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Stroke prevention remains the main objective for management strategies in atrial fibrillation (AF) because there is convincing randomised trial and cohort study evidence that oral anticoagulants (OACs) are remarkably effective in reducing stroke and all-cause mortality. With the introduction of non-vitamin K-dependent oral anticoagulants (NOACs) about 10 years ago, physicians have alternatives to warfarin that are easier to use and reduce major bleeds, particularly intracranial haemorrhage, and further reduce all-cause mortality.1 Accordingly, OACs have become guideline-mandated therapy for patients with a high enough stroke risk (CHA2DS2-VA≥2), with NOACs preferred.2 The widespread adoption and promotion of NOACs, coupled with various quality frameworks and guidelines, have seen an increase in guideline-recommended OAC therapy in many countries, largely due to an increase in NOAC prescription, which has been accompanied by a reduction in AF-related stroke.3
There are five essential steps to prevent strokes in AF, and all need to occur in order to achieve the full potential of reduction of AF-related stroke (figure 1). Early identification of AF followed by appropriate assessment and initiation of OAC thromboprophylaxis is a critical first step, but for many patients this is where the pathway ends. It seems obvious that the benefits of OAC on stroke and mortality documented in randomised trials will not be realised if the medication is not taken long term. A global problem exists with both patient adherence and persistence, with persistence steadily declining from 3 months after the initial OAC prescription.4 However, the issue of poor persistence and adherence is not widely appreciated to be a significant cause of AF-related stroke.
The study by Rodríguez et al 5 in this issue of the journal clearly demonstrates that for OACs to be effective and lead …
Contributors All authors contributed to the content of the review, drafting and redrafting the manuscript, and approved the final version.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests NL reports grants from BMS/Pfizer outside the submitted work. KG has received honoraria from Pfizer for professional activities outside the submitted work. BF reports grants, personal fees and non-financial support from BMS/Pfizer; grants, personal fees and non-financial support from Bayer; personal fees and non-financial support from Daiichi Sankyo; non-financial support from Alivecor; personal fees and non-financial support from Omron outside the submitted work.
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.
Provenance and peer review Not commissioned; externally peer reviewed.
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