Thrombosis in patients with coronavirus disease 2019 (Covid-19) is driven by complex interactions between immune, complement, fibrinolytic, endothelial, and coagulation systems.1 In addition to venous thromboembolism (VTE), microthrombi have also been implicated in contributing to end-organ damage, such as acute respiratory distress syndrome and kidney dysfunction, as well as to overall mortality.1 As available therapies, variants, and vaccines have evolved, so have reported rates of VTE attributable to Covid-19.