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Cessation of non-vitamin K antagonist oral anticoagulants in patients with atrial fibrillation
  1. Melissa E Middeldorp1,2,
  2. Aashray Gupta1,2,
  3. Adrian Elliott1,
  4. Kadhim Kadhim1,2,
  5. Anand Thiyagarajah1,2,
  6. Celine Gallagher1,2,
  7. Jeroen Hendriks2,3,
  8. Dominik Linz1,2,
  9. Mehrdad Emami1,2,
  10. Rajiv Mahajan1,
  11. Dennis Lau1,2,
  12. Prashanthan Sanders1,2
  1. 1Centre for Heart Rhythm Disorders (CHRD), University of Adelaide, Adelaide, South Australia, Australia
  2. 2Royal Adelaide Hospital, Adelaide, South Australia, Australia
  3. 3College of Nursing and Health Sciences, Flinders University, Adelaide, South Australia, Australia
  1. Correspondence to Professor Prashanthan Sanders, Centre for Heart Rhythm Disorders, University of Adelaide CHRD, Adelaide, SA 5000, Australia; prash.sanders{at}adelaide.edu.au

Abstract

Objective To characterise the rate, causes and predictors of cessation of non-vitamin K antagonist oral anticoagulants (NOACs) in patients with atrial fibrillation (AF).

Patients and methods Consecutive patients with AF with a long-term anticoagulation indication treated with NOACs (dabigatran, apixaban and rivaroxaban) in our centre from September 2010 through December 2016 were included. Prospectively collected data with baseline characteristics, causes of cessation, mean duration-to-cessation and predictors of cessation were analysed.

Results The study comprised 1415 consecutive patients with AF, of whom 439 had a CHA2DS2-VASc≥1 and were on a NOAC. Mean age was 71.9±8.7 years and 37% were females. Over a median follow-up of 3.6 years (IQR=2.7–5.3), 147 (33.5%) patients ceased their index-NOAC (113 switched to a different form of OAC), at a rate of 8.8 per 100 patient-years. Serious adverse events warranting NOAC cessation occurred in 28 patients (6.4%) at a rate of 1.6 events per 100 patient-years. The mean duration-to-cessation was 4.9 years (95% CI 4.6 to 5.1) and apixaban had the longest duration-to-cessation with (5.1, 95% CI 4.8 to 5.4) years, compared with dabigatran (4.6, 95% CI 4.2 to 4.9) and rivaroxaban (4.5, 95% CI 3.9 to 5.1), pairwise log-rank p=0.002 and 0.025, respectively. In multivariable analyses, age was an independent predictor of index-NOAC cessation (HR 1.03, 95% CI 1.01 to 1.05; p=0.006). Female gender (HR 2.2, 95% CI 1.04 to 4.64; p=0.04) independently predicted serious adverse events.

Conclusion In this ‘real world’ cohort, NOAC use is safe and well-tolerated when prescribed in an integrated care clinic. Whether apixaban is better tolerated compared with other NOACs warrants further study.

  • atrial fibrillation
  • pharmacology
  • stroke
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Footnotes

  • Twitter @Kadhimad, @Rajiv_EP, @PrashSanders

  • Contributors MEM, AG, AE, KK and PS had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: MEM, DL and PS. Drafting of the manuscript: MEM, KK and PS. Critical review of the manuscript for intellectual content: MEM, AG, AE, KK, AT, CG, JH, DL, ME, RM, DL and PS.

  • Funding This study was supported by the Centre for Heart Rhythm Disorders at the University of Adelaide, Adelaide, Australia.

  • Competing interests MEM is supported by a Postgraduate Scholarship from the National Health and Medical Research Council of Australia and the Robert J. Craig Scholarship from the University of Adelaide. AE is supported by an Early Career Fellowship from the National Heart Foundation of Australia. CG is supported by the Leo J. Mahar Cardiovascular Nursing Scholarship from the University of Adelaide. JH is supported by an Early Career Fellowship from the National Heart Foundation of Australia and the Derek Frewin Lectureship from the University of Adelaide. DL is supported by the Beacon Research Fellowship from the University of Adelaide. KK is supported by the Leo J. Mahar Scholarship from the University of Adelaide. ME is supported by the Jitendra K Vohra Electrophysiology Scholarship from the University of Adelaide. RM is supported by a Health Professional Fellowship co-funded by the National Health and Medical Research Council of Australia and the National Heart Foundation of Australia, and by the Leo J. Mahar Lectureship from the University of Adelaide. DL is supported by the Robert J. Craig Lectureship from the University of Adelaide. PS is supported by Practitioner Fellowships from the National Health and Medical Research Council of Australia and by the National Heart Foundation of Australia. JH reports that the University of Adelaide has received on his behalf lecture and/or consulting fees from Medtronic and Pfizer/BMS. DL reports having received lecture fees and research funding from Medtronic, ResMed, Sorin, Sanofi-Aventis and Pfizer. RM reports that the University of Adelaide has received on his behalf lecture fees and research funding from Medtronic and St Jude Medical. PS reports having served on the advisory board of Medtronic, St Jude Medical, Boston-Scientific and CathRx. PS reports that the University of Adelaide has received on his behalf lecture and/or consulting fees from Medtronic, St Jude Medical, Boston Scientific and Pfizer. PS reports that the University of Adelaide has received on his behalf research funding from Medtronic, St Jude Medical, Boston Scientific, Biotronik and Sorin.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Ethics approval The study was approved by the Human Research Ethics Committee of the University of Adelaide and Royal Adelaide Hospital.

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

  • Data availability statement Data are available on reasonable request. Data used in this study may be made available on request to the PI (prash.sanders@adelaide.edu.au) pending acceptance of the proposal by the steering committee.

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