Abstract
It is now well established that besides being the most common sustained arrhythmia, atrial fibrillation (AF) is a major healthcare burden. Risk of debilitating stroke is increased in AF patients, but even in the absence of stroke, this population is at heightened risk of cognitive decline, depression, and dementia. The reasons for this are complex, multifactorial, and incompletely understood. One potential contributing mechanism is cerebrovascular dysfunction. Cerebral blood flow is regulated by chemical, metabolic, autoregulatory, neurogenic, and systemic factors. The dysfunction in one or more of these mechanisms may contribute to the elevated risk of cognitive decline and cerebrovascular events in AF. This short review presents the evidence for diminished cerebral blood flow, cerebrovascular carbon dioxide reactivity (i.e., cerebrovascular vasodilatory reserve), cerebral autoregulation, and neurovascular coupling in AF patients when compared to control participants in sinus rhythm. Further work is needed to understand the physiological mechanisms underpinning these observations and their clinical significance in atrial fibrillation patients.
Highlights
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia characterized by an irregularly irregular cardiac output that leads to disrupted peripheral blood flow kinetics
Similar findings regarding cerebral perfusion in fibrillating and non-fibrillating atrial fibrillation (AF) patients have been documented with phasecontrast MRI in a cross-sectional study (Gardarsdottir et al, 2017)
In AF, an attenuated brachial artery flow mediated dilatation response (FMD) (Freestone et al, 2008) and raised plasma von Willlebrand concentrations (Conway et al, 2003; Freestone et al, 2008), a factor related to adverse cardiovascular outcomes (Conway et al, 2003; Lip et al, 2006), have been identified and indicate endothelial damage/dysfunction
Summary
Reviewed by: Stefano Tarantini, The University of Oklahoma Health Sciences Center, United States Joseph Arnold Fisher, University Health Network (UHN), Canada. Risk of debilitating stroke is increased in AF patients, but even in the absence of stroke, this population is at heightened risk of cognitive decline, depression, and dementia. The reasons for this are complex, multifactorial, and incompletely understood. The dysfunction in one or more of these mechanisms may contribute to the elevated risk of cognitive decline and cerebrovascular events in AF. This short review presents the evidence for diminished cerebral blood flow, cerebrovascular carbon dioxide reactivity (i.e., cerebrovascular vasodilatory reserve), cerebral autoregulation, and neurovascular coupling in AF patients when compared to control participants in sinus rhythm.
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