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Clinical research

A randomised study of dabigatran in elective percutaneous coronary intervention in stable coronary artery disease patients

1. Department of Cardiac Intensive Care & Interventional Cardiology, Hartcentrum, Hasselt, Belgium; 2. Cardialysis, Clinical Research Management & Core Laboratories, Rotterdam, The Netherlands; 3. Department of Cardiology, Onze Lieve Vrouw Gasthuis, Amsterdam, The Netherlands; 4. Department of Haematology, Erasmus University Medical Center, Rotterdam, The Netherlands; 5. Department of Cardiology, Medical Center Alkmaar, Alkmaar, The Netherlands; 6. Department of Interventional Cardiology, Erasmus University Medical Center, Rotterdam, The Netherlands; 7. Department of Interventional Cardiology, Maasstadziekenhuis, location Zuider, Rotterdam, The Netherlands; 8. Department of Cardiology. Antonius Hospital, Nieuwegein, The Netherlands; 9. TSTAT Boehringer Ingelheim Limited, Bracknell, United Kingdom; 10. Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, CT, USA

Aims: Patients receiving long-term anticoagulant treatment with dabigatran may need to undergo a percutaneous coronary intervention (PCI). We studied markers of coagulation activation during elective PCI in patients using dabigatran in order to investigate whether coagulation activation upon balloon inflation and stenting is suppressed by dabigatran without additional heparin treatment.

Methods and results: This phase IIa, exploratory, multicentre, randomised, open-label study included 50 stable patients having an elective PCI. Patients on standard dual antiplatelet therapy (DAPT) were randomised (2:2:1) to either pre-procedural dabigatran 110 mg BID (n=19) or 150 mg BID (n=21), as compared to standard intraprocedural unfractionated heparin (UFH) (n=10). Following PCI, a significant increase in the levels of prothrombin fragment 1+2 (F1+2) in the combined dabigatran group was observed compared to the level just before the start of PCI (159.1 [1.4] pmol/l; geometric mean [gSD]). Levels at 0.5, 1.0, 1.5 and 2 hrs after the start of PCI ranged from 193.5 (1.4) to 270.6 pmol/l (1.7); (p-value for paired analysis=0.015, 0.022, 0.2342, 0.0379, respectively). Also, thrombin-antithrombin (TAT) complexes were increased significantly in the combined dabigatran group compared to pre-PCI levels (4.2 [2.2] ug/l). Levels ranged from 5.2 (2.5) to 8.5 (2.3) (p=0.0497, 0.0343, 0.005 and 0.1628, respectively). In contrast, in the control group of patients treated with UFH, no increase was observed in F1+2 and TAT complexes during PCI. Five out of 40 (12.5%) patients required bail-out anticoagulation in the dabigatran group, of whom four experienced a procedural myocardial infarction (MI), versus one out of 10 in the UFH group, who had a stent thrombosis without MI prior to the study-PCI. One minor access-site bleeding occurred in the dabigatran group.

Conclusions: Dabigatran treatment (110 mg or 150 mg BID) may not provide sufficient anticoagulation during PCI. ClinicalTrials.gov Identifier: NCT00818753 EudraCT. No: 2007-007536-25.

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