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Arrhythmias
Book chapter   Open access

Arrhythmias

Barry London
Principles of Molecular Medicine, pp.157-165
Humana Press
2006
DOI: 10.1007/978-1-59259-963-9_18
url
https://doi.org/10.1007/978-1-59259-963-9_18View
Published (Version of record) Open Access

Abstract

Ion channel mutations cause long QT syndrome, Brugada syndrome, conduction disorders, catecholinergic ventricular tachycardia, and some forms of familial atrial fibrillation and pre-excitation. Transgenic and gene-targeted mouse models of these disorders have further increased the understanding of links between ion channel mutations and these rare arrhythmia syndromes. Molecular genetics, pathophysiology, and implications of these findings are discussed later. It is important to realize, however, that the genetic basis of other inherited arrhythmic syndromes remains unclear, as does the role of genes that are not ion channels. In addition, the relationship of common genetic variants (polymorphisms) to arrhythmic risk is only beginning to be studied. This chapter highlights the avenues of future research that seem most likely to yield results.
Arrhythmias atrial fibrillation Brugada syndrome conduction disease ion channel long QT syndrome Wolff-Parkinson-White syndrome (WPW)

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