"Bonded by one chain, related to one purpose": what is primary in the development of thrombotic complications in COVID-19 — mechanisms of inflammation or endothelium damage?

The ongoing COVID-19 pandemic has caused significant morbidity and mortality worldwide, as well as a profound impact on society. Among the nosologies that increase the risk of a severe course of COVID-19, coronary heart disease, chronic heart failure, cardiomyopathy. The main complications caused by coronavirus infection include thrombotic ones. Spike protein SARS-CoV-2 can interact directly with platelets and fibrin, causing blood hypercoagulation and obstructing blood flow. The presence of the spike protein in circulation leads to structural changes in fibrin, complement 3 and prothrombin, which can contribute to hypercoagulability in COVID-19 positive patients and cause a significant violation of fibrinolysis. Endothelial damage and systemic inflammation, being interrelated triggers of coagulopathy characteristic of COVID-19, trigger a cascade of reactions resulting in thrombotic complications against the background of endothelial dysfunction and hyperinflammation, which may be of clinical importance in the treatment of hypercoagulability in patients with COVID-19 (bibliography: 14 refs).