Abstract
At the time of this writing, > 3 million cases of the SARS-CoV-2 virus-induced human disease, the Coronavirus disease 2019 (COVID-19), have been reported worldwide with > 210,000 deaths. Although the lungs are ‘‘ground zero’’ [1], the virus’s reach can extend to any organs including the heart and blood vessels, kidneys, gut and brain. Evidence of abnormal coagulation markers in COVID-19 appeared in early reports from China [2]. It includes elevated fibrinogen and D-dimers, minimal changes in PT, PTT and platelet count in early stages of infection, no antithrombin deficiency, coagulopathy being related to severity of illness, overt Disseminated Intravascular Coagulation (DIC; ISTH criteria) being an end-stage evolution in the most severe cases, mainly in non- survivors. Further studies evidenced elevated D-dimers on admission (> 1000 ng/mL) associated with increased mortality [3]. Then accumulating reports described a high incidence of venous thromboembolic events VTE, also of arterial events, in ICU patients. The COVID-19 associated coagulopathy (CAC) quickly became an issue of clinical management, hoping to limit deleterious clinical consequences and improve the prognosis.