SUBACUTE AND CHRONIC POST-COVID MYOENDOCARDITIS: CLINICAL PRESENTATION, ROLE OF CORONAVIRUS PERSISTENCE AND AUTOIMMUNE MECHANISMS

Aim: To study the clinical features of myoendocarditis and its possible mechanisms, including the persistence of SARS-Cov-2 in the myocardium, in the long-term period following COVID-19. Materials and methods: This cohort, prospective study included 15 patients aged 47.8 +/- 13.4 years (8 men) with post-COVID myocarditis. The COVID-19 diagnosis was confirmed for all patients. Median time to seeking medical care after COVID-19 was 4 [3; 7] months. The diagnosis of myocarditis was confirmed by magnetic resonance imaging (MRI) of the heart (n=10) and by endomyocardial biopsy of the right ventricle (n=6). The virus was detected in the myocardium with PCR; an immunohistochemical (IHC) study with antibody to SARS-Cov-2 was performed; anticardiac antibody level was measured; and echocardiography and Holter monitoring were performed. Hemodynamically significant coronary atherosclerosis was excluded for all patients older than 40 years. Results: All patients showed a clear connection between the emergence or exacerbation of cardiac symptoms and COVID-19. About 11 patients did not have any signs of heart disease before COVID-19; 4 patients had previously moderate arrhythmia or heart failure (HF) without myocarditis. The symptoms of myocarditis emerged at 1-5 months following COVID-19. MRI revealed typical late gadolinium accumulation, the signs of hyperemia, and one case of edema. The level of anticardiac antibodies was increased 3-4 times in 73% of the patients. Two major clinical variants of post-COVID myocarditis were observed. 1. Arrhythmic (n=6), with newly developed extrasystole or atrial fibrillation without systolic dysfunction. 2. Decompensated variant with systolic dysfunction and biventricular HF (n=9). Mean left ventricular ejection fraction was 34.1 +/- 7.8%, and left ventricular end-diastolic dimension was 5.8 +/- 0.7 cm. In one case, myocarditis was associated with the signs of IgG4-negative aortitis. SARS-Cov-2 RNA was found in five of six biopsy samples of the myocardium. The longest duration of SARS-Cov-2 persistence in the myocardium was 9 months following COVID-19. By using antibody to the Spike antigen and nucleocapsid, SARS-Cov-2 was detected in cardiomyocytes, endothelium, and macrophages. Five patients were diagnosed with lymphocytic myocarditis; one with giant-cell myocarditis; three patients had signs of endocarditis (infectious, lymphocytic with mural thrombosis). Conclusion: Subacute/chronic post-COVID myocarditis with isolated arrhythmias or systolic dysfunction is characterized by long-term (up to 9 months) persistence of SARS-Cov-2 in the myocardium in combination with a high immune activity. Endocarditis can manifest either as infectious or as nonbacterial thromboendocarditis. A possibility of using corticosteroids and anticoagulants in the treatment of post-COVID myoendocarditis should be studied.