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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.
  • Onohuean H; Department of Pharmacology and Toxicology, Biopharmaceutics Unit, School of Pharmacy, Kampala International University, Western-Campus, Kampala, Uganda. hope.onohuean1@kiu.ac.ug.
  • Al-Kuraishy HM; Department of Clinical Pharmacology and Medicine, College of Medicine, ALmustansiriyia University, Baghdad, Iraq.
  • Al-Gareeb AI; Department of Clinical Pharmacology and Medicine, College of Medicine, ALmustansiriyia University, Baghdad, Iraq.
  • Qusti S; Biochemistry Department, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia.
  • Alshammari EM; Department of Chemistry, College of Sciences, University of Ha'il, Ha'il, Saudi Arabia.
  • Batiha GE; Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, AlBeheira, 22511, Egypt. gaberbatiha@gmail.com.
Naunyn Schmiedebergs Arch Pharmacol ; 394(10): 2013-2021, 2021 10.
Article in English | MEDLINE | ID: covidwho-1391844
ABSTRACT
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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Full text: Available Collection: International databases Database: MEDLINE Main subject: SARS-CoV-2 / COVID-19 / Heart Failure Type of study: Prognostic study Topics: Long Covid Limits: Humans Language: English Journal: Naunyn Schmiedebergs Arch Pharmacol Year: 2021 Document Type: Article Affiliation country: S00210-021-02147-6

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Full text: Available Collection: International databases Database: MEDLINE Main subject: SARS-CoV-2 / COVID-19 / Heart Failure Type of study: Prognostic study Topics: Long Covid Limits: Humans Language: English Journal: Naunyn Schmiedebergs Arch Pharmacol Year: 2021 Document Type: Article Affiliation country: S00210-021-02147-6