Myocarditis is one of the relatively common complications of respiratory infection with SARSCoV- 2. As several patients confirmed with the new SARS-CoV-2 are known with cardiovascular disease (CVD) and data from the literature show negative prognosis and a higher risk of complications, this subgroup of subjects represents a particular situation. Therefore, an adequate understanding of the mechanisms involved in myocardial injury and interaction between COVID-19 and CVD is essential for optimal further management. Studies have proved that in COVID-19 patient myocarditis is determined via three pathological mechanisms of cardiomyocyte injury: direct viral cell entry and binding to ACE2, vasculitis-mediated injury, and systemic inflammatory response leading to pro-inflammatory cytokine discharge. Studies show that the incidence of myocarditis in patients with SARS-CoV-2 is relatively low, 4.8%, but myocardial damage occurs in more than 25% of critical cases in the form of acute fulminant myocarditis with severe hemodynamic degradation, or develops when the severity of SARS-CoV-2 infection intensifies. The mortality rate in myocarditis from COVID-19 infection ranges between 50–70%, with poorer prognosis and a higher risk of complications in CVD patients. As in all of these cases increased troponin and natriuretic peptide levels proved to be a negative prognostic factor, for risk stratification and prompt treatment, cardiac biomarkers should be evaluated in all patients with COVID-19.