Systemic inflammation and oxidative stress are emerging as key pathophysiological contributors to the development and persistence of atrial fibrillation.
Inflammation and oxidative stress are emerging as key pathophysiological mechanisms in the development and persistence of atrial fibrillation.
Atrial fibrillation (AF) remains the most commonly encountered sustained arrhythmia in clinical practice and contributes to increased morbidity and mortality. Management of AF poses a challenge due to the refractory nature of the arrhythmia and the associated thromboembolic complications. Recent studies have implicated both systemic and local cardiac inflammation in the development as well as persistence of AF. This has been validated by the occurrence of high levels of systemic markers of inflammation in patients with post operative as well as chronic AF. High levels of markers of oxidative stress have also been found in patients with chronic AF when compared with controls, indicating a role of systemic reactive oxidative species in the perpetuation of this arrhythmia. Renin angiotension system (RAS) is believed to be unregulated in AF and may contribute to the pathogenesis of AF by producing a state of cardiac or systemic oxidative stress and /or inflammation. In this review, we aim to discuss the emerging evidence linking inflammation, and oxidative stress with AF.
Negi et al. (Wed,) conducted a review in Atrial Fibrillation. Systemic inflammation and oxidative stress are emerging as key pathophysiological contributors to the development and persistence of atrial fibrillation.
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