Author + information
- Received March 23, 2018
- Revision received July 5, 2018
- Accepted July 9, 2018
- Published online October 1, 2018.
- Caroline Sindet-Pedersen, MSca,b,c,∗ (, )@uni_copenhagen,
- Morten Lamberts, MD, PhDa,d,
- Laila Staerk, MDa,b,
- Anders Nissen Bonde, MDa,b,
- Jeffrey S. Berger, MD, MSc,
- Jannik Langtved Pallisgaard, MD, PhDa,
- Morten Lock Hansen, MD, PhDa,
- Christian Torp-Pedersen, MD, DMSca,b,e,
- Gunnar H. Gislason, MD, PhDa,b,f,g and
- Jonas Bjerring Olesen, MD, PhDa
- aDepartment of Cardiology, Copenhagen University Hospital Herlev and Gentofte, Hellerup, Denmark
- bDepartment of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- cNew York University School of Medicine, New York, New York
- dDepartment of Cardiology, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark
- eDepartment of Health, Science and Technology, Aalborg University, and Department of Epidemiology/Biostatistics and Cardiology, Aalborg University Hospital, Aalborg, Denmark
- fThe National Institute of Public Health, University of Southern Denmark, Copenhagen, Denmark
- gThe Danish Heart Foundation, Copenhagen, Denmark
- ↵∗Address for correspondence:
Ms. Caroline Sindet-Pedersen, Department of Cardiology, Copenhagen University Hospital Herlev and Gentofte, Post 635, Kildegaardsvej 28, 2900 Hellerup, Denmark.
Background The optimal treatment strategy when combining antiplatelets with oral anticoagulants in patients with atrial fibrillation (AF) and myocardial infarction (MI) or undergoing percutaneous coronary intervention (PCI) is unknown.
Objectives The authors investigated the risk of bleeding, ischemic stroke, MI, and all-cause mortality associated with direct oral anticoagulants (DOACs) compared with vitamin K antagonists (VKAs) in combination with aspirin, clopidogrel, or both in patients with AF following MI and/or PCI.
Methods Danish nationwide registries were used to identify patients with AF who were admitted with a MI and/or underwent PCI, between August 2011 and June 2017, treated with OAC in combination with antiplatelet(s). Patients were followed for 12 months or until an outcome, study end, or death. Standardized absolute risks were estimated on the basis of outcome-specific Cox regression models adjusted for potential confounders. Average treatment effects were obtained as standardized absolute risk differences (ARD) in risks at 3 and 12 months using the g-formula.
Results Overall, 3,222 patients were included in the study population, of which 875 (27%) were treated with VKA+single antiplatelet therapy (SAPT), 595 (18%) were treated with DOAC+SAPT, 1,074 (33%) were treated with VKA+dual antiplatelet therapy (DAPT), and 678 (22%) were treated with DOAC+DAPT. At 3 months, there was a significant difference in the absolute risk of MI associated with DOAC+SAPT compared with VKA+SAPT (3-month ARD −1.53% (95% confidence interval: −3.08% to −0.11%), with no significant differences found regarding bleeding, ischemic stroke, and all-cause mortality. Compared with VKA+DAPT, DOAC+DAPT was associated with a significantly reduced risk of bleeding (3-month ARD −1.96%, 95% confidence interval: −3.46% to −0.88%), with no significant difference in the absolute risk of all-cause mortality, stroke, or MI.
Conclusions In a real-world population of AF patients with MI and/or after PCI, the authors found that DOAC in combination with DAPT was associated with a significantly decreased risk of bleeding and similar thromboembolic protection compared with VKA in combination with DAPT.
- atrial fibrillation
- direct oral anticoagulants
- myocardial infarction
- percutaneous intervention
- vitamin K antagonists
This work was supported by The Danish Counsel of Independent Research grant no. 4183-00008. Dr. Lamberts has received speaker fees from Bristol-Myers Squibb and Bayer. Dr. Staerk has received funding for research from Boehringer Ingelheim. Dr. Berger has received research support from AstraZeneca; and has been a consultant for Merck, AstraZeneca, and Janssen. Dr. Pallisgaard has received funding for research from Boehringer Ingelheim and Bayer. Dr. Lock Hansen has received speaker fees from Bristol-Myers Squibb, Boehringer Ingelheim, and Bayer. Dr. Torp-Pedersen has received research contracts from Bayer and Biotronic; and speaker fees from Bayer and Bristol-Myers Squibb. Dr. Gislason has received funding for research from Boehringer Ingelheim, Pfizer, Bristol-Myers Squibb, AstraZeneca, and Bayer; and has been a stockholder in Lundbeck A/S, Novo Nordisk A/S, and ALK Abello Pharmaceuticals. Dr. Olesen has received speaker fees from Bristol-Myers Squibb, Boehringer Ingelheim, Bayer, and AstraZeneca; and funding for research from the Lundbeck Foundation, Bristol-Myers Squibb, and the Capital Region of Denmark, Foundation for Health Research. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received March 23, 2018.
- Revision received July 5, 2018.
- Accepted July 9, 2018.
- 2018 American College of Cardiology Foundation
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