Relationships between paroxysmal atrial fibrillation, total oxidant status, and DNA damage

Structural and electrophysiological changes play a critical role in the development of atrial fibrillation (AF). Although the pathophysiology of paroxysmal AF (PAF) has not been fully elucidated, oxidative stress (OS) and DNA damage appear to be important triggers. Thus far, no studies have investigated the relationships among total oxidant status (TOS), DNA damage, and PAF. The goal of this study was to assess TOS and DNA damage in patients with PAF.

This cross-sectional study included 56 patients with PAF and 31 healthy controls. OS was assessed based on TOS, total antioxidant capacity (TAC), and oxidative stress index (OSI). The level of DNA damage was assessed using 8-hydroxy-2'-deoxyguanosine (8-OHdG).

There were no significant differences between the groups in terms of baseline characteristics. However, patients with PAF had significantly higher high-sensitivity C-reactive protein (p=0.018), TOS (p=0.001), OSI (p=0.001), and 8-OHdG (p=0.019) levels, compared with the control group. Multivariate logistic regression analysis showed that serum TOS level (odds ratio: 1.608; 95% confidence interval [CI]: 1.188-2.176, p=0.002) was the only independent predictor of PAF. TOS ≥12.2 predicted PAF with a sensitivity of 82% and specificity of 76% (AUC: 0.785, 95% CI: 0.687-0.883, p<0.001).

We found that TOS and DNA damage were significantly greater in patients with PAF than in the control group. Therefore, we propose that TOS and DNA damage can be used to detect patients at higher risk of AF.