Cardiac injury and acute myocarditis are well-established results of viral infections. In regards to COVID-19, reports of myocyte necrosis and mononuclear cell infiltrates suggests that myocarditis could be important in the occurrence of cardiac injury in patients. Mycarditis has the potential to turn into a conduciton block, tachyarrhythmia, and impairment of left ventricular function. Though the details of these findings are still unclear. Clinically, COVID-19 related myocarditis may only manifest as mild chest pain and could be rather indistinguishable from other causes in most patients. Sympotoms of myocarditis in COVID-19 patients usually do not present themselves until 10-14 days after the initial onset of symptoms. Data suggests that the delay in myocardial inflammation has to two with two pathogenic mechanisms. First, 'cytokine storm' promotes subclinical autoimmune myocarditis. Secondly, myocardial damage and/or molecular mimicry "initiate a de Novo autoimmune reaction".