Higher ventricular rate during atrial fibrillation relates to increased cerebral hypoperfusions and hypertensive events

TL;DR

This study uses computational models to show that higher ventricular rates during atrial fibrillation increase critical cerebral hypoperfusions and hypertensive events, suggesting rate control around 60 bpm may benefit cognitive health.

Contribution

It provides novel insights into how ventricular rate during AF impacts cerebral hemodynamics, highlighting potential benefits of rate control for cognitive outcomes.

Findings

Higher ventricular rates increase critical cerebral hemodynamic events.

Lower ventricular rates are associated with more hypoperfusions at proximal cerebral levels.

Rate control around 60 bpm may reduce risks of cerebral hypoperfusions and hypertensive events.

Abstract

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.