Transient cerebral hypoperfusion and hypertensive events during atrial fibrillation: a plausible mechanism for cognitive impairment

TL;DR

This study uses computational models to show that atrial fibrillation causes significant variability in cerebral blood flow, leading to hypoperfusions and hypertensive events that may contribute to cognitive decline.

Contribution

It introduces a novel simulation approach to analyze cerebral hemodynamics during AF, revealing mechanisms potentially linked to AF-related cognitive impairment.

Findings

AF increases variability in cerebral blood flow at distal levels.

Hypoperfusions and hypertensive events are more frequent during AF than sinus rhythm.

Cerebral hemodynamic instability during AF may underlie cognitive decline.

Abstract

Atrial fibrillation (AF) is associated with an increased risk of dementia and cognitive decline, independent of strokes. 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 distal cerebral circulation, at the arteriolar and capillary level. Two coupled lumped-parameter models (systemic and cerebrovascular circulations, respectively) were here used to simulate sinus rhythm (SR) and AF. For each simulation 5000 cardiac cycles were analyzed and cerebral hemodynamic parameters were calculated. With respect to SR, AF triggered a higher variability of the cerebral hemodynamic variables which increases proceeding towards the distal circulation, reaching the maximum extent at the arteriolar and capillary levels. This variability led to critical cerebral hemodynamic events of excessive pressure or reduced blood flow: 303 hypoperfusions occurred at the arteriolar level, while 387 hypertensive events occurred at the capillary level during AF. By contrast, neither hypoperfusions nor hypertensive events occurred during SR. Thus, the impact of AF per se on cerebral hemodynamics candidates as a relevant mechanism into the genesis of AF-related cognitive impairment/dementia.