Abstract
The increased plasma levels of von Willebrand factor (VWF) in patients with COVID-19 was reported in many studies, and its correlation with disease severity and mortality suggest its important role in the pathogenesis of thrombosis in COVID-19. We performed histological and immunohistochemical studies of the lungs of 29 patients who died from COVID-19. We found a significant increase in the intensity of immunohistochemical reaction for VWF in the pulmonary vascular endothelium when the disease duration was more than 10 days. In the patients who had thrombotic complications, the VWF immunostaining in the pulmonary vascular endothelium was significantly more intense than in nonsurvivors without thrombotic complications. Duration of disease and thrombotic complications were found to be independent predictors of increased VWF immunostaining in the endothelium of pulmonary vessels. We also revealed that bacterial pneumonia was associated with increased VWF staining intensity in pulmonary arterial, arteriolar, and venular endothelium, while lung ventilation was an independent predictor of increased VWF immunostaining in arterial endothelium. The results of the study demonstrated an important role of endothelial VWF in the pathogenesis of thrombus formation in COVID-19.
Highlights
The novel coronavirus infection (COVID-19) pandemic caused by SARS-CoV-2, an RNA-containing virus of the family Coronaviridae, genus Betacoronavirus, has claimed more than 5 million lives to date [1]
We found that the lung morphological changes in COVID-19 did not correlate with the stages of acute respiratory distress syndrome (ARDS)
Fibrosis, which is not typical for the first stage of ARDS, was detected in 50% of the patients with a disease duration of less than 10 days, which may have been due to late hospitalization or a specific pattern of fibrosis development in COVID-19
Summary
The novel coronavirus infection (COVID-19) pandemic caused by SARS-CoV-2, an RNA-containing virus of the family Coronaviridae, genus Betacoronavirus, has claimed more than 5 million lives to date [1]. The predominantly respiratory clinical manifestations of COVID-19, morphological evidence of lung damage, and respiratory failure as the most frequent cause of death suggest that the lungs are the main target organ for the SARS-CoV-2 virus. Morphological study of internal organs of patients who died of COVID-19 shows damage and circulatory disturbances in the lungs (corresponding to acute respiratory distress syndrome) and other organs [2,3]. The reported complications of COVID-19 indicate the involvement of the hemostatic, central nervous, cardiovascular, and genitourinary systems in the disease mechanisms [4–7]. One of the possible mechanisms contributing to extrapulmonary complications in COVID19 is viremia, which has been identified in patients with severe infection in several studies [8,9]
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