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See Latest ArticlesInherited Cardiac Diseases Caused by Mutations in the Nav1.5 Sodium Channel
Journal of Cardiovascular Electrophysiology, 10/23/09
Tfelt–Hansen J et al. – In this comprehensive review, the authors describe the functional role of Nav1.5 and its associated proteins in propagation and depolarization both in a normal– and in a pathophysiological setting. Furthermore, several of the arrhythmogenic diseases, such as long–QT syndrome, Brugada syndrome, and AF, reported to be associated with mutations in SCN5A, are thoroughly described.
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