Elias Kyriakou1, Ignatios Ikonomidis2, Dimitrios Stylos1, Stefanos Bonovas3, Ioannis Papadakis2, Georgios K Nikolopoulos4, Styliani Kokoris1, Dimitrios Kalantzis1, Christine Economopoulou1, Petros Kopterides5, John Lekakis2, Argirios E Tsantes6. 1. Laboratory of Haematology & Blood Bank Unit, "Attiko" University Hospital, School of Medicine, University of Athens, Athens, Greece. 2. Second Cardiology Department, "Attiko" University Hospital, School of Medicine, University of Athens, Athens, Greece. 3. Department of Pharmacology, School of Medicine, University of Athens, Athens, Greece. 4. National Development and Research Institutes, Inc, New York, NY, USA Hellenic Centre for Diseases Control and Prevention, Athens, Greece. 5. Second Department of Critical Care Medicine, "Attiko" University Hospital, School of Medicine, University of Athens, Athens, Greece. 6. Laboratory of Haematology & Blood Bank Unit, "Attiko" University Hospital, School of Medicine, University of Athens, Athens, Greece atsantes@yahoo.com.
Abstract
BACKGROUND: Our aim was to identify laboratory assays in order to assess the anticoagulant effects of dabigatran etexilate (DE). METHODS: Twenty patients with nonvalvular atrial fibrillation treated on DE (110 mg per os twice daily) and 20 on acenocoumarol were studied. Conventional coagulation tests, endogenous thrombin potential (ETP), thromboelastometry (ROTEM), epinephrine-induced light transmission aggregometry (LTA), and Hemoclot Thrombin Inhibitors (HTI) were performed in all patients. RESULTS: In ROTEM analysis, the lysis index at 60 minutes was significantly lower in patients receiving DE (P = .011). In LTA, patients on DE showed decreased aggregation compared to those on acenocoumarol, marginally insignificant (P = .068). Regarding ETP, acenocoumarol affected thrombin generation more than dabigatran (area under the curve [AUC], P < .001), while statistically significant associations were detected between dabigatran levels, as determined by the HTI assay, and almost all parameters of ETP assay (AUC, P < .001). CONCLUSION: The role of ETP in estimating anticoagulant activity of dabigatran possibly requires further research.
BACKGROUND: Our aim was to identify laboratory assays in order to assess the anticoagulant effects of dabigatran etexilate (DE). METHODS: Twenty patients with nonvalvular atrial fibrillation treated on DE (110 mg per os twice daily) and 20 on acenocoumarol were studied. Conventional coagulation tests, endogenous thrombin potential (ETP), thromboelastometry (ROTEM), epinephrine-induced light transmission aggregometry (LTA), and Hemoclot Thrombin Inhibitors (HTI) were performed in all patients. RESULTS: In ROTEM analysis, the lysis index at 60 minutes was significantly lower in patients receiving DE (P = .011). In LTA, patients on DE showed decreased aggregation compared to those on acenocoumarol, marginally insignificant (P = .068). Regarding ETP, acenocoumarol affected thrombin generation more than dabigatran (area under the curve [AUC], P < .001), while statistically significant associations were detected between dabigatran levels, as determined by the HTI assay, and almost all parameters of ETP assay (AUC, P < .001). CONCLUSION: The role of ETP in estimating anticoagulant activity of dabigatran possibly requires further research.
Authors: Irina V Gribkova; Elena N Lipets; Irina G Rekhtina; Alex I Bernakevich; Dorzho B Ayusheev; Ruzanna A Ovsepyan; Fazoil I Ataullakhanov; Elena I Sinauridze Journal: Sci Rep Date: 2016-07-05 Impact factor: 4.379