A mutation in the atrial-specific myosin light chain gene (MYL4) causes familial atrial fibrillation

Nathan Orr, Rima Arnaout, Lorne J. Gula, Danna A. Spears, Peter Leong-Sit, Qiuju Li, Wadea Tarhuni, Sven Reischauer, Vijay S. Chauhan, Matthew Borkovich, Shaheen Uppal, Arnon Adler, Shaun R. Coughlin, Didier Y. R. Stainier and Michael H. Gollob ()
Additional contact information
Nathan Orr: Toronto General Research Institute, University Health Network
Rima Arnaout: University of California San Francisco
Lorne J. Gula: University Hospital, Western University
Danna A. Spears: Toronto General Hospital, University Health Network
Peter Leong-Sit: University Hospital, Western University
Qiuju Li: Toronto General Research Institute, University Health Network
Wadea Tarhuni: University Hospital, Western University
Sven Reischauer: University of California San Francisco
Vijay S. Chauhan: Toronto General Hospital, University Health Network
Matthew Borkovich: Toronto General Hospital, University Health Network
Shaheen Uppal: Toronto General Hospital, University Health Network
Arnon Adler: Toronto General Hospital, University Health Network
Shaun R. Coughlin: University of California San Francisco
Didier Y. R. Stainier: University of California San Francisco
Michael H. Gollob: Toronto General Research Institute, University Health Network

Nature Communications, 2016, vol. 7, issue 1, 1-8

Abstract: Abstract Atrial fibrillation (AF), the most common arrhythmia, is a growing epidemic with substantial morbidity and economic burden. Mechanisms underlying vulnerability to AF remain poorly understood, which contributes to the current lack of highly effective therapies. Recognizing mechanistic subtypes of AF may guide an individualized approach to patient management. Here, we describe a family with a previously unreported syndrome characterized by early-onset AF (age

Date: 2016
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DOI: 10.1038/ncomms11303

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