Markers of oxidative stress after ablation of atrial fibrillation are associated with inflammation, delivered radiofrequency energy and early recurrence of atrial fibrillation

The role of oxidative stress after radiofrequency ablation of atrial fibrillation (AF) has not yet been well characterized. We sought to evaluate the time course of biomarkers of oxidative stress and inflammation after AF ablation and their association with clinical variables. Thirty consecutive patients (57.9 +/- A 1.7 years, 63% males) with paroxysmal AF underwent pulmonary vein isolation and ablation of complex fractionated atrial electrograms. Biomarkers were determined in blood samples before ablation and 6 h, 1, 2, 7, 30, 90 and 180 days post-ablation. The pro-oxidant enzyme myeloperoxidase and oxidized low-density lipoprotein reflecting oxidant damage of lipoproteins increased 2.9 +/- A 0.2-fold and 1.2 +/- A 0.1-fold, respectively, and were significantly up-regulated until day 2 post-ablation. The anti-oxidant enzyme copper/zinc superoxide dismutase did not change significantly. Inflammatory markers significantly increased (high-sensitivity C-reactive protein (hs-CRP): 41 +/- A 8-fold; interleukin-6: 4.4 +/- A 0.7-fold) for 7 and 2 days, respectively. The increase of myeloperoxidase and hs-CRP was interrelated and both predicted early recurrence of AF within the first post-ablation week (both p < 0.05). The increase of both markers was associated with the amount of delivered radiofrequency energy (p < 0.05). The up-regulation of hs-CRP correlated with troponin T (p = 0.008), while myeloperoxidase and troponin T were borderline associated (p = 0.054). However, the oxidative and inflammatory responses did not predict long-term ablation outcome (p > 0.05). Markers of oxidative stress showed a significant up-regulation during the first 2 days after AF ablation. Their up-regulation was linked to inflammation, delivered radiofrequency energy, and early recurrence of AF, but did not predict long-term ablation outcome.