Atrial Fibrillation and Cognition

Poggesi, Anna; Inzitari, Domenico; Pantoni, Leonardo

doi:10.1161/strokeaha.115.008225

Cited by 56 publications

(27 citation statements)

References 48 publications

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“…Therefore, there seems to be continuity in AF through ischemic stroke leading to post-stroke, or vascular, dementia. AF may also induce cerebral hypoperfusion based on low cardiac output [ 16 ], which may cause vascular dementia of hypoperfusive etiology, regardless of whether AF leads to ischemic stroke [ 16–18 ]. Indeed, basic research using rodent models has suggested cerebral hypoperfusion induces white matter changes, such as demyelination and axonal damage, and causes working memory impairment [ 19, 20 ].…”

Section: Mechanistic Insightsmentioning

confidence: 99%

“…In the same study, the relative risk of cerebral infarction was 1.84 (95% CI 1.12–3.01) in permanent, and 1.81 (95% CI 1.13–2.84) in nonpermanent, AF with no apparent difference, making it unlikely that CES caused by AF mediates the difference. However, the crucial difference between permanent and nonpermanent AF is the reduction in cardiac output in permanent AF, which increases the likelihood of cerebral hypoperfusion [ 16 ]. In general, in vital organs, such as the brain, the mechanism of autoregulation maintains circulation, even if cardiac output decreases [ 26 ].…”

Section: Mechanistic Insightsmentioning

confidence: 99%

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Linking Atrial Fibrillation with Alzheimer’s Disease: Epidemiological, Pathological, and Mechanistic Evidence

Ihara

Washida

2018

JAD

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Many studies have shown a relationship between atrial fibrillation (AF) and vascular dementia. AF is a major risk factor for stroke, and stroke is the greatest risk factor for vascular dementia. However, the relationship between Alzheimer’s disease (AD), the leading cause of dementia, and AF remains unclear. At least four epidemiological studies have reported AF significantly raises the risk of AD 1.5- to 2.5-fold. Chronic cerebral hypoperfusion, resulting from persistent AF, could explain the link as hypoperfusion may mechanistically exacerbate amyloid-β (Aβ) neuropathology, such as senile plaques and amyloid angiopathy, by upregulating Aβ-producing enzymes and lowering Aβ clearance efficiency. In addition, hypoperfusion may exacerbate tau pathology directly through upregulation of tau-phosphorylating enzymes and indirectly via the amyloid cascade. However, most neuropathological studies do not support the direct link between AD pathology and AF but rather suggests vascular neuropathology is related to, or coexistent with, AF and lowers the threshold for clinically-evident AD. Vascular neuropathology may thus mediate the link between AD and AF. From a treatment perspective, an observational study has shown that catheter ablation is associated with less incidence of AD in AF patients, suggesting rhythm-control suppresses hypoperfusion-induced AD neuropathology. In addition, rate-control may lower the rate of cognitive decline in cognitively impaired elderly subjects with AF. Further studies are warranted to clarify the mechanisms underlying the linkage between AF and AD. However, anticoagulation and rhythm-/rate-control against AF may hold promise even for AD patients.

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Section: Mechanistic Insightsmentioning

confidence: 99%

Section: Mechanistic Insightsmentioning

confidence: 99%

Linking Atrial Fibrillation with Alzheimer’s Disease: Epidemiological, Pathological, and Mechanistic Evidence

Ihara

Washida

2018

JAD

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“…Beyond that, a lower cardiac output in AF could lead to chronic cerebral hypoperfusion, which may in turn cause damage to the brain (de Bruijn et al, 2015 ). Furthermore, AF was also identified to be a risk factor for Alzheimer's disease, the most common type of dementia (Bunch et al, 2010 ; Poggesi et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Non-vitamin K Antagonist Oral Anticoagulants and Cognitive Impairment in Atrial Fibrillation: Insights From the Meta-Analysis of Over 90,000 Patients of Randomized Controlled Trials and Real-World Studies

Zhang

Shen

et al. 2018

Front. Aging Neurosci.

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Background: The relationship between the use of non-vitamin K antagonist oral anticoagulants (NOACs) and the impairment of cognition in atrial fibrillation (AF) remains unknown.Methods: A comprehensive database search of Medline, Embase, Cochrane Library databases, and ClinicalTrials.gov Website was performed for randomized controlled trials (RCTs) reporting cognitive impairment events and observational nationwide database studies reporting adjusted hazard ratio (HR) in AF patients with NOACs. The primacy outcome was a composite of any cognitive impairment. Summary of HRs and 95% confidence intervals (95%CI) were calculated using the fixed- and random-effects models. Subgroup analyses were undertaken according to the individual NOACs, study types, and duration of follow-up.Results: Finally, eight studies including 97,595 patients (77,643 patients in 6 RCTs and 19,952 patients in 2 observational database studies) met the inclusion criteria, among which 55,337 (56.7%) patients were receiving NOACs and 42,258 (43.3%) patients were receiving vitamin K Antagonists (VKAs) or acetylsalicylic acid. The results showed a borderline significant association between the use of NOACs and the lower risk of cognitive impairment when compared with VKAs/ acetylsalicylic acid (HR: 0.80, 95%CI: 0.63–0.98 for fixed-effects model; HR: 0.77; 95%CI: 0.53–1.01 for random-effects model), with no significant heterogeneity between the studies (I2 = 39.4%, P = 0.12). The results were consistent across the key subgroups (Pinteraction > 0.05 for each).Conclusions: The results indicated that the use of NOACs might lower the tendency on the risk of cognitive impairment in comparison to VKAs/acetylsalicylic acid, and further RCTs and real-world studies are required on an urgent basis to obtain a robust result.

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“…Несмотря на растущую осведомленность о взаимосвязи между ФП и КН [9, 49,51], клинические рекомендации по ведению пациентов с ФП не включают оценку когнитивных функций. Оценка когнитивных функций должна быть многогранной, в которой психометрическое тестирование -всего лишь один из компонентов.…”

Section: клинические семинары §unclassified

Atrial fibrillation as Risk Factor for Development of Cognitive Function Impairment and Dementia. Potential of Anticoagulant Therapy in Their Prevention

Остроумова

Chernyaeva

Головина

2018

CARDIO

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Фибрилляция предсердий как фактор риска развития когнитивных нарушений и деменции. Возможности антикоагулянтной терапии в их профилактике Ключевые слова: фибрилляция предсердий, когнитивные функции, когнитивные нарушения, деменция, пожилой и старческий возраст, прямые пероральные антикоагулянты, ривароксабан.

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Atrial Fibrillation and Cognition

Cited by 56 publications

References 48 publications

Linking Atrial Fibrillation with Alzheimer’s Disease: Epidemiological, Pathological, and Mechanistic Evidence

Linking Atrial Fibrillation with Alzheimer’s Disease: Epidemiological, Pathological, and Mechanistic Evidence

Non-vitamin K Antagonist Oral Anticoagulants and Cognitive Impairment in Atrial Fibrillation: Insights From the Meta-Analysis of Over 90,000 Patients of Randomized Controlled Trials and Real-World Studies

Atrial fibrillation as Risk Factor for Development of Cognitive Function Impairment and Dementia. Potential of Anticoagulant Therapy in Their Prevention

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