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Familial atrial rapid fibrillation associated with double mutations of SCN5A and KCNQ1

Part of: Electrophysiology

Published online by Cambridge University Press:  26 February 2021

Miwa Kanai ,
Keiko Toyohara Open the ORCID record for Keiko Toyohara [Opens in a new window]  and
Morio Shoda Open the ORCID record for Morio Shoda [Opens in a new window]
Miwa Kanai
Affiliation:
Department of Cardiology, Tokyo Women’s Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, Japan
Keiko Toyohara
Affiliation:
Department of Pediatric Cardiology, Tokyo Women’s Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, Japan
Morio Shoda*
Affiliation:
Department of Cardiology, Tokyo Women’s Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, Japan Clinical Research Division for Heart Rhythm Management, Department of Cardiology, Tokyo Women’s Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, Japan
*
Author for correspondence: Morio Shoda, Department of Cardiology, Tokyo Women’s Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo162-8666, Japan. Tel: +81-3-3353-8111. E-mail: [email protected]
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Abstract

Familial atrial fibrillation is inherited and sporadically occurs in the paediatric population. Generally, fibrillated wavelets are reported at a frequency of approximately 6 Hz. Herein, we report a familial case presenting rapidly fibrillated wavelets at frequencies of approximately 12 to 30 Hz associated with KCNQ1 and SCN5A mutations.

Keywords

Familial atrial fibrillationKCNQ1 mutationSCN5A mutation
Type
Brief Report
Information
Cardiology in the Young , Volume 31 , Issue 8 , August 2021 , pp. 1356 - 1358
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Copyright
© The Author(s), 2021. Published by Cambridge University Press

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References

Lubitz, SA, Yin, X, Fontes, JD, et al. Association between familial atrial fibrillation and risk of new-onset atrial fibrillation. JAMA 2010; 304: 2263–2269.10.1001/jama.2010.1690CrossRefGoogle ScholarPubMed
Chen, YH, Xu, SJ, Bendahhou, S, et al. KCNQ1 gain-of-function mutation in familial atrial fibrillation. Science 2003; 299: 251–254.10.1126/science.1077771CrossRefGoogle ScholarPubMed
Hong, K, Piper, DR, Diaz-Valdecantos, A, et al. De novo KCNQ1 mutation responsible for atrial fibrillation and short QT syndrome in utero. Cardiovasc Res 2005; 68: 433–440.CrossRefGoogle ScholarPubMed
McNair, WP, Ku, L, Taylor, MR, et al. SCN5A mutation associated with dilated cardiomyopathy, conduction disorder, and arrhythmia. Circulation 2004; 110: 2163–2167.CrossRefGoogle ScholarPubMed
Makiyama, T, Akao, M, Shizuta, S, et al. A novel SCN5A gain-of-function mutation M1875T associated with familial atrial fibrillation. J Am Coll Cardiol 2008; 52: 1326–1334.CrossRefGoogle ScholarPubMed
Wilde, AAM, Amin, AS Clinical spectrum of SCN5A mutations: long QT syndrome, Brugada syndrome, and cardiomyopathy. JACC Clin Electrophysiol 2018; 4: 569–579.CrossRefGoogle ScholarPubMed
Vatta, M, Dumaine, R, Varghese, G, et al. Genetic and biophysical basis of sudden unexplained nocturnal death syndrome (SUNDS), a disease allelic to Brugada syndrome. Hum Mol Genet 2002; 11: 337–345.CrossRefGoogle Scholar