Inflammation and endothelial toxicity: pathogenetic aspects of central nervous system damage due to novel coronavirus disease

Introduction. There are inconsistent data on the incidence of stroke in patients with COVID-19, including acute cerebrovascular accidents in younger people without obligate risk factors, as well as the risk of SARS-CoV-2 infection in patients with acute stroke.

The aim of the study was to evaluate the features of concomitant stroke and COVID-19, and the role of inflammation and endothelial toxicity in cerebral damage.

Materials and methods. The study included 1,524 patients admitted to vascular clinics across St. Petersburg in 2020–2021, including 1,068 people with confirmed COVID-19 infection and 551 death cases. The patients were divided into four groups depending on disease severity, for clinical and laboratory data analysis.

Results. There were marked changes in the laboratory markers of inflammation, haemostasis, fibrinolysis, cytolysis, iron metabolism, cerebral ischaemia, proteolysis, immunodeficiency (lymphocytopenia, monocytopenia, elevated white blood cell count, elevated levels of C-reactive protein, fibrinogen, D-dimer, creatine kinase, ferritin and neutrophil elastase), with statistically significant differences when compared with patients without COVID-19. Changes in inflammatory markers in the first 24–72 hours provided the most information. A multifold increase (escalation) in the marker values was always correlated with an imminent adverse outcome and was usually accompanied by subsequent laboratory confirmation of COVID-19 infection or specific signs of viral pneumonia.

Conclusion. COVID-19 should be considered an independent risk factor for acute stroke, while the virus-induced thrombosis, manifesting in an escalation in inflammatory factors and products of endothelial damage, should be considered a pathogenetic link leading to cerebral tissue damage.