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MeSH Disease

Human Phenotype

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    Myocardial Injury MESHD in Post Mortem Biopsies of Patients with COVID-19

    Authors: Camila Hartmann; Anna Flavia dos Santos Miggiolaro; Jarbas da Silva Motta Junior; Lucas Baena Carstens; Caroline Busatta Vaz De Paula; Larissa Hermann de Souza Nunes; Gustavo Lenci Marques; Lidia Zytinsky Moura; Jose Rocha Faria Neto; Lucia de Noronha; Cristina Pellegrino Baena

    doi:10.21203/rs.3.rs-45192/v1 Date: 2020-07-17 Source: ResearchSquare

    Background: Myocardial injury MESHD is significantly and independently associated with mortality in COVID-19 patients. However, the pathogenesis of myocardial injury MESHD in COVID-19 is still not clear, and cardiac involvement by SARS-CoV-2 remains a major challenge worldwide.Aim: This histopathological and immunohistochemical study seeks to clarify the pathogenesis of myocardial injury MESHD in COVID-19.Methods: Postmortem minimally invasive autopsies were performed in two patients who died from COVID-19, and the myocardium samples were compared to a control patient. Immunohistochemistry (IHC) staining was performed using monoclonal antibodies SERO against the following targets: caspase-1, ICAM-1, TNF-α, IL-4, IL-6, CD163, TGF-β, MMP-9, type 1 and type 3 collagen.Results: The histopathological analysis showed severe pericellular interstitial edema HP edema MESHD surrounding each of the cardiomyocytes. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-4, IL-6, CD163, MMP-9 and type 3 collagen in the COVID-19 patients compared to the control. On the other hand, no difference from the control was observed in expression of TNF-α, TGF-β and type 1 collagen. Conclusion: Our findings point to a pathogenesis related with pyroptosis leading to endothelial disfunction. The subsequent inflammation MESHD with associated interstitial edema HP edema MESHD could explain the myocardial disfunction and arrythmias MESHD in COVID-19 patients. The presence of Th2 response, MMP-9 and type-3 collagen suggests progression to myocardial fibrosis HP myocardial fibrosis MESHD in the long term.

    The Pathogenisis of COVID-19 Myocardial Injury MESHD: an Immunohistochemical Study of Postmortem Biopsies 

    Authors: Camila Hartmann; Anna Flavia dos Santos Miggiolaro; Jarbas da Silva Motta Junior; Lucas Baena Carstens; Caroline Busatta Vaz De Paula; Sarah Fagundes Grobe; Larissa Hermann de Souza Nunes; Gustavo Lenci Marques; Lidia Zytynski Moura; Lucia de Noronha; Cristina Pellegrino Baena

    doi:10.21203/rs.3.rs-45192/v2 Date: 2020-07-17 Source: ResearchSquare

    Rationale: M yocardial injury MESHDis significantly and independently associated with mortality in COVID-19 patients. However, the pathogenesis of m yocardial injury MESHDin COVID-19 is still not clear, and cardiac involvement by SARS-CoV-2 remains a major challenge worldwide. Objective: This histopathological and immunohistochemical study seeks to clarify the pathogenesis and propose a mechanism with pathways involved in COVID-19 m yocardial injury. MESHD Methods and Results: Postmortem minimally invasive autopsies were performed in six patients who died from COVID-19, and the myocardium samples were compared to a control patient. Histopathological analysis was performed using hematoxylin-eosin and toluidine blue staining. Immunohistochemical (IHC) staining was performed using monoclonal antibodies SERO against the following targets: caspase-1, ICAM-1, TNF-α, IL-4, IL-6, CD163, TGF-β, MMP-9, type 1 and type 3 collagen. The samples were also subjected to a TUNEL assay to detect potential apoptosis. The histopathological analysis showed severe pericellular interstitial edema HP dema MESHDsurrounding each of the cardiomyocytes and higher mast cells count by high-power field in all COVID-19 myocardium samples. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-4, IL-6, CD163, MMP-9 and type 3 collagen in the COVID-19 patients compared to the control. No difference from the control was observed in expression of TNF-α, TGF-β and type 1 collagen. The TUNEL assay was positive in all the COVID-19 samples confirming the presence of endothelial apoptosis. Conclusions: The pathogenesis of COVID-19 m yocardial injury MESHDseems to be related with pyroptosis leading to endothelial cell injury and disfunction. The subsequent i nflammation MESHDwith associated interstitial edema HP dema MESHDcould explain the myocardial disfunction and a rrythmias MESHDin these patients. Our findings also show that COVID-19 m yocardial injury MESHDmay cause myocardial fibrosis HP yocardial fibrosis MESHDin the long term. These patients should be monitored for m yocardial dysfunction MESHDand a rrythmias MESHDafter the acute phase of COVID-19.

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MeSH Disease
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Transmission
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