Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the  causal agent of coronavirus disease 2019 (COVID-19), in which  coagulation abnormalities and endothelial dysfunction play a key  pathogenic role. Tissue factor (TF) expression is triggered by  endothelial dysfunction. Activated factor VII-antithrombin (FVIIa-AT)  complex reflects indirectly FVIIa-TF interaction and has been proposed  as a potential biomarker of prothrombotic diathesis. FVIIa-AT plasma  concentration was measured in 40 patients (30 males and 10 females; 64.8  ± 12.3 years) admitted with SARS-CoV-2 pneumonia during the first  pandemic wave in Italy. Two sex- and age-matched cohorts without  COVID-19, with or without signs of systemic inflammation, were used to  compare FVIIa-AT data. The FVIIa-AT plasma levels in COVID-19 patients  were higher than those in non-COVID-19 subjects, either with or without  inflammation, while no difference was observed among non-COVID-19  subjects. The association between COVID-19 and FVIIa-AT levels remained  significant after adjustment for sex, age, C-reactive protein, renal  function, fibrinogen, prothrombin time and activated partial  thromboplastin time. Our results indicate that SARS-CoV-2 infection, at  least during the first pandemic wave, was characterized by high FVIIa-AT  levels, which may suggest an enhanced FVIIa-TF interaction in COVID-19,  potentially consistent with SARS-CoV-2-induced endotheliopathy.

Keywords: activated factor VII-antithrombin (FVIIa-AT); coagulation; coronavirus disease 2019 (COVID-19); severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2); tissue factor (TF).