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Original research article
Use of oral anticoagulants in combination with antiplatelet(s) in atrial fibrillation
  1. Caroline Sindet-Pedersen1,2,3,
  2. Laila Staerk1,2,
  3. Morten Lamberts1,
  4. Thomas Alexander Gerds4,5,
  5. Jeffrey S Berger3,
  6. Anders Nissen Bonde1,2,
  7. Jannik Langtved Pallisgaard1,2,
  8. Morten Lock Hansen1,
  9. Christian Torp-Pedersen1,6,
  10. Gunnar H Gislason1,2,4,7,
  11. Jonas Bjerring Olesen1
  1. 1 Department of Cardiology, Copenhagen University Hospital Herlev and Gentofte, Hellerup, Denmark
  2. 2 Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
  3. 3 School of Medicine, New York University, New York, New York, USA
  4. 4 Department of Research, Danish Heart Foundation, Copenhagen, Denmark
  5. 5 Department of Public Health, Section of Biostatistics, University of Copenhagen, Copenhagen, Denmark
  6. 6 Department of Health, Science and Technology, Department of Epidemiology/Biostatistics and Cardiology, Aalborg University and Hospital, Aalborg, Denmark
  7. 7 National Institute of Public Health, University of Southern Denmark, Odense, Denmark
  1. Correspondence to Caroline Sindet-Pedersen, Department of Cardiology, Copenhagen University Hospital Herlev and Gentofte, Hellerup, Denmark; carolinesindet{at}gmail.com

Abstract

Objectives To investigate temporal trends in the use of non-vitamin K oral anticoagulants (NOACs) and vitamin K antagonists (VKAs) in combination with aspirin and/or clopidogrel in patients with atrial fibrillation (AF) following acute myocardial infarction (MI) and/or percutaneous coronary intervention (PCI).

Methods Using Danish nationwide registries, all patients with AF who survived 30 days after discharge from MI and/or PCI between 22 August 2011 and 30 September 2016 were identified.

Results A total of 2946 patients were included in the study population, of whom 1967 (66.8%) patients were treated with VKA in combination with antiplatelet(s) (VKA+aspirin n=477, VKA+clopidogrel n=439, VKA+aspirin+clopidogrel n=1051) and 979 (33.2%) patients were treated with NOAC in combination with antiplatelet(s) (NOAC+aspirin n=252, NOAC+clopidogrel n=218, NOAC+aspirin+clopidogrel n=509). The overall study population had a median age of 76 years [IQR: 69–82] and consisted of 1995 (67.7%) men. Patients with MI as inclusion event accounted for 1613 patients (54.8%). Patients with high CHA2DS2-VASc score(congestive heart failure, hypertension, age ≥75 years (2 points), diabetes mellitus, history of stroke/transient ischemic attack/systemic thromboembolism (2 points), vascular disease, age 65-75 years, and female sex) accounted for 132 2814 (95.5%) of patients, and patients with high HAS-BLED score (hypertension, abnormal renal/liver function, history of stroke, history of bleeding, age >65 years, non-steroidal anti-inflammatory drug usages, or alcohol abuse, leaving out labile international normalized ratio (not available), and use of antiplatelets (exposure variable)) accounted for 934 (31.7%) of patients. There was an increase from 10% in 2011 to 52% in 2016 in the use of NOACs in combination with antiplatelet(s).

Conclusion From 2011 to 2016, the use of NOAC in combination with antiplatelet(s) increased in patients with AF following MI/PCI and exceeded the use of VKA in combination with antiplatelet(s) by 2016.

  • atrial fibrillation
  • acute myocardial infarction
  • percutaneous coronary intervention
  • drug monitoring

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Footnotes

  • Contributors All authors contributed significantly to the conception and design of the study, acquisition of data, or analysis and interpretation of the data. CS-P drafted the manuscript, and JBO, LS, ML, ANB, JSB, JLP, CT-P, MLH, TAG and GHG interpreted the data and critically revised the manuscript for intellectual content. All authors gave final approval of the version for publication.

  • Funding This work was supported by the Danish Council of Independent Research (grant no: 4183-00008). GHG is supported by an unrestricted clinical research scholarship from the Novo Nordisk Foundation. The sponsor had no influence on the study design, interpretation of results or the decision to submit the manuscript for publication.

  • Competing interests CS-P has nothing to declare. TAG has nothing to declare. LS has received funding for research from Boehringer Ingelheim. JLP has received funding for research from Boehringer Ingelheim and Bayer. CT-P declares research contracts with Bayer and Biotronic and speaker fees for Bayer and BMS. GHG has received funding for research from Boehringer Ingelheim, Pfizer, BMS, AstraZeneca and Bayer, and declares ownership of stocks in Lundbeck A/S, Novo Nordisk A/S and ALK Abello Pharmaceuticals. JBO has received speaker fees from Bristol-Myers Squibb, Boehringer Ingelheim, Bayer and AstraZeneca, previous funding for research from the Lundbeck Foundation, and current funding for research from the Bristol-Myers Squibb and the Capital Region of Denmark, Foundation for Health Research. ML has received speaker fees from Bristol-Meyer Squibb and Bayer. JSB has received research support from AstraZeneca and is a consultant for Merck, AstraZeneca and Janssen. ANB has nothing to declare. MLH has received speaker fees from Bristol-Meyer Squibb.

  • Ethics approval Retrospective registry-based studies do not require approval from the Research Ethics Committee System. The Danish Data Protection Agency had approved use of data for this study (ref no: 2007-58–0015/GEH-2014–012 I-Suite no: 02720.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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