Fig. 1

Hypothetical pathophysiology patterns concurring in cardiovascular involvement in COVID-19. SARS-CoV-2 enters cells via ACE2 receptor in type 2 in pneumocytes, endothelial cells, pericytes and cardiac myocytes, causing direct damage. Systemic inflammation and uncontrolled immune cell activation lead to a ‘cytokine storm’ which can contribute to destabilize atherosclerotic plaques and potentially trigger the onset of myocarditis trough T cells and macrophages infiltrations. Direct viral cardiac injury can provoke the development of arrhythmias, as well as several medications used in COVID-19 patients