Szczegóły publikacji

Opis bibliograficzny

Elevated factor VIIa—antithrombin complexes are associated with stroke or cardiovascular death in patients with atrial fibrillation / Elżbieta Szczygieł-Pilut, Michał Błaż, Elżbieta POCIASK, Elżbieta Paszek, Anetta Undas // European Journal of Clinical Investigation [Dokument elektroniczny]. - Czasopismo elektroniczne ; ISSN  1365-2362 . — 2025 — vol. 55 iss. 12 art. no. e70091, s. 1–12. — Wymagania systemowe: Adobe Reader. — Bibliogr. s. 11–12, Abstr. — Publikacja dostępna online od: 2025-06-19

Autorzy (5)

Słowa kluczowe

cardiovascular deathatrial fibrillationischemic strokeFVIIa AT complexes

Dane bibliometryczne

ID BaDAP164757
Data dodania do BaDAP2025-12-17
Tekst źródłowyURL
DOI10.1111/eci.70091
Rok publikacji2025
Typ publikacjiartykuł w czasopiśmie
Otwarty dostęptak
Czasopismo/seriaEuropean Journal of Clinical Investigation

Abstract

Background Atrial fibrillation (AF) is associated with a prothrombotic state. We investigated whether factor VIIa-antithrombin (FVIIa-AT) complexes, a marker of tissue factor (TF) exposure, are associated with thromboembolic events in AF. Methods In 224 nonvalvular AF patients (66% men, median age 69 years, median CHA2DS2VASc score 4), 71% on direct oral anticoagulants, we measured FVIIa-AT complexes, along with endogenous thrombin potential (ETP), von Willebrand factor (VWF) and 8-isoprostane, reflecting oxidative stress. During a median follow-up of 53 [interquartile range, IQR 47–57] months, we recorded a composite endpoint: ischemic stroke, systemic thromboembolism or cardiovascular (CV) death. Results FVIIa-AT complexes (median 145 [IQR 125–170] pM) were higher in patients with permanent AF (p < .001), vascular disease (p = .02), previous stroke (p < .001) and smoking (p = .006) as compared with patients without these comorbidities. FVIIa-AT correlated with NT-proBNP (r = .15, p = .022) and ETP (r = .25, p < .001). During follow-up, the composite endpoint was recorded in 30 patients (13.4%, 3.0% per year) including 20 with ischemic stroke (8.9%, 2.0% per year, respectively). Patients with the composite endpoint had 29.2% higher baseline FVIIa-AT complexes compared with the remainder. Patients with FVIIa-AT complexes in the top quartile (>170 pM) had an increased risk of the composite endpoint (HR 12.0, 95% CI 5.2–28.0, p < .0001). FVIIa-AT complexes, along with VWF, remained independently associated with the composite endpoint. Conclusions This study is the first to show that high plasma FVIIa-AT complexes are independently associated with thromboembolic events or CV death in AF, suggesting the need for more potent anticoagulation to suppress the residual TF-mediated coagulation.

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