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. 2012 Dec;9(4):379-88.
doi: 10.3724/SP.J.1263.2012.08141.

Atrial fibrillation in the elderly: the potential contribution of reactive oxygen species

Kurt J Schillinger  1 , Vickas V Patel
Affiliations

Atrial fibrillation in the elderly: the potential contribution of reactive oxygen species

Kurt J Schillinger et al. J Geriatr Cardiol. 2012 Dec.

Abstract

Atrial fibrillation (AF) is the most commonly encountered cardiac arrhythmia, and is a significant source of healthcare expenditures throughout the world. It is an arrhythmia with a very clearly defined predisposition for individuals of advanced age, and this fact has led to intense study of the mechanistic links between aging and AF. By promoting oxidative damage to multiple subcellular and cellular structures, reactive oxygen species (ROS) have been shown to induce the intra- and extra-cellular changes necessary to promote the pathogenesis of AF. In addition, the generation and accumulation of ROS have been intimately linked to the cellular processes which underlie aging. This review begins with an overview of AF pathophysiology, and introduces the critical structures which, when damaged, predispose an otherwise healthy atrium to AF. The available evidence that ROS can lead to damage of these critical structures is then reviewed. Finally, the evidence linking the process of aging to the pathogenesis of AF is discussed.

Keywords: Aging; Arrhythmia; Atrial fibrillation; Cardiac; Free radicals; Oxidative stress; Redox.

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Figures

Figure 1.
Figure 1.. Mechanisms of ectopic firing in atrial fibrillation.
(A): A normal atrial myocyte action potential has 5 phases, labeled 0–4; (B): Enhanced automaticity occurs when unmasked pacemaker currents lead to spontaneous depolarization in phase 4; (C): Early afterdepolarizations are associated with reactivation of voltage-dependent sodium channels or L-type calcium channels in phase 2 of the action potential; (D): Late afterdepolarizations are caused by dysfunctional intracellular calcium handling that results in depolarization during phase 4 of the action potential.
Figure 2.
Figure 2.. Role of ROS in the pathogenesis of atrial fibrillation(references in brackets).
ROS-mediated damage impacts multiple cellular and subcellular structures which promotes AF pathogenesis. References are in parenthesis. DADs: delayed afterdepolarizations; EADs: early afterdepolarizations; ETC: electron transport chain; hERG; human ether-a-go-go related gene; MMP: matrix metalloproteinases; NOS: nitric oxide synthase; ROS: reactive oxygen species; SERCA2: Sarcoplasmic reticulum calcium-ATPase, type2.
See this image and copyright information in PMC

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