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This editorial summarizes a collection of articles reviewing the genetic, biophysical, physiological, and modeling mechanisms underlying ventricular arrhythmias and sudden cardiac death.
This editorial introduces a collection of articles surveying genetic, biophysical, physiological, and modeling studies on the mechanisms and translational implications of ventricular arrhythmias and sudden cardiac death.
catecholaminergic polymorphic ventricular tachycardia Sudden cardiac death refers to unexpected death attributable to a cardiac cause occurring within 1 h of the onset of symp-toms (NICE, 2006). It often results from cardiac arrhythmias and is a major worldwide cause of morbidity and mortality. Arrhythmias account for 180,000 to 250,000 deaths per year in the United States and ∼70,000 deaths per year in the United Kingdom (NICE, 2006; Chugh et al., 2008). These commonly present as ventricular fibrillation often preceded by ventricu-lar tachycardia (Turakhia and Tseng, 2007). Cardiac arrhythmias most frequently result from underlying ischaemic heart disease (Behr et al., 2003). However, ∼4 % may arise from ion channel abnormalities (Tung et al., 1994; Martin et al., 2012) with their own implications for management (Martin et al., 2011). In all events, cardiac arrhythmias follow disruption of the normal cell
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Sabir et al. (2013) conducted an editorial in Sudden cardiac death and ventricular arrhythmias. This editorial summarizes a collection of articles reviewing the genetic, biophysical, physiological, and modeling mechanisms underlying ventricular arrhythmias and sudden cardiac death.
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