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

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.

Combination of Panax ginseng C. A. Mey and Febuxostat Boasted Cardioprotective Effects Against Doxorubicin-Induced Acute Cardiotoxicity in Rats

“…DOX produces a variety of reactive oxygen species (ROS), which cause endoplasmic reticulum calcium leakage, DNA damage, and autophagy flux suppression, ultimately resulting in ferroptosis and lipid peroxidation ( Abushouk et al, 2019 ; Podyacheva et al, 2021 ). The heart is sensitive to oxidative damage due to low antioxidant enzymes, large mitochondrial density/volume, and a higher oxygen consumption rate ( Onohuean et al, 2021 ). Oxidative stress due to DOX-induced cardiotoxicity also develops due to the reduction of endogenous antioxidant capacity.…”

Dysregulated miRNAs network in the critical COVID-19: An important clue for uncontrolled immunothrombosis/thromboinflammation

“…Not only do these medications control the hyperinflammatory/hyperoxidant states but they may also recover the efficient functions and optimal expressions of miRNAs resulting in the limitation of uncontrolled immunothrombosis/thromboinflammation. Some other groups of drugs such as anti-heart failure ones, anti-histamines, leukotriene receptor antagonists (LTRAs), the phosphodiesterase (PDE) inhibitors, etc., with confirmed anti-inflammatory and anti-oxidant roles, can also be administrated for the amelioration of miRNAs performances [17] , [18] , [296] , [297] , [298] , [299] , [300] , [301] . Produced in the body, some alarming agents can also be helpful.…”

“…1 ). Venous thromboembolism, ischemic stroke (IS), neurological disorders, acute coronary syndrome, and myocardial damage are among the grave clinical complications ensuing from the above-mentioned processes in patients with the critical COVID-19 [1] , [2] , [3] , [10] , [11] , [12] , [13] , [14] , [15] , [16] , [17] , [18] . Normally, there is a balance between the pro/anticoagulant factors and pro-/anti-inflammatory ones that would maintain homeostasis [1] .…”

Changes in the Blood Viscosity in Patients With SARS-CoV-2 Infection

“…COVID-19 patients with ALI/ARDS require ICU admission and mechanical ventilation for respiratory support (6,7). Moreover, COVID-19 may cause extra-pulmonary manifestations, including neurological complications (8), acute kidney injury (9), testicular injury (10), heart failure (11), newonset diabetes mellitus (12), and thromboembolic disorders (13).…”