Role of inflammation and oxidative stress in atrial fibrillation

Abstract

Atrial fibrillation (AF) is the most common arrhythmia seen in clinical practice. Increasing evidence indicates that inflammation and oxidative stress contribute to the pathogenesis of AF, but their role remains poorly defined. In addition, whether inflammation and oxidative stress are associated with particular types of AF is unclear. The purpose of this study was to define the role of inflammation and oxidative stress in AF. Using a case-control study design, 305 patients with AF were compared with 150 control patients. AF was categorized into lone and typical AF and further subcategorized as paroxysmal, persistent, or permanent AF. Serum concentrations of interleukin (IL)-6, IL-8, IL-10, tumor necrosis factor (TNF)-alpha, monocyte chemoattractant protein (MCP)-1, vascular endothelial growth factor (VEGF), N-terminal pro-brain (B-type) natriuretic peptide (NTpBNP), and urinary F(2)-isoprostanes, a measure of oxidative stress, were measured. IL-6, IL-8, IL-10, TNF-alpha, MCP1, VEGF, and NTpBNP concentrations were independently associated with AF (all P <.05). However, F(2)-isoprostane excretion was not elevated (P = .50). Graded increases in TNF-alpha [median (interquartile range) 6.8 (3.4-11.3), 8.0 (5.6-10.9), 10.1 (5.7-12.4) pg/mL, P <.05] and NTpBNP [170.6 (67.3-481.9), 681.39 (310.3-1,439.0), 1,179.9 (653.1-2,096.0) pg/mL, P <.001] were seen among the subgroups of paroxysmal, persistent, and permanent AF, respectively. Inflammatory biomarkers were significantly increased in patients with AF, supporting a strong association between inflammation and AF. Surprisingly, urinary F(2)-isoprostanes, a sensitive index of systemic oxidative stress in vivo, were not increased in AF overall or in different subtypes of AF.