The aim. To analyze current evidence about etiology, pathogenesis, clinical manifestation, diagnosis, and treatment of patients with COVID-19 associated myocarditis. Multisystem inflammatory syndrome is possible in COVID-19 including inflammatory damage to the myocardium, which may last over several months and worsen the disease outcome. Mechanisms of inflammatory cardiac damage include direct damage by SARS-CoV-2, massive release of cytokines, dysregulation of the renin-angiotensin system. All these factors can aggravate pre-existing overload of the right heart chambers in patients with multifocal pneumonia, thrombosis of coronary arteries and myocardial ischemia. Inflammation of the myocardium manifests with typical symptoms of myocarditis and pericarditis. It can be accompanied by heart failure with rapid decompensation, arrhythmia, acute coronary syndrome or even sudden death. Laboratory findings in COVID-19 associated myocarditis include high levels of CRP, BNP, NT-proBNP, and D-dimer. Transthoracic echocardiography allows for an assessment of the left ventricular dysfunction and diagnosis of a pericardial effusion. Heart MRI according to the Lake Louise Diagnostic Criteria is the most sensitive diagnostic method in acute myocarditis. Medical imaging is indicated only in cases when results obtained can potentially influence the patient management tactics and should be performed according to the shortest protocol due to high risks of virus transmission. Conclusions. ESC experts (2020) do not provide unanimous recommendations for the treatment of SARS-CoV-2 associated myocarditis, considering a lack of the evidence base. Patient management is limited to adequate treatment of heart failure, arrhythmia, acute coronary syndrome, and prevention of thrombotic complications. Ongoing studies are aiming to evaluate potential place of glucocorticoids, intravenous immunoglobulins, antibodies against IL-6 receptor, colchicine in the treatment of COVID-19.