Mechanisms, Clinical Significance, and Prevention of Cognitive Impairment in Patients With Atrial Fibrillation

Atrial fibrillation (AF) and dementia are major health issues, with growing evidence suggesting a consistent association between AF and all forms of dementia. Although dementia and AF share several risk factors, the association appears to be independent of a history of clinical stroke and other comorbidities such as hypertension, heart failure, and diabetes. Proposed mechanisms linking AF to cognitive decline include altered hemodynamics resulting in cerebral hypoperfusion, inflammation, genetic factors, and silent cerebral ischemia due to subclinical microemboli. Evidence in support of the microembolization hypothesis includes the much higher incidence of silent cerebral ischemia detected in imaging studies in patients with AF, the association between presence of silent cerebral ischemia and cognitive dysfunction, and a “dose response” relationship between extent of silent cerebral ischemia and degree of cognitive impairment. Preventive therapies are currently being investigated and include anticoagulation, antiplatelet therapy, statins, pharmacological rhythm and rate control treatment strategies for AF, and catheter ablation procedures. Blinded Randomized Trial of Anticoagulation to Prevent Ischemic Stroke and Neurocognitive Impairment in Atrial Fibrillation (BRAIN-AF) trial is currently assessing whether oral anticoagulation can prevent cognitive decline in patients at low risk of overt stroke. Considering the strong and independent association between AF and neurocognitive outcomes and the major clinical implications, evidence-based preventive approaches are critically required to diminish the health burden from the scourge of dementia and related conditions. La fibrillation auriculaire (FA) et la démence sont des enjeux majeurs de santé pour lesquels de plus en plus d’évidences montrent un lien entre FA et toutes les formes de démence. Bien qu'ils partagent de nombreux facteurs de risques, l'association semble indépendante des antécédents d'accident vasculaire cérébral ou d'autres comorbidités comme l'hypertension, l'insuffisance cardiaque ou le diabète. Les mécanismes suspectés d'expliquer l'association entre FA et démence inclus l'hypoperfusion cérébrale, l'inflammation, les facteurs génétiques et l'ischémie cérébrale silencieuse. Parmi les données probantes supportant l'hypothèse micro-embolique, on note : une augmentation de la prévalence de l'ischémie cérébrale silencieuse sur les examens d'imagerie chez les patients en FA, une association entre