Atherosclerosis as Pathogenetic Substrate for Sars-Cov2 Cytokine Storm

Area of Science:

• Cardiovascular disease
• Immunology
• Infectious disease

Background:

• Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes a global health emergency.
• Lung damage occurs due to SARS-CoV-2 binding to ACE2 receptors on alveolar cells.
• COVID-19 severity ranges from asymptomatic to critical illness requiring intensive care.

Purpose of the Study:

• To investigate the potential link between atherosclerosis and severe COVID-19 outcomes.
• To explore how cardiovascular conditions influence SARS-CoV-2 susceptibility and severity.
• To understand the role of immune dysregulation in both atherosclerosis and severe COVID-19.

Main Methods:

• Review of immune system and inflammation profiles in atherosclerosis.
• Analysis of laboratory results from severe COVID-19 cases.
• Hypothesizing a pathogenetic correlation between atherosclerosis and SARS-CoV-2 infection.

Main Results:

• Cardiovascular conditions like heart failure, coronary heart disease, hypertension, and diabetes mellitus are linked to increased COVID-19 severity.
• Atherosclerosis, characterized by chronic inflammation and immune dysregulation (e.g., elevated IL-6, TNF-α, IL-1β), may create a favorable environment for viral replication.
• SARS-CoV-2 infection might exacerbate atherosclerosis through excessive cytokine release, forming a detrimental feedback loop.

Conclusions:

• Atherosclerosis may serve as a substrate for increased SARS-CoV-2 replication and adverse outcomes.
• The degree of atherosclerotic progression could correlate with infection severity.
• A potential vicious cycle exists where SARS-CoV-2 exacerbates atherosclerosis, and atherosclerosis worsens COVID-19 prognosis.