  Atrial fibrillation (AF) is associated with cognitive impairment/dementia,
independently of clinical cerebrovascular events (stroke/TIA). One of the
plausible mechanisms is the occurrence of AF-induced transient critical
hemodynamic events; however, it is presently unknown, if ventricular response
rate during AF may impact on cerebral hemodynamics. AF was simulated at
different ventricular rates (50, 70, 90, 110, 130 bpm) by two coupled lumped
parameter validated models (systemic and cerebral circulation), and compared to
corresponding control normal sinus rhythm simulations (NSR). Hemodynamic
outcomes and occurrence of critical events (hypoperfusions and hypertensive
events) were assessed along the internal carotid artery-middle cerebral artery
pathway up to the capillary-venous bed. At the distal cerebral circle level
(downstream middle cerebral artery), increasing ventricular rates lead to a
reduced heart rate-related dampening of hemodynamic signals compared to NSR
(p=0.003 and 0.002 for flow rate and pressure, respectively). This response
causes a significant progressive increase in critical events in the distal
cerebral circle (p<0.001) as ventricular rate increases during AF. On the other
side, at the lowest ventricular response rates (HR 50 bpm), at the
systemic-proximal cerebral circle level (up to middle cerebral artery)
hypoperfusions (p<0.001) occur more commonly, compared to faster AF
simulations. This computational study suggests that higher ventricular rates
relate to a progressive increase in critical cerebral hemodynamic events
(hypoperfusions and hypertensive events) at the distal cerebral circle. Thus, a
rate control strategy aiming to around 60 bpm could be beneficial in terms on
cognitive outcomes in patients with permanent AF.
