Abstract
Atrial fibrillation (AF) is one of the most common cardiac arrhythmias. We have discussed the role of hyperuricemia as a predisposing factor for the onset of AF. Numerous clinical and experimental investigators demonstrated the correlation between serum uric acid (SUA) level and arrhythmia development and its complications. The development and progression of AF are connected to a complex of changes in atrial cardiac muscle tissue. The electrical, structural, contractile remodeling, neurohumoral systems, inflammation, fibrosis, oxidative stress, endothelial dysfunction, activation of NLRP3 inflammasome induced by crystals of monosodium urate (MSU), heat shock proteins (HSP), cytokines all have a role in the development of this process. Furthermore, the role of xanthine oxidase (XO) is considered in the pathogenesis of AF through activation of systemic inflammation and oxidative stress, preparing that substrate for AF. The overwhelming data suggest a direct pathophysiological role of the increased SUA and XO activity as risk factors for AF. This article offers a comprehensive review of investigations that shows the interrelation between hyperuricemia and the risk of AF.
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