Abstract
EDITORIAL article Front. Physiol., 25 November 2013Sec. Cardiac Electrophysiology Volume 4 - 2013 | https://doi.org/10.3389/fphys.2013.00339
Highlights
Sudden cardiac death refers to unexpected death attributable to a cardiac cause occurring within 1 h of the onset of symptoms (NICE, 2006)
Ion channel expression depends upon a sequence of processes beginning with DNA transcription into mRNA and its regulation by promoter sites
Gütter et al (2013) throw biophysical light on uncertainties in the relationship between genetic and functional properties: voltage-clamp investigations revealed that only one out of three mutant channels associated with clinical long QT syndrome type 3 (LQT3) and three out of six mutant channels associated with Brugada Syndrome (BrS) showed functional abnormalities in a series of N-terminal, human hNav1.5, mutations
Summary
Sudden cardiac death refers to unexpected death attributable to a cardiac cause occurring within 1 h of the onset of symptoms (NICE, 2006). Jagu et al (2013) outline and illustrate outcomes of genetic studies of biochemical processes underlying relationships between genetic background and protein expression whose alterations lead to arrhythmic tendency. Nielsen et al (2013) further explore uncertainties in relationships between genetic change and their functional consequences for Brugada Syndrome (BrS).
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