Mitochondrial dysfunction and pathomorphological changes in myocardial diagnosis in coronavirus infection

Abstract

Introduction. Mitochondrial destruction is a central event in various mechanisms of cell death, including apoptosis, which is triggered by the p53 gene when reparative processes are disrupted. At the same time, cell breakdown products, for example, in the case of COVID-19 infection, trigger a cascade of inflammatory reactions that threaten the survival of the body. The contribution of mitochondrial dysfunction to the formation of the "cytokine storm" in the complicated course of coronavirus infection and its direct participation in the activation of innate immune reactions is not entirely clear. The article presents the results of a study of functional and structural disorders of mitochondria in patients with severe COVID-19 or who died from this infection. Materials and methods. The study was carried out on mononuclear cells of peripheral blood taken from patients with COVID-19 during the "cytokine storm" and on myocardial tissues obtained during autopsy. The study was approved by the Ethics Committee at the Military Medical Academy (Meeting Minutes No232 dated February 18, 2020). The function of mitochondrial respiration in peripheral blood mononuclear cells was studied using a cellular metabolism analyzer, and structural changes in the myocardium and mitochondria of cardiomyocytes were detected using light microscopy, scanning and transmission electron microscopy. Outcomes. The results of a study of mitochondrial dysfunction in persons with severe coronavirus infection demonstrated the absence of spare breathing in one of the patients with severe COVID-19. In the myocardial tissues of those who died from this infection, disorders were detected, expressed in necrotic changes in cardiomyocytes, changes in the structure of mitochondria, including the loss of cristae, the formation of electron-dense inclusions in the mitochondrial matrix. Discussion. Morphological changes found in the myocardium of patients who died as a result of coronavirus infection should be interpreted as having developed in the premortal period and characterizing the cardiac mechanism of death. Mitochondrial dysfunction, defined structurally and functionally in cardiomyocytes and blood mononuclear cells, is an important determinant of the body's ability to resist SARS-CoV-2 infection. Mitochondrial dysfunction, defined structurally and functionally in cardiomyocytes and blood mononuclear cells, is an important determinant of the body's ability to resist SARS-CoV-2 infection. Conclusion. There is a need to summarize all available data on the pathogenesis, genetic predicators, treatment and course of COVID-19 both in the population of individual countries and in the world as a whole. The study of mitochondrial and nuclear DNA genes involved in intracellular energy metabolism in severe COVID-19 is a promising research goal with high clinical potential.