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Relationship between vitamin D level and left atrial fibrosis in patients with lone paroxysmal atrial fibrillation undergoing cryoballoon-based catheter ablation
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文摘
Left atrial (LA) fibrosis is known as the hallmark for arrhythmogenic substrate in atrial fibrillation (AF). Quantification of LA fibrosis by using delayed-enhanced magnetic resonance imaging (DE-MRI) in AF patients is a pioneering noninvasive technique. Vitamin D (vitD) negatively regulates the renin–angiotensin system, binds to vitD receptors on cardiac myocytes, and has antioxidant properties that may ameliorate the inflammation and proarrhythmic substrate formation. However, its role in LA fibrosis is unclear. We aimed to investigate the association of serum 25(OH)D level with the extent of LA fibrosis by using DE-MRI and also predictors for AF recurrence after cryoablation was assessed in patients with paroxysmal AF.MethodsA total of 48 patients with lone paroxysmal AF (41.7% female; age: 48.5 ± 8.4 years) who underwent DE-MRI at 1.5 T and initial cryoballoon-based catheter ablation along with 48 healthy control subjects were enrolled. Fibrosis degree was categorized according to Utah class defined in the DECAAF study.ResultsSerum 25(OH)D levels were significantly lower in AF group compared to control group (25.8 ± 7.6 ng/ml vs. 31.0 ± 9.5 ng/ml, p = 0.004). Serum 25(OH)D levels were associated with moderate–severe LA fibrosis independent of other measures (OR: 0.72, 95% CI: 0.54–0.97, p = 0.028). At a mean 16.5 ± 2.6 months follow-up, late recurrence was observed in 10 (20.8%) patients. In multivariable Cox regression analysis, LA volume index (HR: 1.42, 95% CI: 1.01–2.01, p = 0.045) and the extent of LA fibrosis (HR: 1.14, 95% CI: 1.01–1.28, p = 0.034) were found as independently associated with late AF recurrence during follow-up.ConclusionLower levels of serum 25(OH)D are significantly associated with more extensive LA fibrosis in patients with lone paroxysmal AF and may be implicated in the pathophysiology of AF recurrence after cryoablation. Further large-scale studies are needed to elucidate the exact role of vitD deficiency and replacement on LA fibrosis.

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