Less dementia with oral anticoagulation in atrial fibrillation

Literature - Friberg L & Rosenqvist M. - Eur Heart J 2017; published online ahead of print

Background

Atrial fibrillation (AF) is associated with an increased risk for stroke, which is significantly reduced by OAC therapy. AF is also associated with dementia, but it is unclear whether OAC therapy is useful for the prevention of dementia, since available studies led to conflicting results [1-4].

In this retrospective cohort study, the incidence of dementia among AF patients with and without OAC treatment was evaluated, using data from the Swedish Patient register and the Dispensed Drug register [5,6]. It was also assessed whether there is a difference between novel anticoagulants and warfarin in this context.

All individuals with a diagnosis of AF between 2006 and 2014 and without a history of dementia were included in the analysis. Information within 30 days after the first contact was used as baseline condition. New dementia during follow-up was detected from day 31 within the time at risk. 444106 patients were included in the study. During over 1.5 million years of follow-up, 26 210 patients were diagnosed with dementia, corresponding to 1.73 per 100 patient years at risk (PYAR).

Main results

• At baseline, 54.3% of patients did not receive OAC, 42.9% used warfarin, 0.04% received phenprocoumon, and 2.9% used a NOAC.
• The strongest predictors for dementia were age (HR per decade: 2.19; 95% CI: 2.16–2.22), Parkinson’s disease (HR: 2.46; 95% CI: 2.25–2.69), absence of OAC treatment (HR: 2.08; 95% CI: 1.73-2.53), and alcohol abuse (HR: 1.53; 95% CI: 1.41–1.66).
• The incidence rate of dementia in patients receiving OAC was lower compared with patients without OAC (1.14 vs. 1.78 per 100 PYAR; P< 0.001).
• Compared with patients who did not receive OAC, patients with OAC at baseline had fewer previous hospitalization with bleeding diagnoses (12.2% vs. 19.3%; P< 0.001), fewer intracranial bleedings (1.7% vs. 3.3%; P < 0.001), and fewer recurrent fall accidents (3.4% vs. 8.0%; P< 0.001).
• Propensity score matching showed that patients with OAC treatment had a 29% lower risk of dementia compared with patients not on OAC at baseline (HR: 0.71; 95% CI: 0.68–0.74).
• In an on-treatment analysis, excluding non-OAC patients who later received OAC and OAC patients covered less than 80% of the time at risk, OAC patients had a 48% lower risk of dementia compared with non-OAC patients (HR: 0.52; 95% CI: 0.50–0.55).
• When NOACs and warfarin were compared to no treatment, the risk of dementia was lower with NOAC (HR: 0.48; 95% CI: 0.40–0.58) compared with warfarin (HR: 0.62; 95% CI: 0.60–0.64). This finding was verified with an on-treatment analysis (NOAC HR: 0.30; 95% CI: 0.22–0.42 vs. VKA HR: 0.53; 95% CI: 0.50–0.56).
• Of note, the NOAC and the VKA group differed in several of the baseline characteristics. A direct comparison between NOACs and warfarin, after propensity score matching for the likelihood of either treatment, showed no difference regarding the risk of dementia (HR: 0.97; 95% CI: 0.67–1.40).

Conclusion

References

Find this article online at Eur Heart J