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Covid-19 and development of heart failure: mystery and truth

Coronavirus disease 2019 (Covid-19) is a novel worldwide pandemic caused by a novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). During Covid-19 pandemic, socioeconomic deprivation, social isolation, and reduced physical activities may induce heart failure (HF), destabilization, and...

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Autores principales: Onohuean, Hope, Al-kuraishy, Hayder M., Al-Gareeb, Ali I., Qusti, Safaa, Alshammari, Eida M., Batiha, Gaber El-Saber
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8417660/
https://www.ncbi.nlm.nih.gov/pubmed/34480616
http://dx.doi.org/10.1007/s00210-021-02147-6
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author Onohuean, Hope
Al-kuraishy, Hayder M.
Al-Gareeb, Ali I.
Qusti, Safaa
Alshammari, Eida M.
Batiha, Gaber El-Saber
author_facet Onohuean, Hope
Al-kuraishy, Hayder M.
Al-Gareeb, Ali I.
Qusti, Safaa
Alshammari, Eida M.
Batiha, Gaber El-Saber
author_sort Onohuean, Hope
collection PubMed
description Coronavirus disease 2019 (Covid-19) is a novel worldwide pandemic caused by a novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). During Covid-19 pandemic, socioeconomic deprivation, social isolation, and reduced physical activities may induce heart failure (HF), destabilization, and cause more complications. HF appears as a potential hazard due to SARS-CoV-2 infection, chiefly in elderly patients with underlying comorbidities. In reality, the expression of cardiac ACE2 is implicated as a target point for SARS-CoV-2-induced acute cardiac injury. In SARS-CoV-2 infection, like other febrile illnesses, high blood viscosity, exaggerated pro-inflammatory response, multisystem inflammatory syndrome, and endothelial dysfunction-induced coagulation disorders may increase risk of HF development. Hypoxic respiratory failure, as in pulmonary edema, severe acute lung injury (ALI), and acute respiratory distress syndrome (ARDS) may affect heart hemodynamic stability due to the development of pulmonary hypertension. Indeed, Covid-19-induced HF could be through the development of cytokine storm, characterized by high proliferation pro-inflammatory cytokines. In cytokine storm-mediated cardiac dysfunction, there is a positive correlation between levels of pro-inflammatory cytokine and myocarditis-induced acute cardiac injury biomarkers. Therefore, Covid-19-induced HF is more complex and related from a molecular background in releasing pro-inflammatory cytokines to the neuro-metabolic derangements that together affect cardiomyocyte functions and development of HF. Anti-heart failure medications, mainly digoxin and carvedilol, have potent anti-SARS-CoV-2 and anti-inflammatory properties that may mitigate Covid-19 severity and development of HF. In conclusion, SARS-CoV-2 infection may lead to the development of HF due to direct acute cardiac injury or through the development of cytokine storms, which depress cardiomyocyte function and cardiac contractility. Anti-heart failure drugs, mainly digoxin and carvedilol, may attenuate severity of HF by reducing the infectivity of SARS-CoV-2 and prevent the development of cytokine storms in severely affected Covid-19 patients.
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spelling pubmed-84176602021-09-07 Covid-19 and development of heart failure: mystery and truth Onohuean, Hope Al-kuraishy, Hayder M. Al-Gareeb, Ali I. Qusti, Safaa Alshammari, Eida M. Batiha, Gaber El-Saber Naunyn Schmiedebergs Arch Pharmacol Review Coronavirus disease 2019 (Covid-19) is a novel worldwide pandemic caused by a novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). During Covid-19 pandemic, socioeconomic deprivation, social isolation, and reduced physical activities may induce heart failure (HF), destabilization, and cause more complications. HF appears as a potential hazard due to SARS-CoV-2 infection, chiefly in elderly patients with underlying comorbidities. In reality, the expression of cardiac ACE2 is implicated as a target point for SARS-CoV-2-induced acute cardiac injury. In SARS-CoV-2 infection, like other febrile illnesses, high blood viscosity, exaggerated pro-inflammatory response, multisystem inflammatory syndrome, and endothelial dysfunction-induced coagulation disorders may increase risk of HF development. Hypoxic respiratory failure, as in pulmonary edema, severe acute lung injury (ALI), and acute respiratory distress syndrome (ARDS) may affect heart hemodynamic stability due to the development of pulmonary hypertension. Indeed, Covid-19-induced HF could be through the development of cytokine storm, characterized by high proliferation pro-inflammatory cytokines. In cytokine storm-mediated cardiac dysfunction, there is a positive correlation between levels of pro-inflammatory cytokine and myocarditis-induced acute cardiac injury biomarkers. Therefore, Covid-19-induced HF is more complex and related from a molecular background in releasing pro-inflammatory cytokines to the neuro-metabolic derangements that together affect cardiomyocyte functions and development of HF. Anti-heart failure medications, mainly digoxin and carvedilol, have potent anti-SARS-CoV-2 and anti-inflammatory properties that may mitigate Covid-19 severity and development of HF. In conclusion, SARS-CoV-2 infection may lead to the development of HF due to direct acute cardiac injury or through the development of cytokine storms, which depress cardiomyocyte function and cardiac contractility. Anti-heart failure drugs, mainly digoxin and carvedilol, may attenuate severity of HF by reducing the infectivity of SARS-CoV-2 and prevent the development of cytokine storms in severely affected Covid-19 patients. Springer Berlin Heidelberg 2021-09-04 2021 /pmc/articles/PMC8417660/ /pubmed/34480616 http://dx.doi.org/10.1007/s00210-021-02147-6 Text en © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Review
Onohuean, Hope
Al-kuraishy, Hayder M.
Al-Gareeb, Ali I.
Qusti, Safaa
Alshammari, Eida M.
Batiha, Gaber El-Saber
Covid-19 and development of heart failure: mystery and truth
title Covid-19 and development of heart failure: mystery and truth
title_full Covid-19 and development of heart failure: mystery and truth
title_fullStr Covid-19 and development of heart failure: mystery and truth
title_full_unstemmed Covid-19 and development of heart failure: mystery and truth
title_short Covid-19 and development of heart failure: mystery and truth
title_sort covid-19 and development of heart failure: mystery and truth
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8417660/
https://www.ncbi.nlm.nih.gov/pubmed/34480616
http://dx.doi.org/10.1007/s00210-021-02147-6
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