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Atrial Fibrillation (AF), the most common sustained arrhythmia, is characterized by atrial electrical, contractile, and structural remodeling [1,2]. Structural remodeling includes interstitial fibrosis, cellular remodeling in atrial myocytes, such as degradation/loss of myofibrils and glycogen deposition (also known as myolysis) [3]. AF itself further augments these responses to perpetuate AF [4,5]. The mechanisms underlying both the initiation and perpetuation of AF are not well established but are thought to involve inflammation and oxidative stress [6-8]. Recently oxidative stress has been linked with atrial fibrillation [9]. There is evidence for enhanced oxidative stress in atrial tissue samples from AF patients [10].
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