COVID-19, caused by SARS-CoV-2, can trigger endothelial injury and immunothrombosis, an inflammatory process involving activation of the endothelium, platelets, and procoagulant factors such as von Willebrand factor (vWF). This factor acts in platelet adhesion and tissue remodeling. Understanding tissue expression of vWF in the lungs of patients with COVID-19 may help predict clinical outcomes, given the limited number of studies on its reduced tissue levels in the disease. The aim of this study is to evaluate pulmonary immunoexpression of vWF and histopathological findings in patients with COVID-19, comparing them with a control group. Case-control study conducted in a large hospital in Curitiba and in an experimental pathology laboratory. Between April and August 2020, 24 post-mortem lung samples were collected from patients with COVID-19, older than 18 years, with diagnosis confirmed by molecular/immunological tests, and post-mortem time shorter than 4 hours. The control group included 11 samples from patients who died from cardiovascular causes or non-pulmonary neoplasms. Samples were fixed, stained with hematoxylin-eosin, and submitted to immunohistochemistry for vWF. Images were obtained from 30 high-power fields per slide and analyzed blindly. Quantification of immunoexpression was performed using Image Pro-Plus 4.5 software, converted to percentage per HPF, and submitted to statistical analysis. The COVID-19 group had a higher mean age (71.96 ± 12.5 vs. 42.31 ± 4.4; p < 0.001) and longer hospitalization time (15.87 ± 10.2 vs. 7.6 ± 13.1; p < 0.003). Median vWF immunoexpression was significantly lower in the COVID-19 group (2.02) compared with the control group (4.41) (p < 0.048). There was a greater presence of microthrombosis in the COVID-19 group (83.33% vs. 9%; p < 0.001) and endothelial activation (100% vs. 54.55%; p < 0.001). Reduced pulmonary tissue immunoexpression of vWF was observed in patients with COVID-19, associated with significant microthrombosis and endothelial activation. These findings reinforce the importance of immunothrombosis in the pathophysiology of the disease and suggest that such alterations may be predictive factors for unfavorable clinical outcomes.
Valerio et al. (Sun,) studied this question.