2 January 2018
Regarding atrial fibrillation (AF), post-stroke cognitive impairment (PSCI), and post-stroke dementia (PSD), a recently published article in October 2017 by Chander and colleagues  reported that AF is a significant and independent risk factor for PSCI even after correction of other risk factors and that we should do follow up for patients with AF regardless of infarction type. This agrees with a meta-analysis done in 2012 . Also in a systemic review done in 2017 , stroke patients with AF have a risk of dementia which is 1.68 times compared with patients without AF. AF was found to cause hippocampal atrophy and cognitive impairment even in patients without symptomatic stroke or with silent infarctions . However, cognitive impairment sometimes may be associated with increasing age in AF patients and age-related pathologies as the prevalence of AF doubles every decade of life after the age of 50 years and reaches 10–20% in patients over the age of 80 years .
Another meta-analysis showed that although the risk is higher in stroke patients, there is association between AF and cognitive impairment or dementia, irrespective of occurrence of stroke . This may be related to other mechanisms mentioned by Chander and colleagues as hypoperfusion, endothelial dysfunction, and neuroinflammation. We should not forget the role of brain resilience in PSCI; including cognitive reserve and brain reserve. Cognitive reserve refers to the brain capacity to maintain the same level of cognitive function despite having brain pathology; it is largely affected by age, educational level, and the performance of exercise and recreational activities . The Stroke Registry Investigating Cognitive Decline (STRIDE) study showed that people who performed regular intellectual and leisure activities such as reading a newspaper and/or stretching physical exercise before stroke had a lower risk of early-onset PSD, after controlling for other factors . Brain reserve refers to variation between individuals in brain size and number of neurons and synapses available, and is capable of resisting brain injury or pathologies . This includes amyloid plaques, neurofibrillary tangles, and white matter hyperintensities. Although they are sometimes subclinical, they decrease brain reserve and resilience and increase the possibility of PSCI with vascular insults .
Last, I would like to highlight the Rotterdam study, in which AF was shown to be more likely associated with Alzheimer’s dementia with cerebrovascular disease than vascular dementia . What is the possible mechanism? And is the relation between AF and dementia or AF and PSCI partially explained by Alzheimer’s pathology, being accelerated with stroke? Future prospective studies are needed to ensure the possible mechanisms responsible for cognitive impairment in AF patients, the relation between AF and Alzheimer’s disease and to identify the best treatment approach if possible for preventing or delaying the progression to dementia in patients with or without stroke.
Heba Mohamed Tawfik, MD
Lecturer and consultant of Geriatrics and Gerontology
Faculty of Medicine, Ain-Shams University
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