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Citations to this article

Electrophysiological abnormalities and arrhythmias in alpha MHC mutant familial hypertrophic cardiomyopathy mice.
C I Berul, … , J G Seidman, M E Mendelsohn
C I Berul, … , J G Seidman, M E Mendelsohn
Published February 15, 1997
Citation Information: J Clin Invest. 1997;99(4):570-576. https://doi.org/10.1172/JCI119197.
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Electrophysiological abnormalities and arrhythmias in alpha MHC mutant familial hypertrophic cardiomyopathy mice.

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Abstract

A new mouse cardiac electrophysiology method was used to study mice harboring an alpha-myosin heavy chain Arg403Gln missense mutation (alpha-MHC403/+), which results in histological and hemodynamic abnormalities characteristic of familial hypertrophic cardiomyopathy (FHC) and sudden death of uncertain etiology during exercise. Wild-type animals had completely normal cardiac electrophysiology. In contrast, FHC mice demonstrated (a) electrocardiographic abnormalities including prolonged repolarization intervals and rightward axis; (b) electrophysiological abnormalities including heterogeneous ventricular conduction properties and prolonged sinus node recovery time; and (c) inducible ventricular ectopy. These data identify distinct electrophysiologic abnormalities in FHC mice with a specific alpha-myosin mutation, and also validate a novel method to explore in vivo the relationship between specific genotypes and their electrophysiologic phenotypes.

Authors

C I Berul, M E Christe, M J Aronovitz, C E Seidman, J G Seidman, M E Mendelsohn

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Total citations by year

Year: 2023 2020 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 2005 2004 2003 2002 2001 2000 1999 1998 1985 Total
Citations: 1 2 1 1 1 2 1 3 2 1 1 3 3 1 2 5 9 6 10 8 5 10 1 79
Citation information
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