Key result
AF is independently linked to reduced cerebral peak systolic and mean flow velocities.
Why the study?
Atrial fibrillation is associated with cognitive impairment and dementia, but the underlying mechanisms remain unclear. Disrupted cerebral autoregulation and altered cerebral hemodynamics may link AF to cognitive decline, motivating an evaluation of the association between AF and cerebral hemodynamics in cognitively healthy individuals.
Cross-Sectional (n=3,027)
In a large population-based cohort of cognitively healthy individuals, atrial fibrillation is independently associated with reduced cerebral peak systolic velocity and mean flow velocity, especially when AF is present during the examination.
AF may impair cerebral perfusion in healthy adults; hypothesis-generating for hypoperfusion-mediated cognitive risk.
Background Atrial fibrillation (AF) is associated with cognitive impairment and dementia, but the underlying mechanisms remain unclear. Altered cerebral hemodynamics may link AF to cognitive decline.1 Cerebral autoregulation appears to be disrupted in AF, potentially reducing the brain’s ability to buffer blood pressure variability and increasing vulnerability to cerebral hypoperfusion.2 We therefore investigated the association between AF and cerebral hemodynamics in a large, population-based cohort of cognitively healthy individuals. Methods This study is based on the inclusion visit (2012–2015) of the Akershus Cardiac Examination (ACE) 1950 Study, which includes participants born in 1950 and residing in Akershus County. Peak systolic velocity (PSV), end-diastolic velocity (EDV), resistance index (RI), and mean flow velocity (MFV) were assessed using transcranial Doppler (TCD) ultrasonography through the right transtemporal bone window. AF was self-reported and validated by electrocardiography and medical record review. Linear regression models were used to explore associations between AF and cerebral hemodynamic parameters. Results We analyzed 3,027 individuals (82% of the cohort) with available transcranial hemodynamic measurements. The mean age was 63.9 years (SD 0.6), 1,277 (42%) were women, and the mean systolic blood pressure was 137.7 mmHg (SD 18.4). In all, 143 (5%) had diagnosed AF. In univariate analyses, AF was associated with all four TCD measures (PSV, EDV, RI, and MFV). After adjustment for age, sex, and systolic blood pressure, AF remained significantly associated with PSV and MFV (Figure 1). The effect of AF on cerebral hemodynamics was more pronounced when comparing participants with AF present at the time of examination (n = 40; 28% of those with AF) to those in sinus rhythm. Conclusion In this large population-based study, AF was associated with altered cerebral hemodynamics, manifested as reduced PSV and MFV. These alterations were most pronounced among participants with atrial fibrillation present at the time of examination. Future studies should investigate whether altered cerebral hemodynamics precede cognitive decline and whether the magnitude of these changes influences the development of cognitive impairment.
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Ihle‐Hansen et al. (2026) conducted a cross-sectional in Atrial fibrillation (n=3,027). Atrial fibrillation vs. Sinus rhythm / no diagnosed atrial fibrillation was evaluated on Cerebral hemodynamic parameters: peak systolic velocity (PSV), end-diastolic velocity (EDV), resistance index (RI), and mean flow velocity (MFV) on transcranial Doppler ultrasonography. Atrial fibrillation (present in 5% of 3,027 participants) was significantly associated with reduced cerebral peak systolic and mean flow velocities after multivariable adjustment.
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