Po-02-199 a novel finding: serum microrna-122 correlates with left atrial substrate in patients with atrial fibrillation

MicroRNA-122 (miR-122) is the most abundant miR in the liver, and previous studies revealed its anti-inflammatory function. Growing evidence shows the association of miR-122 with the pathophysiology of several heart diseases. However, little is known about the role of miR-122 in maintaining the left atrial substrate in atrial fibrillation (AF). The aim of the present study was to investigate the relationship between serum miR-122 and the presence of AF, and the impact of miR-122 on left atrial substrate and ablation outcomes. Patients undergoing their first AF ablation were enrolled. Blood samples were taken immediately before ablation for measuring the serum miR-122 level. The left atrial electroanatomic map was constructed and the bipolar peak-to-peak voltage was obtained. For patients with persistent AF, external cardioversion was performed to convert the patients to sinus rhythm to allow mapping. The AF types, left atrial voltage, and the outcomes after ablation were analyzed. Another cohort of subjects who underwent health examination and had no underlying cardiovascular comorbidity were randomly selected as the controls. This study consisted of 64 AF patients and 80 normal subjects as controls. Patients with AF had significantly lower serum miR-122 levels compared with the controls (136.1 vs. 560.0 copies/mL, P = 0.016, Figure). Among patients with AF, 10 (15.9%) patients had persistent AF. The average bipolar mapping sites in the left atrium were 536 ± 268 points for each patient and the voltage was 1.3 ± 0.6 mV. After a median follow-up for 7.5 years, AF recurrence rate was 68.4%. Serum miR-122 had a positive correlation with the left atrial mean voltage (P = 0.036, Table), but no correlation with the AF types or recurrence after catheter ablation. Patients with AF had significantly lower serum MiR-122 levels. Among them, low serum MiR-122 can further predict poor left atrial substrates. Further studies are warranted to clarify the causality and the role of miR-122 in the molecular mechanisms underlying AF.