syncope as compared to those without SCN5A mutations.
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spelling pubmed-61744142018-10-16 SCN5A gene mutations and the risk of ventricular fibrillation and syncope in Brugada syndrome patients: A meta‐analysis Raharjo, Sunu Budhi Maulana, Rido Maghfirah, Irma Alzahra, Fatimah Putrinarita, Agnes Dinar Hanafy, Dicky A. Yuniadi, Yoga J Arrhythm Clinical Reviews Mutations in the gene encoding the main cardiac sodium channel (SCN5A) are the commonest genetic cause of Brugada syndrome (BrS). However, the effect of SCN5A mutations on the outcomes of ventricular fibrillation (VF) and syncope remains uncertain. To clarify this relationship, a meta‐analysis was performed. A comprehensive search was conducted to identify all eligible studies from PubMed, MEDLINE, EBSCO, ProQuest, Science Direct, Clinical Key, and Cochrane database for cohort studies of BrS populations that had been systematically tested for SCN5A mutations. We did meta‐analysis to see the relationship between SCN5A mutations and the occurrence of VF and/or syncope using RevMan 5.3. Five clinical studies met our criteria and included a total of 665 BrS patients. These studies included 45 patients with VF and 178 patients with syncope. We found that in BrS patients with SCN5A mutations the rate of VF event was 30.7% while in patients without mutations was 28.5% (Risk Ratio [RR] = 1.11, [95% CI: 0.61, 2.00], P = 0.73, I (2) = 0%). The occurrence of syncope events was 35.9% in patients with SCN5A mutations and 34.5% in patients without mutations (RR = 1.12, [95% CI: 0.87, 1.45], P = 0.37, I (2) = 39%). Furthermore, the occurrence of combined VF and syncope events were similar between the 2 groups (RR = 1.12, [95% CI: 0.89, 1.42], P = 0.34, I (2) = 11%). BrS patients with SCN5A mutations exhibit a similar risk of future occurence of VF and/or syncope as compared to those without SCN5A mutations. John Wiley and Sons Inc. 2018-07-26 /pmc/articles/PMC6174414/ /pubmed/30327691 http://dx.doi.org/10.1002/joa3.12097 Text en © 2018 The Authors. Journal of Arrhythmia published by John Wiley & Sons Australia, Ltd on behalf of the Japanese Heart Rhythm Society. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Clinical Reviews
Raharjo, Sunu Budhi
Maulana, Rido
Maghfirah, Irma
Alzahra, Fatimah
Putrinarita, Agnes Dinar
Hanafy, Dicky A.
Yuniadi, Yoga
SCN5A gene mutations and the risk of ventricular fibrillation and syncope in Brugada syndrome patients: A meta‐analysis
title SCN5A gene mutations and the risk of ventricular fibrillation and syncope in Brugada syndrome patients: A meta‐analysis
title_full SCN5A gene mutations and the risk of ventricular fibrillation and syncope in Brugada syndrome patients: A meta‐analysis
title_fullStr SCN5A gene mutations and the risk of ventricular fibrillation and syncope in Brugada syndrome patients: A meta‐analysis
title_full_unstemmed SCN5A gene mutations and the risk of ventricular fibrillation and syncope in Brugada syndrome patients: A meta‐analysis
title_short SCN5A gene mutations and the risk of ventricular fibrillation and syncope in Brugada syndrome patients: A meta‐analysis
title_sort scn5a gene mutations and the risk of ventricular fibrillation and syncope in brugada syndrome patients: a meta‐analysis
topic Clinical Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6174414/
https://www.ncbi.nlm.nih.gov/pubmed/30327691
http://dx.doi.org/10.1002/joa3.12097
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