Cerebral hypoperfusions and hypertensive events during atrial fibrillation: a mechanism for cognitive impairment?

Background: atrial fibrillation (AF) is associated with an increased risk of dementia and cognitive decline, independent of clinical strokes/TIAs. Several mechanisms have been proposed to explain this association, but altered cerebral blood flow dynamics during AF has been poorly investigated: in particular, it is unknown how AF influences hemodynamic parameters of the deepest cerebral circulation. Purpose: aim of the present study was to study AF impact on cerebral circulation through a computational hemodynamic analysis. Methods: two coupled lumped-parameter models (systemic and cerebrovascular circulations, respectively) were used to simulate sinus rhythm (SR) and AF. For each simulation 5,000 cardiac cycles were analyzed, computing main statistics (mean and standard deviation) for different cerebral hemodynamic parameters. Results: with respect to SR, AF triggered a greater variability (represented by the standard deviation) of the parameters, especially in the deepest circulation (cerebral arterioles and capillaries; see Figure, top panel). This variability led to critical cerebral hemodynamic events: during AF 303 hypoperfusions (maximum duration: 2 beats) occurred at the arteriolar level, while 387 hypertensive events (maximum duration: 5 beats) occurred at the capillary level (see Figure, lower panel). By contrast, neither hypoperfusions nor hypertensive events occurred during SR. Conclusion: during AF, the higher variability of the cerebral hemodynamic variables increases proceeding towards the peripheral circulation, reaching the maximum extent at the arteriolar and capillary levels and possibly resulting in local transient periods of excessive pressure or reduced blood flow. Thus, the impact of AF per se on cerebral hemodynamics candidates as a relevant mechanism into the genesis of AF-related cognitive impairment/dementia