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

Matteo Anselmino,Fiorenzo Gaita,Luca Ridolfi,Stefania Scarsoglio,Andrea Saglietto

doi:10.1038/srep28635

Matteo Anselmino, Fiorenzo Gaita + Show 3 more

Open Access

https://doi.org/10.1038/srep28635

Copy DOI

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.

Highlights

Atrial fibrillation (AF) is associated with an increased risk of dementia and cognitive decline, independent of strokes
Among all hemodynamic variables of the cerebral system, we focused on those related to the left ICA-middle cerebral artery (MCA) pathway (Pa, QICA,left, PMCA,left, QMCA,left, Pdm,left, Qdm,left, Pc, Qpv), highlighted in orange in Fig. 2, as representative of the blood flow distribution from large arteries to the capillary and venous circulation
AF and sinus rhythm (SR) are considered in absence of other associated pathologies, such as hypertension, that could themselves affect cerebral hemodynamics: as a consequence, the reported results strictly focus on the hemodynamic impact exerted by heart rhythm alone on the cerebral circulation

Summary

Introduction

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. 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. While the role of SCI6,7 and microbleeds[8,9] in the genesis of cognitive impairment has been investigated, the same is not true for the altered cerebral blood flow It is unknown how abnormal heart rhythm influences hemodynamic parameters of the distal cerebral circulation, as determined by time-variable pressure and flow rate signals at the arteriolar and capillary levels. The results of the present computational approach provide physiopathological insights into the genesis of early dementia and cognitive impairment in AF patients

Methods

Results

Discussion

Conclusion