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Covid-19 and development of heart failure: mystery and truth
Hope Onohuean1, Hayder M Al-Kuraishy2, Ali I Al-Gareeb2
1Department of Pharmacology and Toxicology, Biopharmaceutics Unit, School of Pharmacy, Kampala International University, Western-Campus, Kampala, Uganda. hope.onohuean1@kiu.ac.ug.
Insights
Coronavirus disease 2019 (Covid-19) can cause heart failure (HF) through direct cardiac injury or cytokine storms. Certain heart failure medications like digoxin and carvedilol may reduce Covid-19 severity and HF risk.
Area of Science:
- Cardiology
- Infectious Diseases
- Molecular Biology
Background:
- Coronavirus disease 2019 (Covid-19), caused by SARS-CoV-2, presents risks for heart failure (HF), especially in elderly patients with comorbidities.
- SARS-CoV-2 targets cardiac ACE2, potentially leading to acute cardiac injury.
- Factors like inflammation, coagulation disorders, and hypoxic respiratory failure in Covid-19 can exacerbate HF risk.
Purpose of the Study:
- To explore the mechanisms linking Covid-19 infection to heart failure development.
- To investigate the role of cytokine storms and molecular pathways in Covid-19-induced cardiac dysfunction.
- To evaluate the potential therapeutic benefits of anti-heart failure medications in mitigating Covid-19 severity and HF.
Main Methods:
- Review of existing literature on Covid-19, cardiovascular complications, and potential therapeutic targets.
- Analysis of molecular mechanisms including ACE2 expression, cytokine storm pathways, and their impact on cardiomyocyte function.
- Examination of the anti-viral and anti-inflammatory properties of digoxin and carvedilol in the context of Covid-19 and HF.
Main Results:
- Covid-19 infection can precipitate HF through direct myocardial injury or via a 'cytokine storm' response.
- Cytokine storms lead to increased pro-inflammatory cytokines, myocarditis, and impaired cardiac contractility.
- Elevated blood viscosity, endothelial dysfunction, and pulmonary hypertension contribute to HF development in Covid-19 patients.
Conclusions:
- SARS-CoV-2 infection poses a significant risk for developing heart failure through multiple pathways.
- Digoxin and carvedilol demonstrate potential in reducing SARS-CoV-2 infectivity and mitigating the inflammatory response, thereby offering protection against Covid-19-induced HF.
- Targeting molecular pathways and utilizing specific anti-heart failure drugs may be crucial in managing cardiovascular complications of Covid-19.
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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