Researchers have recently delivered sobering news for the assessment of cognitive decline among younger adults with atrial fibrillation (AFib). Their findings—the culmination of the BRAIN-AF trial—reveal anticoagulants cannot help mitigate cognitive decline in individuals under the age of 65 who do not possess additional stroke risk factors.
At the American Heart Association's (AHA) Scientific Sessions 2024, which took place from November 16-18 in Chicago, Dr. Lena Rivard, the lead author and electrophysiologist at the Montreal Heart Institute, detailed this pivotal study. She noted the results of the trial, which was necessitated by rising evidence linking AFib with cognitive impairments, showed no significant benefits of using rivaroxaban, commonly known as Xarelto, or similar anticoagulation measures.
Traditionally, anticoagulants, often prescribed to reduce stroke risk, target severe urological issues. Case studies had indicated those with AFib might also face cognitive impairment, which led researchers to believe anticoagulants could be effective against cognitive decline, too. This was not the case, as indicated by the early termination of the study, labelled 'futile' after the data safety committee found minimal benefits after almost four years of average follow-up, shorter than the project’s five-year expectations.
The trial had originally involved over 1,200 participants, primarily young and healthy, with their ages averaging around 53. Participants were randomly assigned to take either rivaroxaban or placebo. At the conclusion of the study, the data revealed no discernible difference in cognitive health between those taking the anticoagulant and those on placebo. Notably, the rates of cognitive decline, stroke, or transient ischemic attack (TIA) were virtually identical — 7% per year for the rivaroxaban group compared to 6.4% for the placebo group.
Among those who did experience cognitive decline, stroke, or TIA, cognitive impairment easily topped the list, accounting for 91% of the recorded outcomes. Rivard emphasized the observation mirrored broader trends where adults younger than 65, who should ideally be extrapolated from anticoagulant practices reserved for older individuals, were being treated unnecessarily.
Dr. Andrea Russo, from Cooper University Health Care, who was not involved with the trial, expressed concerns over the mechanisms linking AFib with cognitive decline. Questions remain as to whether cognitive decline and AFib merely coexist or if one precipitates the other. Russo suggested, "Presence of microemboli is only one mechanism. We need to study other mechanisms, such as cerebral hypoperfusion, maybe the impact of drugs used to treat AFib."">
Despite the rise of research-focused results, the connection between AFib and cognitive decline isn't effortless to unravel. Past literature has pointed to tendencies toward higher cognitive decline and incidence of stroke among those with AFib, leading many to believe anticoagulants could stave off such complications.
Doctors have long acknowledged the complex interaction between AFib symptoms, cognitive performance, and potential treatment impacts. Most of the participants were excluded from the trial if they displayed any signs of dementia on the Mini-Mental State Evaluation or were at heightened risk of bleeding due to other health conditions. This exclusion criterion muddles the findings, as it raises new questions about what alternative interventions might yield different outcomes.
Over the years, it’s important to highlight the risks existing with AFib itself. Afib is the most prevalent heart rhythm disorder across the U.S., impacting approximately 5.2 million people. Experts predict this figure could climb to over 12 million by 2030, prompting the need for effective management strategies to both limit stroke risks and understand cognitive consequences.
Results from the BRAIN-AF trial may also reinforce current clinical guidelines emphasizing the importance of healthy lifestyles and mental stimulation as preventive strategies against cognitive decline, rather than solely relying on pharmaceutical interventions. Rivard remarked on how people younger than 65 with AFib and no standard risk factors face significantly low stroke rates; hence, anticoagulation efforts yield little utility for cognitive preservation.
The researchers plan to analyze their data, including over 5,700 Montreal Cognitive tests conducted during the study, to advance their comprehension of cognitive decline as it relates to AFib. The insights gained may help formulate personalized treatment pathways addressing the cognitive health of future patients.
While the findings raise alarms about traditional anticoagulation strategies for younger AFib patients, Dr. Hooman Kamel of Weill Cornell Medicine posited this study may not completely rule out microemboli as causal contributors to cognitive decline. With its limitations and applicability primarily to younger, healthier populations devoid of stroke indicators, BRAIN-AF may still serve as the foundation for forthcoming studies exploring cognition as a clinical endpoint alongside standard health assessments.
Consequently, AFib treatment strategies must incorporate awareness of cognition and neurological factors from the onset to provide holistic approaches to dealing with this pervasive condition. Rivard poignantly concluded, “The BRAIN-AF trial confirmed a high rate of cognitive decline during follow-up in younger adults. It is not known whether other interventions such as ablation of AFib could have a positive impact on cognition in this population.” Through continuous dialogue and study, the medical community hopes to unravel the intricacies of AFib and its wider health ramifications, directing future interventions toward more effective and compassionate care.
