Objective Atrial fibrillation (AF) is common in patients with heart failure (HF), and oral anticoagulants (OAC) are indicated. The aim was to assess prevalence of, predictors of and consequences of OAC non-use.
Methods We included patients with AF, HF and no previous valve replacement from the Swedish Heart Failure Registry. High and low CHA2DS2-VASc and HAS-BLED scores were defined as above/below median. Multivariable logistic regressions were used to assess the associations between baseline characteristics and OAC use and between CHA2DS2-VASc and HAS-BLED scores and OAC use. Multivariable Cox regressions were used to assess associations between CHA2DS2-VASc and HAS-BLED scores, OAC use and two composite outcomes: all-cause death/stroke and all-cause death/major bleeding.
Results Of 21 865 patients, only 12 659 (58%) received OAC. Selected predictors of OAC non-use were treatment with platelet inhibitors, less use of HF treatments, paroxysmal AF, history of bleeding, no previous stroke, planned follow-up in primary care, older age, living alone, lower income and variables associated with more severe HF. For each 1-unit increase in CHA2DS2-VASc and HAS-BLED, the ORs (95% CI) of OAC use were 1.24 (1.21–1.27) and 0.32 (0.30–0.33), and the HRs for death/stroke were 1.08 (1.06–1.10) and for death/major bleeding 1.18 (1.15–1.21), respectively. For high versus low CHA2DS2-VASc and HAS-BLED, the ORs of OAC use were 1.23 (1.15–1.32) and 0.20 (0.19–0.21), and the HRs for death/stroke were 1.25 (1.19–1.30) and for death/major bleeding 1.28 (1.21–1.34), respectively.
Conclusions Patients with AF and concomitant HF do not receive OAC on rational grounds. Bleeding risk inappropriately affects decision-making more than stroke risk.
- medication adherence
- atrial fibrillation
- heart failure
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Contributors GS contributed to the conception and design of the research, analysis and interpretation of data, drafting and revising the manuscript. LHL contributed to the conception and design of the research, drafting and revising the manuscript, obtaining funding and supervising work. US, LF and UD performed a critical revision of the manuscript for important intellectual content.
Funding This study was supported in part by grants to LHL’s institution from the Swedish Research Council [grants 2013-23897-104604-23 and 523-2014-2336], the Swedish Heart Lung Foundation [grants 20120321 and 20150557], the Stockholm County Council [grant 20110120].
Competing interests GS: none related to this manuscript. Research grant from MSD Italy and Swedish Heart- Lung Foundation. US: none related to this manuscript. US was supported by grants from the Swedish Society of Medicine, Karolinska Institutet Foundations and Funds, the Mats Kleberg Foundation (grant number 2016-00015), the Swedish Heart-Lung Foundation (grant numbers 20160522 and 20160525), the Swedish Heart and Lung Association (grant number E101/16), Regional ALF agreement between Stockholm County Council and Karolinska Institutet (grant number 20160329), Åke Wiberg Foundation (grant number M16-0081) and Magnus Bergvall Foundation (grant number 2016-01396) LF: none related to this manuscript. Research grants and consultancy fees from Bayer, BMS, Pfizer and Sanofi. UD: none related to this manuscript. Research grant to the author’s institution from AstraZeneca and honoraria/consultancies to author’s institution from Novartis and AstraZeneca. LHL: there are no conflicts of interest related to the work submitted. Outside the work submitted, there are the following potential conflicts of interest: research grants to author’s institution, speaker’s and/or consulting fees: AstraZeneca, Novartis, Bayer, Vifor Pharma, Relypsa, Boston Scientific, StJude, Medtronic, HeartWare.
Ethics approval Regionala erikprövningsnämnden i Linköping.
Provenance and peer review Not commissioned; externally peer reviewed.