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Atrial fibrillation (Afib) patients on oral anticoagulation -- whether non-vitamin K oral anticoagulants (NOACs) or warfarin (Coumadin) -- are less likely to develop dementia over the years, according to a Swedish registry study.

That national register showed that the for anticoagulated individuals than for those with Afib but not treated for it (1.14 versus 1.78 per 100 patient-years at risk, P<0.001). That difference was observed across all subgroups, reported Leif Friberg, MD, PhD, and Mårten Rosenqvist, MD, PhD, both of Sweden's Danderyd University Hospital in Stockholm.

Even with propensity score matching to compensate for anticoagulant recipients being younger and healthier, these drugs were still associated with 29% lower odds of dementia (HR 0.71, 95% CI 0.68-0.74), the authors found. With further adjustment for group crossovers, there was a 48% lower risk with oral anticoagulation in on-treatment analysis (HR 0.52, 95% CI 0.50-0.55).

The reduced risk of dementia was similar whether patients were on NOACs or warfarin (HR 0.97, 95% CI 0.67-1.40).

"Our results strongly suggest that oral anticoagulation treatment protects against dementia in Afib. In order to prove this assumption, randomized placebo controlled trials would be needed, but ... such studies cannot be done because of ethical reasons," Friberg and Rosenqvist noted.

"It is not possible to give placebo to Afib patients and then wait for dementia or stroke to occur. Therefore, we have to do the second best, which is to use the information in population-wide health databases for retrospective studies while trying to control for biases and confounders the best we can," they continued. "More registry studies in this field are therefore important in order to confirm or reject our findings."

"The benefit of oral anticoagulation treatment appeared to be more pronounced among patients in whom treatment had been initiated early after the first diagnosed Afib episode[,] suggesting a dose response relationship between unprotected time in Afib and development of dementia," the authors wrote.

"This suggests that early initiation of anticoagulant treatment in patients with Afib could be of value in order to preserve cognitive function."

There was also a trend towards more benefit from treatment in patients with higher CHA₂DS₂-VASc scores, "suggesting that microembolization indeed might be a cause of dementia in Afib patients."

With a well-established link between Afib and dementia, it is thought that if oral anticoagulation protects against large stroke-causing emboli, it should also protect against small ones that cause microinfarctions and subsequent cognitive deterioration.

Friberg and Rosenqvist used a retrospective registry of Swedish Afib patients with no previous diagnosis of dementia for their study (n=444,106). At baseline, 54.3% were not on oral anticoagulation; 42.9% were on warfarin; and 2.9% were on NOACs.

In general, 1.73 patients received a new diagnosis of dementia for every 100 years at risk.

The strongest predictors of developing dementia were:

• Age (HR 2.19 per decade, 95% CI 2.16-2.22)
• Parkinson's disease (HR 2.46, 95% CI 2.25-2.69)
• Absence of oral anticoagulant treatment (HR 2.08, 95% CI 1.73-2.53)
• Alcohol abuse (HR 1.53, 95% CI 1.41-1.66)

Along with the usual limitations of a retrospective registry study, the authors noted that two out of four falsification endpoints showed a weak relationship with oral anticoagulation status -- leaving room for possible residual confounding in their analysis. Furthermore, it is unknown if patients actually took all the drugs they were recorded as getting from the pharmacy.

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