Inhibitory mechanisms of very low–dose rivaroxaban in non–ST-elevation myocardial infarction

Author:

Borst Oliver1,Münzer Patrick1,Alnaggar Nada2,Geue Sascha1,Tegtmeyer Roland1,Rath Dominik1,Droppa Michal1,Seizer Peter1,Heitmeier Stefan3,Heemskerk Johan W. M.4,Jennings Lisa K.56789,Storey Robert F.10,Angiolillo Dominick J.11,Rocca Bianca12,Spronk Henri413,Ten Cate Hugo41314,Gawaz Meinrad1,Geisler Tobias1

Affiliation:

1. Department of Cardiology and Cardiovascular Medicine, University of Tübingen, Tübingen, Germany;

2. Department of Cardiology, University Hospital Lübeck, Lübeck, Germany;

3. Bayer AG, Wuppertal, Germany;

4. Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands;

5. The Vascular Biology Center of Excellence,

6. Department of Internal Medicine,

7. Department of Microbiology, Immunology, and Biochemistry, and

8. Department of Surgery, University of Tennessee Health Science Center, Memphis, TN;

9. Joint Program of Biomedical Engineering, University of Tennessee Health Science Center and University of Memphis, Memphis, TN;

10. Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom;

11. Division of Cardiology, University of Florida College of Medicine–Jacksonville, Jacksonville, FL;

12. Institute of Pharmacology, Catholic University School of Medicine, Rome, Italy;

13. Department of Internal Medicine, Maastricht University Medical Center, Maastricht, The Netherlands; and

14. Center for Thrombosis and Haemostasis, Gutenberg University Medical Center, Mainz, Germany

Abstract

Key Points VLD rivaroxaban significantly reduces platelet-dependent thrombin generation and thrombus formation on top of DAPT in patients with ACS. Adjunctive treatment with VLD rivaroxaban additionally reduced TG and thrombus formation in both clopidogrel responders and nonresponders.

Publisher

American Society of Hematology

Subject

Hematology

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