Relationships of Overt and Silent Brain Lesions With Cognitive Function in Patients With Atrial Fibrillation.

Conen, David; Rodondi, Nicolas; Müller, Andreas; Beer, Juerg H; Ammann, Peter; Moschovitis, Giorgio; Auricchio, Angelo; Hayoz, Daniel; Kobza, Richard; Shah, Dipen; Novak, Jan; Schläpfer, Jürg; Di Valentino, Marcello; Aeschbacher, Stefanie; Blum, Steffen; Meyre, Pascal; Sticherling, Christian; Bonati, Leo H; Ehret, Georg; Moutzouri, Elisavet; ... (2019). Relationships of Overt and Silent Brain Lesions With Cognitive Function in Patients With Atrial Fibrillation. Journal of the American College of Cardiology, 73(9), pp. 989-999. Elsevier 10.1016/j.jacc.2018.12.039

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BACKGROUND

Patients with atrial fibrillation (AF) have an increased risk of cognitive decline, potentially resulting from clinically unrecognized vascular brain lesions.

OBJECTIVES

This study sought to assess the relationships between cognitive function and vascular brain lesions in patients with AF.

METHODS

Patients with known AF were enrolled in a multicenter study in Switzerland. Brain magnetic resonance imaging (MRI) and cognitive testing using the Montreal Cognitive Assessment (MoCA) were performed in all participants. Large noncortical or cortical infarcts (LNCCIs), small noncortical infarcts (SNCIs), microbleeds, and white matter lesions were quantified by a central core laboratory. Clinically silent infarcts were defined as infarcts on brain MRI in patients without a clinical history of stroke or transient ischemic attack.

RESULTS

The study included 1,737 patients with a mean age of 73 ± 8 years (28% women, 90% taking oral anticoagulant agents). On MRI, LNCCIs were found in 387 patients (22%), SNCIs in 368 (21%), microbleeds in 372 (22%), and white matter lesions in 1715 (99%). Clinically silent infarcts among the 1,390 patients without a history of stroke or transient ischemic attack were found in 201 patients with LNCCIs (15%) and 245 patients with SNCIs (18%). The MoCA score was 24.7 ± 3.3 in patients with and 25.8 ± 2.9 in those without LNCCIs on brain MRI (p < 0.001). The difference in MoCA score remained similar when only clinically silent LNCCIs were considered (24.9 ± 3.1 vs. 25.8 ± 2.9; p < 0.001). In a multivariable regression model including all vascular brain lesion parameters, LNCCI volume was the strongest predictor of a reduced MoCA (β = -0.26; 95% confidence interval: -0.40 to -0.13; p < 0.001).

CONCLUSIONS

Patients with AF have a high burden of LNCCIs and other brain lesions on systematic brain MRI screening, and most of these lesions are clinically silent. LNCCIs were associated with worse cognitive function, even among patients with clinically silent infarcts. Our findings raise the question of MRI screening in patients with AF.

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