Structural reorganization of the myocardium in COVID-19
Authors:   Novosibirsk State Medical University, Novosibirsk, Russia, Savchenko S.V. , Lamanov A.N. ,   Novosibirsk State Medical University, Novosibirsk, Russia, Aizikovich B.I. ,   Novosibirsk State University, Novosibirsk, Russia, Gritsinger V.A. ,   Novosibirsk State Medical University, Novosibirsk, Russia, Bgatova N.P. ,   Research Institute of Clinical and Experimental Lymphology – Branch of the Institute of Cytology and Genetic, Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russia, Taskaeva Yu.S. ,   Research Institute of Clinical and Experimental Lymphology – Branch of the Institute of Cytology and Genetic, Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russia, Pozdnyakova L.L. ,   City Infectious Clinical Hospital No. 1, Novosibirsk, Russia, Shishkova О.M. ,   City Infectious Clinical Hospital No. 1, Novosibirsk, Russia, Ulyanova Ya.S. ,   City Infectious Clinical Hospital No. 1, Novosibirsk, Russia, Filina E.I. ,   City Infectious Clinical Hospital No. 1, Novosibirsk, Russia
Published: September 2024

Introduction. The development of a novel coronavirus infection (COVID-19) is not limited to respiratory damage. Adverse outcomes in patients with COVID-19 may be associated with cardiac damage. Aim. Study of the structural changes in the myocardium and the molecular biological characteristics of the endothelium of blood capillaries in severe forms of COVID-19. Materials and methods. An analysis of the medical documentation – inpatient records of 73 deceased with bilateral multisegmental viral pneumonia caused by the SARS-CoV-2 virus, as well as data from 43 autopsies of patients who died (sudden coronary death) between September 2020 to July 2021, was performed. An assessment of some clinical and laboratory data (degree of lung damage; levels of C-reactive protein, troponin I, D-dimer; left ventricular ejection fraction, etc.), structural changes in the myocardium and molecular biological characteristics (CD31, CD34) of the endothelium of blood capillaries in severe forms of COVID-19 was carried out. Results. The analysis of clinical and laboratory data has shown that a decrease in myocardial contractility in severe forms of COVID-19 due to an extensive lung damage was accompanied by an increase in the level of C-reactive protein, D-dimer, troponin I and indicated acute myocardial damage. According to electrocardiography (ECG) monitoring and echocardiography, repolarization disorders and a decrease in myocardial contractility were noted, which was accompanied by a decrease in ejection fraction by 32%. In more than 70% of cases, various arrhythmic disorders (atrial fibrillation, etc.) were observed during ECG. Light microscopy revealed the presence of sludge phenomenon, as well as swelling, desquamation and proliferation of the endothelium of blood capillaries, formation of diapedetic and focal hemorrhages, in some places leukocyte margination and their migration beyond vascular bed. Fibrin masses were observed in the lumen of blood vessels. Polarization microscopy, along with contractures in cardiomyocytes, revealed groups of cells with myocytolysis and primary granularity. In all observations, lipofuscinosis of cardiomyocytes was detected. Immunohistochemical examination showed a marked decrease in the expression level of CD31 (PECAM-1) and CD34 proteins – markers of blood vessels. Conclusion. The performed clinical and morphological analysis in severe forms of COVID-19 allowed us to obtain new data on degenerative changes in the myocardium and the structure of endothelial cells of blood capillaries, which can be used as a basis for methodological approaches to studying the mechanisms of development of heart failure in a novel coronavirus infection.