The pathophysiology of PE seen during the COVID-19 process has been tried to be explained in various ways: (a) Direct invasion of cardiomyocytes with a virus (binding to ACE2 receptor) results in myocardial injury, myocarditis, and cardiomyopathy; (b) Pericarditis or myopericarditis occurs with indirect effects of inflammatory cytokines (TNF-a, IL-1, IL-6); (c) As a result of ARDS or hypoxia triggering a myocardial injury or pulmonary hypertension; (d) Finally, it was suggested that PE occurs as a result of direct involvement of the pericardium [4]. This evidence concerns the gene TNF and cardiomyopathy.