We appreciate the interest shown by Kow et al. in our work.1 We fully agree with the comment that the lower cardiovascular risk profile in the cohort of patients with coronavirus disease 2019 (COVID-19), as well as the simultaneous thrombosis in different territories, supports the hypothesis of a systemic prothrombotic state in close relation to the inflammatory response associated with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)1,2.

Regarding the potential use of prophylactic antiplatelet therapy for its antithrombotic effect and perhaps even, as noted by the authors, its antiviral effect in patients with COVID-19, we recognize that this is an attractive proposal, but currently there is no clear clinical evidence of its usefulness in SARS-CoV-2 infection. There is no doubt about the importance of antiplatelet therapy in patients with arterial thrombotic complications, but its use in patients with high cardiovascular risk without established disease provides minimal benefit and an increased risk of bleeding complications.3 One might think that with COVID-19 this would be different due to the endothelial dysfunction and inflammatory response it causes, but we must avoid empiricism and not support its de novo use in patients with COVID-19 without a specific cardiovascular reason, except in research studies specifically designed to test its efficacy.

We also thank and congratulate Valga et al.4 for their recent publication on the role played by endothelial injury, complement, and coagulation in the pathogenesis of coronavirus disease. In our scientific letter,1 we focused exclusively on the 1.8% (n=38) of COVID-19 positive patients with arterial thrombotic complications treated at our hospital in March 2020. Although they had a higher score according to the International Society on Thrombosis and Haemostasis (ISTH) diagnostic criteria for disseminated intravascular coagulation (DIC), only 3 strictly met the diagnostic criteria. As other authors have noted,5 it is likely that patients with COVID-19 have a severe hypercoagulability, more so than a consumption coagulopathy, as is the case of classical DIC. Indeed, the pattern is different, as in patients with COVID-19, fibrinogen is characteristically elevated and thrombocytopenia is uncommon, and if it occurs, it is usually mild or moderate. We agree with the hypothesis of Valga et al. of multiple interactions between the immune system, coagulation (immunothrombosis), and associated endothelial dysfunction as a response to SARS-CoV-2 to explain the prothrombotic state of coronavirus disease.