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Updated: Nov 29, 2025
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Hydra, a Computer-Based Platform for Aiding Clinicians in Cardiovascular Analysis and Diagnosis
Published on: September 26, 2018
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Cardiovascular risk in COVID-19 infection
Valter Lubrano1, Silvana Balzan2
1Fondazione G. Monasterio, CNR/Regione Toscana Pisa, Italy.
American Journal of Cardiovascular Disease
|November 23, 2020
Summary
COVID-19 infection can cause severe cardiovascular damage and multiorgan failure, leading to increased mortality. Anti-inflammatory and anticoagulant treatments, such as heparin, may help prevent cardiovascular events in patients with severe COVID-19.
Area of Science:
- Cardiology
- Virology
- Immunology
Background:
- A novel coronavirus, COVID-19, has been identified, causing severe respiratory illness and multiorgan failure.
- While respiratory failure is a known complication, cardiovascular complications are increasingly recognized as a major cause of mortality.
Purpose of the Study:
- To review the effects of COVID-19 on the cardiovascular system.
- To elucidate the mechanisms by which SARS-CoV-2 induces cardiovascular damage and inflammation.
Main Methods:
- Review of existing literature on COVID-19 pathophysiology.
- Analysis of molecular pathways involved in viral infection and immune response.
Main Results:
- COVID-19 patients exhibit elevated cardiac troponin I and inflammatory cytokines, indicating cardiac damage.
- Viral binding to ACE-2 receptors promotes angiotensin II production, leading to hypertension.
- Elevated cytokines (IL-6, IL-1B, IL-8, TNF-α) are linked to plaque instability, thrombotic risk, and coagulation activation.
Conclusions:
- Cardiovascular damage and inflammation are significant contributors to COVID-19 mortality.
- Anti-inflammatory and anticoagulant therapies, like heparin, show promise in mitigating cardiovascular complications and inflammation associated with COVID-19.
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