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This report presents a clinical case of a 57-year-old female patient who was admitted for dyspnea, productive cough, reduced left ventricular (LV) systolic function, and who had previously undergone thoracocentesis for significant pleural effusion. This case is a unique combination of lymphocytic myocarditis and massive intracardiac and ileo-caval thrombosis. Morphological verification of the diagnosis, that was necessary prior to the administration of immunosuppressive therapy due to the prothrombogenic effect of glucocorticoids, provided a justification for a basis therapy for myocarditis, which significantly improved the patient's condition.

Aim    To study clinical features of myoendocarditis and its possible mechanisms, including persistence of SARS-Cov-2 in the myocardium, in the long-term period following COVID-19.Material 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; 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. 11 patients did not have any signs of heart disease before COVID-19; 4 patients had previously had moderate arrhythmia or heart failure (HF) without myocarditis. Symptoms of myocarditis emerged at 1-5 months following COVID-19. MRI revealed typical late gadolinium accumulation, signs of hyperemia, and one case of edema. The level of anticardiac antibodies was increased 3-4 times in 73 % больных. 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 signs of IgG4‑negative aortitis. SARS-Cov-2 RNA was found in 5 of 6 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.

Anesthesiologist daily encounters the need for maintaining an airway patency. This manuscript is devoted to the development of this technique from ancient times to the present. Three areas including tracheostomy, endoscopy and tracheal intubation are comprehensively described.

Immunophenotype of mobilized stem blood cells (CD34+) was studied in 29 patients with late post-traumatic spinal lesions. The CD34+ cells demonstrated different levels of expression of CD45, CD38, monomorphic determinants HLA-DR and gp130 epitopes. Most patients presented with a CD34+ cell fraction with no or low expression of common leukocytic antigen CD45. Only 2 patients had greater than 15 percent of HLA-DR-CD38- cells in the CD34+ fraction. A common transducer molecule of interleukin-6 family cytokines gp130 was expressed on stem (CD34+) cells in all the cases, 26 percent of the patients had an activated gp130 phenotype, i.e. a combination of C7+ and A1- epitopes.