Clinic, laboratory and instrumental features COVID-19-myocarditis

The pandemic of recent years caused by the new COVID-19 virus has been associated with a number of cardiovascular complications, including myocarditis. Therefore, the issue of timely detection and treatment of heart muscle damage in patients with the SARS-CoV-2 virus has become relevant. There are several hypotheses for the pathogenesis of coronavirus myocarditis: direct damage to cardiomyocytes by the virus; severe inflammation and cytokine storm with overproduction of inflammatory cytokines; production of autoantibodies due to molecular mimicry between viral antigens and autoantigens, as well as the release of autoantigens from virus-infected cardiomyocytes. The article presents the results of examination of 19 patients, including 10 (64.6 %) women and 9 (47.37 %) men aged 44 to 81 years. They were diagnosed with myocarditis 7–12 days after diagnosis of COVID-19 infection, on average, 8.63 ± 1.54 days. The patients’ complaints were as follows: weakness (in 100 %), cough (in 100 %), feeling of interruptions in the heart’s work (in 78.95 %), shortness of breath (in 63.16 %), pain in the left half of the chest (in 63.16 %), discomfort in the chest (42.1 %), headache (in 57.89 %), muscle pain (in 52.63 %). The following laboratory changes were revealed: C-reactive protein was, on average, 184.21 ± 113.2 mg/l, troponin I – 0.69 ± 0.37 ng/ml, D-dimer level – 1209.53 ± 855.95 ng/ml, NT-proBNP level – 791 ± 418.63 pg/ml, procalcitonin – 0.56 ± 0.34 ng/ml, ferritin – 1221.55 ± 802.58 μg/l, the number of lymphocytes in the blood plasma – 1.07 ± 0.63 * 109/l. All patients had heart rhythm and conduction disturbances. According to echocardiography, the left ventricular ejection fraction was reduced in 26.3 % of patients.