Key result
Reactive oxygen species contribute to cardiac sympathovagal imbalance and autonomic dysfunction, which can trigger arrhythmias in cardiovascular disease and aging.
This review highlights the role of reactive oxygen species in autonomic dysfunction and arrhythmia, and discusses novel targets for modulating sympathovagal balance in cardiac disease.
ROS modulation warrants mechanistic study but should not yet inform arrhythmia management; leaves open clinical relevance.
Sympathetic hyper-activity and diminished parasympathetic activity are a consequence of many primary cardiovascular disease states and can trigger arrhythmias. Emerging evidence suggests that reactive oxygen species (ROS) including nitric oxide, superoxide, and peroxynitrite may contribute to cardiac sympathovagal imbalance in the brainstem, peripheral neurons, and in cardiomyocytes since all experience increased oxidative stress as a result of cardiac disease processes and aging. This article reviews the roles of ROS in autonomic dysfunction and arrhythmia. In addition, novel research directed toward finding targets for modulating sympathovagal balance in cardiac disease is discussed.
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Danson et al. (2006) conducted a review in Cardiovascular disease and arrhythmia. Reactive oxygen species (ROS) was evaluated. Reactive oxygen species contribute to cardiac sympathovagal imbalance and autonomic dysfunction, which can trigger arrhythmias in cardiovascular disease and aging.
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