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Atrial fibrillation (AF) is common in pulmonary hypertension (PH), whereas the mechanisms and treatments remain to be explored. TRPV2 regulates the structure and function of the cardiovascular system; however, little attention has been given to its role in AF. This study was to determine whether TRPV2 was involved in PH-induced AF and the effects of TRPV2 inhibitor tranilast on AF in rat models of PH. Monocrotaline (MCT) and SU5416/hypoxia (SuHx)-induced PH models were performed to detect atrial electrophysiological parameters. Daily tranilast (a TRPV2 inhibitor) or saline was given starting 1 day before PH establishment. PH increased the susceptibility to AF, with TRPV2 up-regulated in the right atria. Compared to PH rats, tranilast reduced AF inducibility and the prolongations of ERP and APD; mitigated cardiopulmonary remodeling and the increases in P-wave duration and P-R interval; partially reversed the down-regulation of ion channels such as Cav1.2, Nav1.5, Kv4.3, Kv4.2, Kv1.5, Kir2.1, Kir3.1, Kir3.4 as well as connexin (Cx) 40 and Cx43; improved right atrial (RA) fibrosis, enlargement, and myocardial hypertrophy; decreased the accumulation of inflammatory cells; down-regulated inflammatory indicators such as TNF-α, IL-1β, CXCL1, and CXCL2; and inhibited the activation of the PI3K-AKT-NF-κB signaling pathway. Our results reveal that TRPV2 participates in PH-induced AF, and TRPV2 inhibitor tranilast prevents PH-induced RA remodeling. TRPV2 might be a promising target for PH-induced AF., Competing Interests: Declaration of Competing Interest The authors declare that they have no competing interests., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Background: Atrial fibrillation (AF) is one of the most prevalent sustained cardiac arrhythmias. The latest studies have revealed a tight correlation between nonalcoholic fatty liver disease (NAFLD) and AF. However, the exact molecular mechanisms underlying the association between NAFLD and AF remain unclear. The current research aimed to expound the genes and signaling pathways that are related to the mechanisms underlying the association between these two diseases., Materials and Methods: NAFLD- and AF- related differentially expressed genes (DEGs) were identified via bioinformatic analysis of the Gene Expression Omnibus (GEO) datasets GSE63067 and GSE79768, respectively. Further enrichment analysis of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), the construction of a protein-protein interaction (PPI) network, the identification of significant hub genes, and receiver operator characteristic curve analysis were conducted. The gene-disease interactions were analyzed using the Comparative Toxicogenomics Database. In addition, the hub genes were validated by quantitative Real-Time PCR (qRT-PCR) in NAFLD cell model., Results: A total of 45 co-expressed differentially expressed genes (co-DEGs) were identified between the NAFLD/AF and healthy control individuals. GO and KEGG pathway analyses revealed that the co-DEGs were mostly enriched in neutrophil activation involved in the immune response and cytokine-cytokine receptor interactions. Moreover, eight hub genes were selected owing to their high degree of connectivity and upregulation in both the NAFLD and AF datasets. These genes included CCR2, PTPRC, CXCR2, MNDA, S100A9, NCF2, S100A12, and S100A8., Conclusions: In summary, we conducted the gene differential expression analysis, functional enrichment analysis, and PPI analysis of DEGs in AF and NAFLD, which provides novel insights into the identification of potential biomarkers and valuable therapeutic leads for AF and NAFLD., (© 2022. The Author(s).)

Background: The CHADS 2 and CHA 2 DS 2 -VASc scores are well-established clinical scales to estimate the risk of stroke in patients with atrial fibrillation (AF). However, the predictive power of the two scales concerning left atrial thrombus (LAT) or spontaneous echo contrast (SEC) has not been well investigated. Therefore, we investigated the predict power of CHADS 2 and CHA 2 DS 2 -VASc scores concerning LAT/SEC; identified clinical, echocardiographic and laboratory predictors of LAT/SEC in addition to the CHADS 2 and CHA 2 DS 2 -VASc scores; and derived a new scale to predict LAT/SEC accurately, it might improve thromboembolic risk stratification in patients with nonvalvular atrial fibrillation., Methods: We identified 1102 consecutive AF patients who underwent transesophageal echocardiography (TEE) for the purpose of the exclusion of LAT before catheter ablation, cardioversion or left atrial appendage occlusion. The clinical, echocardiographic and laboratory characteristics of patients were collected from the electronic medical record system., Results: In the study, the prevalence of LAT/SEC was only 4.36%. In the multivariate logistic analysis, hypertension, left atrial enlargement, prior stroke/TIA, left ventricular dysfunction, and renal dysfunction were predictors of LAT/SEC. Receiver operating characteristic curve analysis showed that c-statistics of the CHADS 2 and CHA 2 DS 2 -VASc scores concerning LAT/SEC were 0.673 and 0.643, respectively. We derived a new scale composed of variables from the multivariate logistic analysis that showed a higher c-statistic value (0.761) than the CHADS 2 and CHA 2 DS 2 -VASc scores for the prediction of LAT/SEC., Conclusion: In our cohort, we found two variables not included in the CHA 2 DS 2 -VASc score (renal dysfunction, left atrial enlargement) were independent predictors of LAT/SEC. A new scale combining clinical, echocardiographic and laboratory predictors might improve thromboembolic risk stratification. And there is a great need to carry out a new prospective and multicenter study, with a population more homogenous and including all the determinants for LAT/SEC to establish the independent degree of each variable and the applicability in clinical practice, facilitating the emergence of a new score of thromboembolic risk in patients with nonvalvular atrial fibrillation., (Copyright © 2020 Elsevier Ltd. All rights reserved.)