COVID-19-associated coagulopathy and immuno-thrombosis

The global pandemic Coronavirus disease 2019 (COVID-19) is caused by a novel highly virulent beta-coronavirus SARS-CoV-2. The infection SARS-CoV-2 is associated with a broad spectrum of clinical syndromes, ranging from mild upper respiratory infection to life-threatening cardiovascular complications in humans. COVID-19-associated coagulopathy, endotelitis and immune-thrombosis are typical examples that thrombosis and inflammation mutually reinforce each other. Among the basic features of the COVID-19 disease are the endothelial vascular changes affecting the whole vascular system and leading to micro-thrombosis, mainly localized in the pulmonary microcirculation. The anticoagulants are gold stone of the therapy also for its increased anti-inflammatory and endothelial protective activity. Patients with COVID-19 are at increased risk of venous thromboembolism, and therefore pharmacologic prophylaxis with use of low-molecular-weight heparin, or fondaparinux is recommended not only when hospitalized but also after discharge for up to 45 days in patients at high risk for VTE and low risk of bleeding, independently of the patient recovering mobility. For hospitalized COVID-19 patients with proximal deep vein thrombosis or pulmonary embolism, standard initial parenteral anticoagulation with therapeutic weight adjusted doses is suggested. In general, a one-size-fits-all strategy cannot be applied to COVID-19 patients. These patients need an individualized approach carefully balancing thrombotic and hemorrhagic risk. Further research is required to provide better knowledge of the pathogenesis of COVID-19, more precisely targeted treatment and the correct timing of thromboprophylaxis for this vascular disease.