Both occlusion-first and ablation-first strategies were efficacious and safe as combined procedures in patients with nonvalvular AF; however, the occlusion-first strategy was associated with lower new peridevice leak rates at follow-up.

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The present study was designed to develop a novel method for identifying significant pathways associated with human hypertrophic cardiomyopathy (HCM), based on gene co-expression analysis. The microarray dataset associated with HCM (E-GEOD-36961) was obtained from the European Molecular Biology Laboratory-European Bioinformatics Institute database. Informative pathways were selected based on the Reactome pathway database and screening treatments. An empirical Bayes method was utilized to construct co-expression networks for informative pathways, and a weight value was assigned to each pathway. Differential pathways were extracted based on weight threshold, which was calculated using a random model. In order to assess whether the co-expression method was feasible, it was compared with traditional pathway enrichment analysis of differentially expressed genes, which were identified using the significance analysis of microarrays package. A total of 1,074 informative pathways were screened out for subsequent investigations and their weight values were also obtained. According to the threshold of weight value of 0.01057, 447 differential pathways, including folding of actin by chaperonin containing T-complex protein 1 (CCT)/T-complex protein 1 ring complex (TRiC), purine ribonucleoside monophosphate biosynthesis and ubiquinol biosynthesis, were obtained. Compared with traditional pathway enrichment analysis, the number of pathways obtained from the co-expression approach was increased. The results of the present study demonstrated that this method may be useful to predict marker pathways for HCM. The pathways of folding of actin by CCT/TRiC and purine ribonucleoside monophosphate biosynthesis may provide evidence of the underlying molecular mechanisms of HCM, and offer novel therapeutic directions for HCM.

Aim-Oxidative stress and the inflammatory response contribute to the progression of cardiovascular disease. The present study aimed to investigate whether the mitochondrial-derived peptide MOTS-c could alleviate H 2 O 2 -induced oxidative stress and inflammatory status in H9c2 cells through activation of nuclear factor erythroid 2-related Factor 2 (Nrf2)/antioxidative response element (ARE) and inhibition of the NF-jB pathway. Methods-Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 lM MOTS-c was pretreated for 24 h before treatment with H 2 O 2. Then, the cell was treated with 100 lM H 2 O 2 for 1 h to induce oxidative stress. An inhibition model of sh-Nrf2 was constructed via a lentivirus expression system, and an activation model of NF-jB was achieved using phorbol 12-myristate-13-acetate (PMA). Cell viability was determined using a Cell Counting kit-8 assay. Relative measurement of relative protein and mRNA expression used western blotting and qRT-PCR, respectively. Intracellular reactive oxygen species (ROS) levels were detected using dichlorodihydrofluorescein diacetate, and malondialdehyde (MDA) and superoxide dismutase (SOD) levels were determined via commercial kits. The protein expression and distribution in the cells were visualized by immunofluorescence analysis. Enzyme-linked immunosorbent assay was used to detect the levels of inflammatory cytokines, including TNF-a, IL-6 and IL-1b. Results-We found that H 2 O 2 treatment significantly decreased cell viability and the level of SOD, increased the levels of ROS and MDA, and upregulated the expression of inflammatory cytokines, including TNF-a, IL-6 and IL-1b, in H9c2 cells. The expression levels of Nrf2, HO-1 and NQO-1 were significantly downregulated in the H 2 O 2 , while the phosphorylation of NF-jBp65 was promoted by H 2 O 2 . However, pretreatment with MOTS-c significantly reversed H 2 O 2 -induced damage in H9c2 cells. Moreover, both inhibition of the Nrf2/ARE pathway and activation of the NF-jB pathway significantly decreased the effects of MOTS-c, suggesting that MOTS-c might play a role in alleviating oxidative damage via the Nrf2/ARE and NF-jB pathways. Conclusions-Our investigation indicated that MOTS-c could protect against H 2 O 2 -induced inflammation and oxidative stress in H9c2 cells by inhibiting NF-jB and activating the Nrf2/ARE pathways.

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Background: This research explores the relationship between the unipolar electrogram (UP-EGM) and lesion size index (LSI) in different regions of continuous circular lesions (CCLs) and to assess the safety and efficacy of UP-EGM-guided versus LSI-guided radiofrequency catheter ablation (RFCA) in patients with paroxysmal atrial fibrillation (PAF). Methods: A total of 120 patients with drug-refractory PAF who underwent index RFCA were scheduled to be consecutively included from March 2020 to April 2021. All the patients were randomly divided 1:1 into two groups: the UP-EGM group and the LSI group. The first-pass PVI rate, acute PVI rate, and the sinus rhythm maintenance rate were compared. Results: A total of 120 patients with PAF were included in the study: the UP-EGM group (n = 60) and the LSI group (n = 60). All the LSI values in the UP-EGM group were less than those in the corresponding regions in the LSI group (all p < 0.001). There were no significant differences in the first-pass PVI rate and acute PVI rate between the two groups. After a mean follow-up period of 11.31 ± 1.70 months, the sinus rhythm maintenance rate in the UP-EGM group was comparable to that in the LSI group (90% vs. 91.7%, p = 0.752). Conclusion: UP-EGM-guided and LSI-guided RFCA are both effective and safe in patients with PAF. However, UP-EGM may be more suitable than LSI for guiding individual RFCA.