"When," "Where," and "How" of SARS-CoV-2 Infection Affects the Human Cardiovascular System: A Narrative Review

Area of Science:

• Cardiology
• Infectious Diseases
• Pathophysiology

Background:

• The COVID-19 pandemic, caused by SARS-CoV-2, has led to significant cardiovascular complications.
• Myocardial injury in COVID-19 patients is linked to mechanisms like coronary spasm, microthrombi, plaque rupture, hypoxia, and cytokine storm.

Approach:

• This review elucidates the mechanisms by which SARS-CoV-2 impacts the cardiovascular system.
• It explores the roles of the angiotensin-converting enzyme 2 (ACE2) and kinin-kallikrein systems in COVID-19-related cardiovascular pathology.
• The review examines how viral entry via ACE2 receptors on endothelial cells triggers prothrombotic and inflammatory cascades.

Key Points:

• SARS-CoV-2 infection downregulates ACE2 receptors, leading to angiotensin II accumulation and prothrombotic effects, including coagulation cascade activation and impaired fibrinolysis.
• The virus disrupts the kinin-kallikrein system, impairing vasodilation, tissue repair, and platelet regulation.
• These disruptions contribute to a wide spectrum of cardiovascular conditions, including myocarditis, heart failure, arrhythmias, and thromboembolic events.

Conclusions:

• COVID-19 affects the cardiovascular system through complex interactions involving ACE2 and KKS pathways.
• The virus can cause endothelial dysfunction, inflammation, and thrombosis, predisposing patients to diverse cardiac complications.
• Understanding these mechanisms is crucial for managing cardiovascular risks in COVID-19 patients across all demographics, including children and athletes.