Interv Akut Kardiol. 2021;20(2):98-101 | DOI: 10.36290/kar.2021.028
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.
Published: July 9, 2021 Show citation
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to original source...