Figure 1.

Cardiovascular involvement in COVID-19 – key manifestations and hypothetical mechanisms. SARS-CoV-2 anchors on trans-membrane angiotensin-converting enzyme-2 to enter the host cells including type-2 pneumocytes, macrophages, endothelial cells, pericytes and cardiac myocytes leading to inflammation and multi- organ failure. Infection of endothelial cells or pericytes is of particular importance because this could lead to severe microvascular and macrovascular dysfunction. In addition, immune over-reactivity can potentially destabilize atherosclerotic plaques and explain the development of acute coronary syndromes. Infection of the respiratory tract, particularly type-2 pneumocytes, by SARS-CoV-2 is manifested by the progression of systemic inflammation and immune cell over-reaction leading to “cytokine storm”, resulting in increased levels of cytokines such as IL-6, IL-7, IL-22 and CXCL10. Subsequently, it is possible that activated T cell and macrophages may infiltrate infected myocardium resulting in the development of fulminant myocarditis and sever cardiac damage. This process may be further intensified by a cytokine storm. Similarly, the viral invasion my case cardiac myocyte damage directly leading to myocardial dysfunction and contribute to the development of arrhythmias.⁶ Reproduced from the original work “ESC Guidance for the Diagnosis and Management of CV Disease during the COVID-19 Pandemic” https://www.escardio.org/Education/COVID-19-and-Cardiology/ESC-COVID-19-Guidance.⁷ Permission obtained from © The European Society of Cardiology 2020. All rights reserved.