Cargando…
Transient cerebral hypoperfusion and hypertensive events during atrial fibrillation: a plausible mechanism for cognitive impairment
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 ho...
Autores principales: | , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4917883/ https://www.ncbi.nlm.nih.gov/pubmed/27334559 http://dx.doi.org/10.1038/srep28635 |
_version_ | 1782439013734416384 |
---|---|
author | Anselmino, Matteo Scarsoglio, Stefania Saglietto, Andrea Gaita, Fiorenzo Ridolfi, Luca |
author_facet | Anselmino, Matteo Scarsoglio, Stefania Saglietto, Andrea Gaita, Fiorenzo Ridolfi, Luca |
author_sort | Anselmino, Matteo |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4917883 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-49178832016-06-28 Transient cerebral hypoperfusion and hypertensive events during atrial fibrillation: a plausible mechanism for cognitive impairment Anselmino, Matteo Scarsoglio, Stefania Saglietto, Andrea Gaita, Fiorenzo Ridolfi, Luca Sci Rep Article 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. Nature Publishing Group 2016-06-23 /pmc/articles/PMC4917883/ /pubmed/27334559 http://dx.doi.org/10.1038/srep28635 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Anselmino, Matteo Scarsoglio, Stefania Saglietto, Andrea Gaita, Fiorenzo Ridolfi, Luca Transient cerebral hypoperfusion and hypertensive events during atrial fibrillation: a plausible mechanism for cognitive impairment |
title | Transient cerebral hypoperfusion and hypertensive events during atrial fibrillation: a plausible mechanism for cognitive impairment |
title_full | Transient cerebral hypoperfusion and hypertensive events during atrial fibrillation: a plausible mechanism for cognitive impairment |
title_fullStr | Transient cerebral hypoperfusion and hypertensive events during atrial fibrillation: a plausible mechanism for cognitive impairment |
title_full_unstemmed | Transient cerebral hypoperfusion and hypertensive events during atrial fibrillation: a plausible mechanism for cognitive impairment |
title_short | Transient cerebral hypoperfusion and hypertensive events during atrial fibrillation: a plausible mechanism for cognitive impairment |
title_sort | transient cerebral hypoperfusion and hypertensive events during atrial fibrillation: a plausible mechanism for cognitive impairment |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4917883/ https://www.ncbi.nlm.nih.gov/pubmed/27334559 http://dx.doi.org/10.1038/srep28635 |
work_keys_str_mv | AT anselminomatteo transientcerebralhypoperfusionandhypertensiveeventsduringatrialfibrillationaplausiblemechanismforcognitiveimpairment AT scarsogliostefania transientcerebralhypoperfusionandhypertensiveeventsduringatrialfibrillationaplausiblemechanismforcognitiveimpairment AT sagliettoandrea transientcerebralhypoperfusionandhypertensiveeventsduringatrialfibrillationaplausiblemechanismforcognitiveimpairment AT gaitafiorenzo transientcerebralhypoperfusionandhypertensiveeventsduringatrialfibrillationaplausiblemechanismforcognitiveimpairment AT ridolfiluca transientcerebralhypoperfusionandhypertensiveeventsduringatrialfibrillationaplausiblemechanismforcognitiveimpairment |