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Am J Med. 2014 Apr;127(4):329-336.e4. doi: 10.1016/j.amjmed.2013.12.005. Epub 2013 Dec 19.

Myocardial ischemic events in 'real world' patients with atrial fibrillation treated with dabigatran or warfarin.

Author information

1
Department of Cardiology, Aalborg AF Study Group, Aalborg University Hospital, Aalborg, Denmark; Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Faculty of Health, Aalborg University, Aalborg, Denmark.
2
Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Faculty of Health, Aalborg University, Aalborg, Denmark.
3
Division of Pharmacovigilance and Medical Devices, Danish Health and Medicines Authority, Copenhagen, Denmark.
4
Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Faculty of Health, Aalborg University, Aalborg, Denmark; University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, United Kingdom.
5
Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Faculty of Health, Aalborg University, Aalborg, Denmark; University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, United Kingdom. Electronic address: g.y.h.lip@bham.ac.uk.

Abstract

BACKGROUND:

Dabigatran may provide less protection against myocardial infarction than vitamin K antagonists (VKAs) in patients with atrial fibrillation. This may be particularly evident among "switchers" to dabigatran from VKA, as a result of discontinuation effects.

METHODS AND RESULTS:

We identified in nationwide Danish registries a cohort of VKA-naïve "new starters" on dabigatran (110 mg twice daily [bid] and 150 mg bid dose regimes) or warfarin, and a cohort of prior VKA-experienced "switchers" to dabigatran or "continuers" on warfarin. Cohorts were followed for an average of 16.0 months. Adjusted Cox regression models were used to compare event rates. Relative to warfarin, there was a nonsignificant trend to lower myocardial infarction rates with dabigatran among VKA-naïve users (110 mg hazard ratio [HR] 0.71; 95% confidence interval [CI], 0.47-1.07; 150 mg HR 0.94; 95% CI, 0.62-1.41); however, there was a nonsignificant trend to increased myocardial infarction rates among prior VKA-experienced users (110 mg HR 1.45; 95% CI, 0.98-2.15; 150 mg HR 1.30; 95% CI 0.84-2.01). An increased myocardial infarction rate relative to warfarin among prior VKA-experienced users was clearly significant during the early follow-up period of <60 days (110 mg HR 3.01; 95% CI, 1.48-6.10; 150 mg HR 2.97; 95% CI, 1.31-6.73). Comparable results were obtained for a composite end point (myocardial infarction, unstable angina, or cardiac arrest) among both VKA-naïve and prior VKA-experienced users.

CONCLUSIONS:

In this large-scale nationwide cohort study, we found that switching to dabigatran increased the risk of myocardial infarction compared with continued warfarin usage in the early period after switching. Caution may be warranted, especially when switching prior VKA-experienced patients with atrial fibrillation to dabigatran.

KEYWORDS:

Dabigatran; Effectiveness; Myocardial infarction; Warfarin

PMID:
24361757
DOI:
10.1016/j.amjmed.2013.12.005
[Indexed for MEDLINE]

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