Introduction. An essential point in the pathogenesis of COVID-19 is endothelial dysfunction with the development of thrombosis and 
microangiopathy of pulmonary vessels, which is one of the causes of high mortality. At the same time, electron microscopic examination of 
the pulmonary vascular bed in COVID-19 coronavirus infection is rarely performed.
Objective: To investigate ultrastructural changes in the pulmonary microcirculatory bed by determining the features of endothelial damage 
and the role of vascular disorders in the pathogenesis of severe COVID19 coronavirus infection.
Methods. The material was collected at autopsy, no later than 2 hours after the fact of death of patients, fixed in Millonig's fixative with 
pH 7.36. Dehydration was carried out in increasing-strength ethanol, transferred to propylene oxide, and tarred in a mixture of Araldite. 
Ultrathin sections with a thickness of 60 nμ were made using an LKB 2188 Ultrotome NOVA ultramicrotome. According to Reynolds, sections were mounted on support grids and contrasted with uranyl acetate and lead citrate. The obtained samples were viewed in a transmission electron microscope TEM 100-01, and photofixation was carried out using a KAPPA Image Base digital camera.
Results. Significant structural changes in type 2 pneumocytes were observed with the development of degeneration and reactive hyperplasia, 
the formation of syncytial elements, dyscirculatory disorders with endothelial alteration, pronounced hyperemia and stasis, coagulopathy, 
and thrombosis. In the lumen of the alveoli, in addition to the deposition of fine-grained masses of fibrin hyaline membranes, fibrinous exudate, 
desquamated type 2 pneumocytes, macrophages, lymphocytes, plasma cells, single neutrophils, and erythrocytes were detected.
Individual type 2 pneumocytes were characterized by the appearance of “giant lamellar bodies” measuring 2-4 μm, which occupied a
significant part of the cytoplasm. Hyperplasia of type 2 pneumocytes was observed in some areas of the lung tissue. The proliferation of 
fibroblasts and collagen fibrils was detected in the interstitium of the interalveolar septa.
Conclusions. As a result of transmission electron microscopy of the lungs of patients who died due to severe COVID-19 coronavirus infection, pronounced dyscirculatory changes were found in the vessels of the microcirculatory bed, characterized by the development of hyperemia, stasis, and microthrombosis with pronounced degenerative, necrotic changes in the endothelium and the development of endotheliitis.

Introduction. Worldwide, more than 182 million cases of COVID-19 and more than 3.9 million deaths have been confi rmed since the virus was fi rst identifi ed. Advanced age and some comorbid conditions, such as diabetes and cardiovascular diseases, are considered risk factors for the adverse course of the discussed pathology. In recent years, several reports have been published about the results of the pathological examination of patients with COVID-19. Most often, in fatal cases, diff use alveolar damage is described, which is characterized by intraalveolar edema, the appearance of “hyaline” membranes and the proliferation of pneumocytes and fi broblasts. However, the nature of the damage caused by SARS-CoV-2 remains unclear. The study of pathomorphological changes in severe fatal cases of COVID-19 is important for a better understanding of pathogenetic mechanisms of the development of pulmonary complications and the development of new eff ective methods of antiviral treatment. The aim of the current study is to evaluate the gross and microscopic fi ndings in COVID-19 patients’ autopsy to investigate the clinicopathologic basis for adverse outcomes with a fatal course of the disease. Methods. A retrospective analysis of 1036 consecutive autopsies associated with COVID-19 in 2020 was conducted based on Lviv Regional Offi ce for Autopsy and Lviv Railway Clinical Hospital. The diagnosis of COVID-19 was confi rmed by clinical signs of viral pneumonia, nasopharyngeal smear analysis, and radiological changes. A statistical study was performed with IBM SPSS Statistics 24.0. Results. The majority (72.4%) were elderly (60+) males (54.1±1.5%) and females (45.9±1.5%), with an age range from 19 to 93 years (mean age 66.9 ± 0.4 years). All examined patients had pneumonia, which was detected during a clinical examination with CT diagnosis and confi rmed at autopsy. The acute exudative phase of pneumonia was diagnosed in 18.5±1.2% of cases, proliferative phase – in 18.5±1.2%, and fi brotic phase – in 5.9±0.7%. And in 53.5±1.5% of cases, signs of progressive fi brosis associated with exudative lesions prevailed. COVID-19 was the single original cause of death in 88.7±1.0% of cases. The following were identifi ed in the lungs: typical virus-induced changes in epithelial cells of the trachea, bronchi, bronchioles and alveoli (100%, n=1036); diff erent phases of diff use alveolar damage in the majority of cases (96.5±0.6%); manifestations of innate immunity were described; pathological changes in the microvasculature (large vessel thrombi were detected in 37.9±1.5%). Conclusion. Our study results prove the importance of pathological examination of tissues during autopsies to determine the pathophysiological mechanisms and underlying causes of death of patients with COVID-19. Keywords: COVID-19, SARS-CoV-2, diff use alveolar damage, vessel thrombi, elderly males.