Abstract
Thrombotic complications in covid-19 patients affect the vessels of the lungs, limbs, spleen, heart, brain and/or kidneys (1). These complications are typically associated with multiple organ failure and a high mortality rate.
Pulmonary embolism and deep vein thrombosis are the most frequent thrombotic events in covid-19 (1). The risk of venous thromboembolism remains high in hospitalized patients in spite of anticoagulation prophylaxis.
Cytokines, protein proinflammatory mediators serving as a key signalling pathway, are responsible for a shift of endothelial function from homeostatic to defensive mode. A critical covid-19 stage usually involves a cytokine storm, a previously well-described positive feedback which controls cytokine production and overwhelms antiregulatory mechanisms.
Studies of covid-19 patients have shown elevated levels of blood neutrophils and neutrophil extracellular traps (NETs). The failure of anticoagulants in preventing and treating thrombotic complications of covid-19 is explained by an impossibility to inhibit the effect of inflammatory cytokines on the endothelium by influencing the development of NETs.