Duygu, AliGazi, EmineDeveci, BülentArslan, MehmetÖztopuz, ÖzlemAdalı, Yasemen2025-01-272025-01-2720222602-3164https://doi.org/10.14744/ejmi.2022.80484https://search.trdizin.gov.tr/tr/yayin/detay/534096https://hdl.handle.net/20.500.12428/14707Objectives: The aim of this study is to investigate the efficacy of sacubitril-valsartan treatment in the early period of\rExperimental Autoimmune Myocarditis (EAM) model, under the perspective of fibrosis and inflammatory cytokines.\rMethods: The study was performed using 18 rats in three groups of EAM (n=6), EAM treatment (n=6) and control (n=6).\rEAM was induced by footpad injections of porcine cardiac myosin and Complete Freund’s Adjuvant (CFA). The EAM group\rwas not given any medical care. 20 mg/kg sacubitril-valsartan was given to EAM treatment (marked as treatment) group\rtwice a day beginning from the 21st day to the 42nd day. No procedure was applied to the control group. Histopathological,\rbiochemical and RT-PCR analyses were performed on the heart tissues taken after the 42nd day of sacrificing.\rResults: Significant congestion, fibrosis, and cellular changes were observed in the EAM and treatment groups. There was\r50% less severe fibrosis,which is 3rd degree, in the Treatment group compared to EAM. Severe congestion rate was lower\rin the treatment group compared to EAM; with the percentage of 16,6% to 50%. Though the average values of treatment\rgroup were lower than EAM group, there was obvious difference in TNF ?, TGF ?1 and NT-proBNP levels (p>0.05) between\rthe EAM and the treatment groups. There was no significant difference in IL-6 levels between the three groups.\rConclusion: In view of findings, the treatment of ARNI in acute autoimmune myocarditis may be promising on cardiac\rrisk markers (cytokine, BNP values) and fibrosis parameters. Studies to be conducted in high-numbered groups will\rreveal more statistical significance.eninfo:eu-repo/semantics/openAccessKalp ve Kalp Damar SistemiCould ARNI have an Effect on LV Fibrosis and Inflammatory Parameters in an Experimental Autoimmune Myocarditis Model?Article6219019710.14744/ejmi.2022.80484534096