Production of some cytokines as a reflection of various immunoregulatory mechanisms in post-covid myocarditis

Currently, the problem of persistent myocardial damage in patients who have had COVID-19 has become one of the most pressing in the practice of cardiologists. The main mechanisms of the pathogenesis of post-COVID myocarditis are associated with a violation of immunoregulation caused by long-term persistence of the virus in the heart muscle and the launch of autoimmune processes that can lead to myocardial remodeling, the formation of myocardiosclerosis and the development of heart failure or arrhythmia. The purpose of this study was to assess the dynamics of the production of certain cytokines (IFNg, IL-4, IL-17А), which may indirectly reflect the activation of various immune response pathways in patients with post-COVID myocarditis, depending on the duration of the disease and the degree of heart failure. The study included 32 patients with post-COVID myocarditis, 36 patients with myocardial cardiosclerosis, and 10 apparently healthy individuals. It was found that in all patients with post-COVID myocarditis, the content of IFNg, IL-4, IL-17А in the blood serum was higher than in patients with myocardial cardiosclerosis (p 0.001; p 0.05; p 0.01, respectively) and conditionally healthy individuals (p 0.001; p 0.01; p 0.001, respectively). Compared with the group of patients with no or moderate severity of symptoms of heart failure (functional class 0–II), those with more severe heart failure (functional class III) had a higher level of interferon gamma (p 0.05). When comparing the results obtained with similar indicators in patients with myocardial cardiosclerosis who have the same degree of heart failure, no statistically significant differences were obtained. The maximum content of IFNg in post-COVID myocarditis was observed in the 2nd week of the disease (p 0.001 compared with the control group); then its level gradually decreased and by the end of the 2nd month there were no longer any significant differences. The opposite trend was observed in relation to the content of IL-4 and IL-17А: in the first two weeks, no statistically significant differences were detected with the control group, but then their content increased quite quickly (p 0.001 compared with the control group by the end of the first month of the disease) and continued to remain the same high until the end of the 2nd month. Thus, monitoring the content of IFNg, IL-4, IL-17А in blood serum can to some extent provide an idea of the sequence of development of the immune response in post-COVID myocarditis. An increase in IFNg levels in the early stages of the disease is probably associated with an increase in the manifestations of heart failure. Th17-mediated mechanisms may be involved in the process of myocardial remodeling resulting in myocardial cardiosclerosis.