Abstract
Atrial fibrillation is the most common persistent cardiac arrhythmia [1]. Rates of hospitalisation and the cost of treatment of AF are increasing in epidemic proportions [2, 3]. AF can predispose to stroke, ventricular fibrillation, heart attack and in some cases lead to sudden cardiac death [1, 4]. Despite this, the mechanisms underlying the development and sustenance of AF are incompletely understood [5], although the large degree of electrical heterogeneity and structural anisotropy are thought to be important [6–12]. Further to this, current treatment of AF is relatively poor [5]. Many drug therapies have adverse side effects in the ventricles. IKur is an ion channel of interest as a potential target for drug therapies because it is not expressed in the ventricles. The role which electrical remodelling associated with AF plays in the genesis and sustenance of AF is also incompletely understood. Hence, the aims of this Chapter are to (1) provide insight into the underlying mechanisms of AF; (2) analyse the most vulnerable regions of the atria to the development of AF (3) quantify the effect of AF-induced remodelling in the behaviour of AF and (4) to investigate the possibility of IKur as a potential target for drug therapies.
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Colman, M.A. (2014). Atrial Fibrillation. In: Mechanisms of Atrial Arrhythmias. Springer Theses. Springer, Cham. https://doi.org/10.1007/978-3-319-01643-6_8
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DOI: https://doi.org/10.1007/978-3-319-01643-6_8
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