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Abstract
Oxidative stress in atrial tissue may be causally related to atrial fibrillation as suggested by clinical and animal studies. Reactive oxygen species (ROS) are known to play a key role in fibrosis and the induction of after-depolarization and triggered activity. Therefore, suppressing oxidative stress may have a potential beneficial role in the management of atrial fibrillation. Since increased NADPH oxidase activity is shown to play a key role in generation of ROS in atrial tissue and in atrial fibrillation, our proposed strategy to target upstream inhibition of ROS production by inhibition of NADPH oxidase activity may provide a novel approach to prevent atrial fibrillation recurrences. We hypothesize that apocynin could be effective against atrial fibrillation, by virtue of its potent inhibitory effect of a major oxidative system (i.e. NADPH oxidase) combined with its demonstrated anti-inflammatory, antifibrotic and antihypertensive effects which partially are driven from its antioxidant property. Atrial fibrillation is known to be initiated by the interaction of these multiple factors.