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 persistent AF when compared with controls, indicating a role of systemic reactive oxidative species in the perpetuation of this arrhythmia. The renin angiotensin system (RAS) is believed to be upregulated 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.
Keywords: Atrial fibrillation, inflammation, oxidative stress, fibrosis, Atrial fibrillation (AF), thromboembolic, renin angiotensin system (RAS), hemodynamic instability, thromboembolism, cardiac arrhythmias, paroxysmal, sinus rhythm, Angiotensin II, cardiomyopathies, hyperthyroidism, alcoholism, tumor necrosis, factor alpha (TNF), interleukin-1, interleukin-6 (IL-6), C-reactive protein, pleiotropic cytokine, glycopeptide, nitrotyrosine, reactive oxygen species (ROS), arrhythmogenic effect, fibroproliferative, Nuclear factor, kappa, anticoagulation, angiotensin receptor blockers, ascorbic acid, Vitamin C, arrhythmia, corticosteroids, atrial myocardium, thrombosis, upstream therapies
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