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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. [ABSTRACT FROM AUTHOR]

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_circ_0000672/hsa_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_circ_0000672 and hsa_circ_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_circ_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_circ_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_circ_0000672 exerted biological functions as a sponge of miR-516a-5p to regulate expression of its target gene TRAF6. Hsa_circ_0000672 expression in peripheral blood monocytes may be associated with atrial fibrosis. The hsa_circ_0000672 may be involved in atrial fibrosis by indirectly regulating TRAF6 as a ceRNA by sponging miR-516a-5p. [ABSTRACT FROM AUTHOR]

Abstract: Aims: To examine the effects of metoprolol on expression of myocardial inflammatory cytokines and myocardial function in rats following coronary microembolization (CME). Main methods: Male rats were randomly assigned to receive either sham-operation (control group), CME plus saline (CME group), or CME plus metoprolol (metoprolol group). CME was induced by injecting 3000 polyethylene microspheres (42μm) into the left ventricle during a 10-second occlusion of the ascending aorta. Metoprolol (2.5mg/kg) or saline was administered as three intravenous bolus injections after CME. At 3h, 6h, 12h, 24h and 4weeks after CME, myocardial function was measured with echocardiography; and the mRNA and protein levels of tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10) and interleukin 1-β (IL-1β) were determined. Key findings: Induced CME led to markedly higher mRNA and protein levels of TNF-α, IL-1β and IL-10 at 3, 6, 12, and 24h, as well as reduced left ventricular function, compared to the control group. Metoprolol administration reduced TNF-α and IL-1β levels, but increased IL-10 levels at 3, 6, 12, and 24h compared to the CME group. Moreover, metoprolol treatment resulted in significantly improved left ventricular function at 12h, 24h and 4weeks, but afforded no cardiac protection at 3h and 12h, compared to the CME group. Significance: Higher levels of TNF-α and IL-1β in rats following CME are associated with the development of myocardial contractile dysfunction. Metoprolol-conferred protection against progressive contractile dysfunction following CME may be mediated by its anti-inflammation potential. [Copyright &y& Elsevier]