David Conen1, Nicolas Rodondi2, Andreas Müller3, Juerg H Beer4, Peter Ammann5, Giorgio Moschovitis6, Angelo Auricchio7, Daniel Hayoz8, Richard Kobza9, Dipen Shah10, Jan Novak11, Jürg Schläpfer12, Marcello Di Valentino13, Stefanie Aeschbacher14, Steffen Blum14, Pascal Meyre14, Christian Sticherling14, Leo H Bonati15, Georg Ehret10, Elisavet Moutzouri2, Urs Fischer16, Andreas U Monsch17, Christoph Stippich18, Jens Wuerfel19, Tim Sinnecker20, Michael Coslovsky21, Matthias Schwenkglenks22, Michael Kühne14, Stefan Osswald14. 1. Cardiology Division, Department of Medicine, University Hospital Basel, Basel, Switzerland; Cardiovascular Research Institute Basel, Basel, Switzerland; Population Health Research Institute, McMaster University, Hamilton, Canada. Electronic address: conend@mcmaster.ca. 2. Institute of Primary Health Care (BIHAM), University of Bern, Bern, Switzerland; Department of General Internal Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. 3. Department of Cardiology, Triemli Hospital Zurich, Zurich, Switzerland. 4. Departement of Medicine, Cantonal Hospital of Baden and Molecular Cardiology, University Hospital of Zurich, Zurich, Switzerland. 5. Department of Cardiology, Kantonsspital St. Gallen, St. Gallen, Switzerland. 6. Department of Cardiology, Ospedale Regionale di Lugano, Lugano, Switzerland. 7. Division of Cardiology, Fondazione Cardiocentro Ticino, Lugano, Switzerland. 8. Department of Internal Medicine, HFR-Hôpital Cantonal Fribourg, Fribourg, Switzerland. 9. Department of Cardiology, Luzerner Kantonsspital, Lucerne, Switzerland. 10. Division of Cardiology, Department of Medical Specialties, University Hospital Geneva, Geneva, Switzerland. 11. Department of Cardiology, Bürgerspital Solothurn, Solothurn, Switzerland. 12. Department of Cardiology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. 13. Department of Cardiology, Ospedale San Giovanni, Bellinzona, Switzerland. 14. Cardiology Division, Department of Medicine, University Hospital Basel, Basel, Switzerland; Cardiovascular Research Institute Basel, Basel, Switzerland. 15. Department of Neurology and Stroke Center, University Hospital Basel, University of Basel, Basel, Switzerland. 16. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. 17. Memory Clinic, Universitäre Altersmedizin, Felix Platter Spital Basel, University of Basel, Basel, Switzerland. 18. Department of Neuroradiology, University Hospital Zurich, Zurich, Switzerland. 19. Medical Image Analysis Center (MIAC AG) and Department of Biomedical Engineering, University of Basel, Basel, Switzerland. 20. Department of Neurology and Stroke Center, University Hospital Basel, University of Basel, Basel, Switzerland; Medical Image Analysis Center (MIAC AG) and Department of Biomedical Engineering, University of Basel, Basel, Switzerland. 21. Cardiovascular Research Institute Basel, Basel, Switzerland. 22. Epidemiology, Biostatistics, and Prevention Institute, University of Zurich, Zurich, Switzerland.
Abstract
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.
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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Authors: George Markousis-Mavrogenis; Dimos D Mitsikostas; Loukia Koutsogeorgopoulou; Theodoros Dimitroulas; Gikas Katsifis; Panayiotis Argyriou; Dimitrios Apostolou; Stella Velitsista; Vasiliki Vartela; Dionysia Manolopoulou; Maria G Tektonidou; Genovefa Kolovou; George D Kitas; Petros P Sfikakis; Sophie I Mavrogeni Journal: J Clin Med Date: 2020-02-06 Impact factor: 4.241
Authors: Fabienne Witassek; Anne Springer; Luise Adam; Stefanie Aeschbacher; Jürg H Beer; Steffen Blum; Leo H Bonati; David Conen; Richard Kobza; Michael Kühne; Giorgio Moschovitis; Stefan Osswald; Nicolas Rodondi; Christian Sticherling; Thomas Szucs; Matthias Schwenkglenks Journal: PLoS One Date: 2019-12-23 Impact factor: 3.240