Apixaban enhances endogenous fibrinolysis in patients with atrial fibrillation.


Journal

Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology
ISSN: 1532-2092
Titre abrégé: Europace
Pays: England
ID NLM: 100883649

Informations de publication

Date de publication:
01 Sep 2019
Historique:
received: 18 04 2019
accepted: 30 05 2019
entrez: 11 9 2019
pubmed: 11 9 2019
medline: 15 12 2020
Statut: ppublish

Résumé

Approximately 20% of ischaemic stroke patients exhibit spontaneous arterial recanalization, attributable to endogenous fibrinolysis, which strongly relates to improved functional outcome. The impact of oral anticoagulants on endogenous fibrinolysis is unknown. Our aim was to test the hypothesis that apixaban enhances endogenous fibrinolysis in non-valvular atrial fibrillation (NVAF). In a prospective cross-sectional analysis, we compared endogenous fibrinolysis in NVAF patients (n = 180) taking aspirin, warfarin, or apixaban. In a prospective longitudinal study, patients were tested before and after apixaban (n = 80). Endogenous fibrinolysis was assessed using the Global Thrombosis Test (GTT) and thromboelastography (TEG). Endogenous fibrinolysis [measured by GTT lysis time (LT)] was shorter on apixaban compared with warfarin or aspirin [median 1850 (IQR 1591-2300) vs. 2758 (2014-3502) vs. 2135 (1752-2463) s, P < 0.0001]. Among TEG indices, a small but significant difference in clot lysis time (CLT) was observed [apixaban 60.0 (45.0-61.0) vs. warfarin 61.0 (57.0-62.0) vs. aspirin 61.0 (59.0-61.0) min, P = 0.036]. Apixaban improved endogenous fibrinolysis measured using the GTT [LT pre-treatment 2204 (1779-2738) vs. on-treatment 1882 (1607-2374) s, P = 0.0003], but not by using TEG. Change in LT (ΔLT) with apixaban correlated with baseline LT (r = 0.77, P < 0.0001). There was weak correlation between ΔLT and ΔCLT in response to apixaban (r = 0.28, P = 0.02) and between on-apixaban LT and CLT (r = 0.25, P = 0.022). Apixaban enhances endogenous fibrinolysis, with maximal effect in those with impaired fibrinolysis pre-treatment. Apixaban-treated patients exhibit more favourable fibrinolysis profiles than those taking warfarin or aspirin. Whether apixaban may confer additional thrombotic risk reduction in NVAF patients with impaired fibrinolysis, compared to warfarin, merits further study.

Identifiants

pubmed: 31505618
pii: 5522956
doi: 10.1093/europace/euz176
pmc: PMC6735819
doi:

Substances chimiques

Anticoagulants 0
Factor Xa Inhibitors 0
Platelet Aggregation Inhibitors 0
Pyrazoles 0
Pyridones 0
apixaban 3Z9Y7UWC1J
Warfarin 5Q7ZVV76EI
Aspirin R16CO5Y76E

Types de publication

Journal Article Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

1297-1306

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Cardiology.

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Auteurs

Nikolaos Spinthakis (N)

School of Life and Medical Sciences, Postgraduate Medical School, University of Hertfordshire, Hertfordshire, UK.
Department of Cardiology, East and North Hertfordshire NHS Trust, Hertfordshire, UK.

Ying Gue (Y)

School of Life and Medical Sciences, Postgraduate Medical School, University of Hertfordshire, Hertfordshire, UK.
Department of Cardiology, East and North Hertfordshire NHS Trust, Hertfordshire, UK.

Mohamed Farag (M)

School of Life and Medical Sciences, Postgraduate Medical School, University of Hertfordshire, Hertfordshire, UK.
Department of Cardiology, East and North Hertfordshire NHS Trust, Hertfordshire, UK.

Manivannan Srinivasan (M)

Department of Cardiology, East and North Hertfordshire NHS Trust, Hertfordshire, UK.

David Wellsted (D)

School of Life and Medical Sciences, Postgraduate Medical School, University of Hertfordshire, Hertfordshire, UK.

Deepa R J Arachchillage (DRJ)

Department of Haematology, Royal Brompton Hospital, London, UK.
Department of Haematology, Imperial College Healthcare NHS Trust, London, UK.

Gregory Y H Lip (GYH)

Liverpool Centre for Cardiovascular Science, University of Liverpool, Liverpool Heart & Chest Hospital, Liverpool, UK.
Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Aalborg University, Aalborg, Denmark.

Diana A Gorog (DA)

School of Life and Medical Sciences, Postgraduate Medical School, University of Hertfordshire, Hertfordshire, UK.
Department of Cardiology, East and North Hertfordshire NHS Trust, Hertfordshire, UK.
Faculty of Medicine, National Heart & Lung Institute, Imperial College, Dovehouse Street, London, London, UK.

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