The existence of pericardial effusion during COVID-19 infection is explained by several pathophysiological mechanisms: (a) by binding to the ACE2 receptor, the virus directly invades cardiomyocytes leading to myocardial injury; (b) indirectly, by means of inflammatory cytokines (tumor necrosis factor-alpha (TNF-a), interleukin (IL)-1, and IL-6) the virus leads to pericarditis or myopericarditis; (c) result of direct involvement of the pericardium; (d) consequence of acute respiratory distress syndrome (ARDS) or hypoxia [44]. Here, TNF is linked to acute respiratory distress syndrome.