Vitamin D was not involved in our article, because there had been no studies focusing on the association of vitamin D and atrial fibrillation (AF) recurrence after catheter ablation.1

We surely agreed with the opinion of Levent et al. that it might be beneficial to exploring the role of pre-ablation vitamin D in evaluating the risk of post-ablation AF recurrence, because series of mechanism studies had indicated the role of vitamin D in the pathogenesis of AF.

But we disagreed with the pathological mechanism stated by Levent et al. (euw289). The mechanism we recognized was as follows: the antioxidant activity of vitamin D could inhibit reactive oxygen species production; reactive oxygen species could trigger AF due to the formation of the inflammation and proarrhythmic substrate. Besides, Vitamin D could negatively regulate RAAS, and angiotensin II might participate in the atrial structural and electrical remodeling.2,3 Moreover, vitamin D could also modulate the calcium homeostasis and had a direct electromechanical effect.4 Besides, Levent et al. referred that vitamin D could up-regulate anti-inflammatory cytokines, but the effect was in immature dendritic cells,5 which had no relationship with AF.

Studies about vitamin D and post-ablation AF recurrence were still lacking. The results of epidemiologic studies about vitamin D deficiency and AF prevalence were still ambiguous.3 The study focusing on the role of vitamin D in preventing and terminating AF was still in the phase of animal testing, which was conducted in five rabbits with heart failure,4 therefore it is valuable and of great urgency to evaluate the role of vitamin D in AF occurrence and recurrence.

Conflict of interest: none declared.

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