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Can COVID 2019 induce a specific cardiovascular damage or it exacerbates pre-existing cardiovascular diseases?
Gelsomina Mansueto1, Massimo Niola2, Claudio Napoli3
1Clinical Department of Internal Medicine and Specialistics, Department of Advanced Medical and Surgical Sciences (DAMSS), University of Campania "Luigi Vanvitelli", 80138 Naples, Italy.
Abstract:
A novel coronavirus SARS-CoV-2 causes acute respiratory distress syndrome (ARDS) with cardiovascular and multiple organ failure till death. The main mechanisms of virus internalization and interaction with the host are down-regulation or upregulation of the ACE2 receptor, the surface glycoprotein competition mechanism for the binding of porphyrin to iron in heme formation as well as interference with the immune system. The interference on renin-angiotensin-aldosterone system (RAAS) activation, heme formation, and the immune response is responsible for infection diffusion, endothelial dysfunction, vasoconstriction, oxidative damage and releasing of inflammatory mediators. The main pathological findings are bilateral interstitial pneumonia with diffuse alveolar damage (DAD). Because ACE receptor is also present in the endothelium of other districts as well as in different cell types, and as porphyrins are transporters in the blood and other biological liquids of iron forming heme, which is important in the assembly of the hemoglobin, myoglobin and the cytochromes, multiorgan damage occurs both primitive and secondary to lung damage. More relevantly, myocarditis, acute myocardial infarction, thromboembolism, and disseminated intravasal coagulation (DIC) are described as complications in patients with poor outcome. Here, we investigated the role of SARSCoV-2 on the cardiovascular system and in patients with cardiovascular comorbidities, and possible drug interference on the heart.
Insights
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause severe organ damage, particularly affecting the cardiovascular system. This study explores SARS-CoV-2
Area of Science:
- Virology and Immunology
- Cardiovascular Pathophysiology
- Molecular Mechanisms of Viral Infection
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection leads to acute respiratory distress syndrome (ARDS), multi-organ failure, and death.
- Viral entry and host interaction involve the ACE2 receptor, porphyrin-heme binding competition, and immune system interference.
- Dysregulation of the renin-angiotensin-aldosterone system (RAAS), heme synthesis, and immune responses contribute to disease progression, endothelial dysfunction, and inflammation.
Purpose of the Study:
- To investigate the impact of SARS-CoV-2 on the cardiovascular system.
- To examine the role of SARS-CoV-2 in patients with pre-existing cardiovascular comorbidities.
- To explore potential cardiac side effects of drugs used in SARS-CoV-2 treatment.
Main Methods:
- Review of pathological findings, including bilateral interstitial pneumonia and diffuse alveolar damage (DAD).
- Analysis of viral mechanisms affecting ACE2 receptors and porphyrin metabolism.
- Examination of cardiovascular complications such as myocarditis, myocardial infarction, thromboembolism, and disseminated intravascular coagulation (DIC).
Main Results:
- SARS-CoV-2 infection causes multi-organ damage due to ACE2 receptor presence in various tissues and porphyrin's role in heme formation.
- Cardiovascular complications, including myocarditis and DIC, are significant in severe cases and patients with comorbidities.
- The virus interferes with RAAS, heme synthesis, and immune responses, leading to endothelial dysfunction and inflammation.
Conclusions:
- SARS-CoV-2 poses a significant threat to the cardiovascular system, exacerbating existing conditions and causing new cardiac pathologies.
- Understanding the virus's interaction with ACE2, heme synthesis, and RAAS is crucial for managing severe disease and multi-organ damage.
- Further research is needed to address drug-induced cardiac interference in SARS-CoV-2 patients.
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