%0 Journal Article
%T High Plasma Levels of Activated Factor VII-Antithrombin Complex Point to Increased Tissue Factor Expression in Patients with SARS-CoV-2 Pneumonia: A Potential Link with COVID-19 Prothrombotic Diathesis.
%A Martinelli N
%A Rigoni AM
%A De Marchi S
%A Osti N
%A Donini M
%A Montagnana M
%A Castagna A
%A Pattini P
%A Udali S
%A De Franceschi L
%A Tinazzi E
%A Mazzi F
%A Moruzzi S
%A Argentino G
%A Delfino L
%A Sartori G
%A Azzini AM
%A Tacconelli E
%A Van Dreden P
%A Lippi G
%A Girelli D
%A Olivieri O
%A Friso S
%A Pizzolo F
%J Diagnostics (Basel)
%V 12
%N 11
%D Nov 2022 14
%M 36428852
%F 3.992
%R 10.3390/diagnostics12112792
%X 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.