Search

Atrial fibrosis is a crucial contributor to initiation and perpetuation of atrial fibrillation (AF). This study aimed to identify a circRNA-miRNA-mRNA competitive endogenous RNA (ceRNA) regulatory network related to atrial fibrosis in AF, especially to validate hsa&#95;circ&#95;0000672/hsa&#95;miR-516a-5p/TRAF6 ceRNA axis in AF preliminarily. The circRNA-miRNA-mRNA ceRNA network associated with AF fibrosis was constructed using bioinformatic tools and literature reviews. Left atrium (LA) low voltage was used to represent LA fibrosis by using LA voltage matrix mapping. Ten controls with sinus rhythm (SR), and 20 patients with persistent AF including 12 patients with LA low voltage and 8 patients with LA normal voltage were enrolled in this study. The ceRNA regulatory network associated with atrial fibrosis was successfully constructed, which included up-regulated hsa&#95;circ&#95;0000672 and hsa&#95;circ&#95;0003916, down-regulated miR-516a-5p and five up-regulated hub genes (KRAS, SMAD2, TRAF6, MAPK11 and SMURF1). In addition, according to the results of Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, these hub genes were clustered in TGF-beta and MAPK signaling pathway. In the patients with persistent AF, hsa&#95;circ&#95;0000672 expression in peripheral blood monocytes was significantly higher than those in controls with SR by quantitative real-time polymerase chain reaction (p-value < 0.001). Furthermore, hsa&#95;circ&#95;0000672 expression was higher in peripheral blood monocytes of persistent AF patients with LA low voltage than those with LA normal voltage (p-value = 0.002). The dual-luciferase activity assay confirmed that hsa&#95;circ&#95;0000672 exerted biological functions as a sponge of miR-516a-5p to regulate expression of its target gene TRAF6. Hsa&#95;circ&#95;0000672 expression in peripheral blood monocytes may be associated with atrial fibrosis. The hsa&#95;circ&#95;0000672 may be involved in atrial fibrosis by indirectly regulating TRAF6 as a ceRNA by sponging miR-516a-5p., (© 2023. The Author(s).)

Background: High power shorter duration (HPSD) ablation may lead to safe and rapid lesion formation. However, the optimal radio frequency power to achieve the desired ablation index (AI) or lesion size index (LSI) is insubstantial. This analysis aimed to appraise the clinical safety and efficacy of HPSD guided by AI or LSI (HPSD-AI or LSI) in patients with atrial fibrillation (AF)., Methods: The Medline, PubMed, Embase, Web of Science, and the Cochrane Library databases from inception to November 2020 were searched for studies comparing HPSD-AI or LSI and low power longer duration (LPLD) ablation., Results: Seven trials with 1013 patients were included in the analysis. The analyses verified that HPSD-AI or LSI revealed benefits of first-pass pulmonary vein isolation (PVI) (RR: 1.28; 95% CI: 1.05-1.56, P = 0.01) and acute pulmonary vein reconnection (PVR) (RR: 0.65; 95% CI: 0.48-0.88, P = 0.005) compared with LPLD. HPSD-AI or LSI showed higher freedom from atrial tachyarrhythmia (AT) (RR = 1.32, 95% CI: 1.14-1.53, P = 0.0002) in the subgroup analysis of studies with PVI ± (with or without additional ablation beyond PVI). HPSD-AI or LSI could short procedural time (WMD: -22.81; 95% CI, -35.03 to -10.60, P = 0.0003), ablation time (WMD: -10.80; 95% CI: -13.14 to -8.46, P < .00001), and fluoroscopy time (WMD: -7.71; 95% CI: -13.71 to -1.71, P = 0.01). Major complications and esophageal lesion in HPSD-AI or LSI group were no more than LDLP group (RR: 0.58; 95% CI: 0.20-1.69, P = 0.32) and (RR: 0.84; 95% CI: 0.43-1.61, P = 0.59)., Conclusions: HPSD-AI or LSI was efficient for treating AF with shorting procedural, ablation, and fluoroscopy time, higher first-pass PVI, and reducing acute PVR and may increase freedom from AT for patients with additional ablation beyond PVI compared with LPLD. Moreover, complications and esophageal lesion were low and no different between two groups., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2021 Xing Liu et al.)