Biomarker and cognitive decline in atrial fibrillation: a prospective cohort study

We investigated associations of a broad biomarker panel with cognitive decline in atrial fibrillation (AF) patients to characterize possible mechanisms. We enrolled 1440 AF patients with available baseline biomarkers and cognitive testing by the Montreal Cognitive assessment (MoCA) score at inclusion and at ≥ 2 yearly follow-ups. We investigated the associations of biomarkers with cognitive decline in univariate logistic regression models, LASSO regression analysis and built a combined model. Mean age was 72 years, 75% male, 47% paroxysmal AF. Over 4 years, 93 patients (6.5%) had cognitive decline. These patients had more often permanent AF (32.3 vs 21.5%, p = 0.007) and more often a history stroke (23.7 vs 11.2%, p < 0.001), but similar baseline MoCA scores (24.9 vs 25.3 points, p = 0.22) and anticoagulation rates (93.5 vs 89.5%, p = 0.29). The three biomarkers with the highest univariate AUC for cognitive decline were GDF-15 (0.67 [0.62-0.72]), Cystatin C (0.67 [0.61-0.72]) and high-sensitivity Troponin T (hs-TnT) (0.65 [0.60-0.70]). In LASSO regression analysis, the best cross validation included GDF-15, GFAP, ESM-1, NfL and ALAT. The combined prediction model with the highest AUC of 0.73 (0.68-0.78) included IGFBP-7, GDF-15, Cystatin C, hsCRP, ALAT, GFAP, ESM-1 and FGF23. Over 4 years, 6.5% of AF patients had cognitive decline despite a high rate of anticoagulation. Inflammation, neuronal damage, and increased amyloid-beta might be important non-ischemic mechanisms of cognitive decline in AF patients.

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Publication Details

Journal
Scientific Reports
Published
2025-04-15
DOI
https://doi.org/10.1038/s41598-025-89800-9
Citations
2
Primary Topic
Atrial Fibrillation Management and Outcomes
Type
article
Field-Weighted Citation Impact
2.78

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article

Biomarker and cognitive decline in atrial fibrillation: a prospective cohort study

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2 citations
Scientific Reports
Atrial Fibrillation Management and Outcomes
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article

Biomarker and cognitive decline in atrial fibrillation: a prospective cohort study

Philipp Krisai, Jürg H. Beer, Richard Kobza, Andreas Müller, Nicolas Rodondi, Giorgio Moschovitis, Elia Rigamonti, Stefan Osswald, Sreekar Balasundaram, Stefanie Aeschbacher, Michael Kühne, David Conen, Magdalena Eberl, Leo Hermann Bonati, Patricia Chocano-Bedoya, Vinzent Rolny, Tobias Reichlin, Michael Coslovsky
article en
2 citations

Abstract

We investigated associations of a broad biomarker panel with cognitive decline in atrial fibrillation (AF) patients to characterize possible mechanisms. We enrolled 1440 AF patients with available baseline biomarkers and cognitive testing by the Montreal Cognitive assessment (MoCA) score at inclusion and at ≥ 2 yearly follow-ups. We investigated the associations of biomarkers with cognitive decline in univariate logistic regression models, LASSO regression analysis and built a combined model. Mean age was 72 years, 75% male, 47% paroxysmal AF. Over 4 years, 93 patients (6.5%) had cognitive decline. These patients had more often permanent AF (32.3 vs 21.5%, p = 0.007) and more often a history stroke (23.7 vs 11.2%, p < 0.001), but similar baseline MoCA scores (24.9 vs 25.3 points, p = 0.22) and anticoagulation rates (93.5 vs 89.5%, p = 0.29). The three biomarkers with the highest univariate AUC for cognitive decline were GDF-15 (0.67 [0.62-0.72]), Cystatin C (0.67 [0.61-0.72]) and high-sensitivity Troponin T (hs-TnT) (0.65 [0.60-0.70]). In LASSO regression analysis, the best cross validation included GDF-15, GFAP, ESM-1, NfL and ALAT. The combined prediction model with the highest AUC of 0.73 (0.68-0.78) included IGFBP-7, GDF-15, Cystatin C, hsCRP, ALAT, GFAP, ESM-1 and FGF23. Over 4 years, 6.5% of AF patients had cognitive decline despite a high rate of anticoagulation. Inflammation, neuronal damage, and increased amyloid-beta might be important non-ischemic mechanisms of cognitive decline in AF patients.

Scientific ReportsVol. 15(1)
University of Bern (CH), University of Zurich (CH), Kantonsspital St. Gallen (CH), Triemli Hospital (CH), University Hospital of Bern (CH), University Hospital of Basel (CH), Population Health Research Institute (CA), Hospital Base (CL), Roche Pharma AG (Germany) (DE), Ente Ospedaliero Cantonale (CH), University Hospital of Zurich (CH), Fribourg Development Agency (CH), University Hospital of Geneva (CH), Epatocentro Ticino (CH), Luzerner Kantonsspital (CH), Kantonsspital Baden (CH), Solothurner Spitäler (CH), Hôpital Nestlé (CH), Department of Biomedicine Basel (CH), Reha Rheinfelden (CH), Hamilton Health Sciences (CA), McMaster University (CA)
National Science Foundation, Foundation for Cardiovascular Research, Universität Basel, Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung, Schweizerische Herzstiftung
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Atrial Fibrillation Management and Outcomes
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