Atrial fibrillation and dementia have long been linked, partly because both tend to affect the elderly. But there may be a causal link as well related to management of anticoagulation.
Atrial fibrillation (AF) has long been linked with dementia-partly because both are diseases of the elderly but also because there may be a causal relationship, potentially via the incidence of subclinical or silent ischemic or hemorrhagic cerebral infarcts; this has not yet been determined. Newer insights continue to emerge that may allow better characterization of this relationship.
Data from two abstracts published by the same group in Salt Lake City presented at the annual Heart Rhythm Society meeting in 20141,2 showed that in patients with AF:
1. Increased time in therapeutic range was associated with lower risk of dementia.
2. A higher average heart rate was associated with a lower risk of dementia.
The first study,1 using a prospective observational design, followed 2693 patients from the local anticoagulation clinic for 5 years. The overall incidence of dementia over the study period was low (4%) but the risk was progressively higher for those who had a therapeutic INR (TTR) between 2 and 3 51% to 75% of the time (hazard ratio [HR] = ≈2); 25% to 50% of the time (HR = ≈3.5); or <25% of the time (HR = ≈4) compared with those who had TTR >75% of the time. This risk was high regardless of whether patients were overcoagulated or undercoagulated.
The second study2 included 1071 patients with continuous AF who were followed for 3 years after undergoing 24-hour Holter monitoring. After multivariate adjustment, dementia risk was lower with higher heart rates (risk ≈3.5X for heart rates <60 beats/min; 4.2X for 60 to 70 beats/min; ≈2.5X for heart rates 80 to 99 beats/min, compared with heart rates >100 beats/min), although the results did not achieve statistical significance.
Although the first study provides convincing evidence that risk of dementia may be linked to incidence of microinfarcts or microbleeds, the results of the second study are a bit more difficult to contextualize. Despite the statistical adjustment, there still may be residual confounding. For example, it is possible that patients who achieve lower heart rates receive more intensive pharmacologic therapy, which could be associated with higher dementia risk. Additional studies are needed to determine whether this finding is reproducible and what the pathophysiologic link is between AF and dementia.
For now, no changes to heart rate goals are recommended but patients with lower heart rates while receiving AF therapy may be at somewhat higher risk, perhaps a result of decreased cerebral perfusion.