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Increased stressor‐evoked cardiovascular reactivity is associated with reduced amygdala and hippocampus volume

Exaggerated cardiovascular reactivity to acute psychological stress is associated with an increased risk of developing cardiovascular disease. The amygdala and hippocampus have been implicated in centrally mediating stressor‐evoked cardiovascular reactivity. However, little is known about the associ...

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Autores principales: Trotman, Gavin P., Gianaros, Peter J., Veldhuijzen van Zanten, Jet J. C. S., Williams, Sarah E., Ginty, Annie T.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6849591/
https://www.ncbi.nlm.nih.gov/pubmed/30132921
http://dx.doi.org/10.1111/psyp.13277
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author Trotman, Gavin P.
Gianaros, Peter J.
Veldhuijzen van Zanten, Jet J. C. S.
Williams, Sarah E.
Ginty, Annie T.
author_facet Trotman, Gavin P.
Gianaros, Peter J.
Veldhuijzen van Zanten, Jet J. C. S.
Williams, Sarah E.
Ginty, Annie T.
author_sort Trotman, Gavin P.
collection PubMed
description Exaggerated cardiovascular reactivity to acute psychological stress is associated with an increased risk of developing cardiovascular disease. The amygdala and hippocampus have been implicated in centrally mediating stressor‐evoked cardiovascular reactivity. However, little is known about the associations of amygdala and hippocampus morphology with stressor‐evoked cardiovascular reactivity. Forty (M (age) = 19.05, SD = 0.22 years) healthy young women completed two separate testing sessions. Session 1 assessed multiple parameters of cardiovascular physiology at rest and during a validated psychological stress task (Paced Auditory Serial Addition Test), using electrocardiography, Doppler echocardiography, and blood pressure monitoring. In Session 2, 1 year later, structural MRI was conducted. Brain structural volumes were computed using automated segmentation methods. Regression analyses, following Benjamini‐Hochberg correction, showed that greater heart rate and cardiac output reactivity were associated with reduced amygdala and hippocampus gray matter volume. Systolic blood pressure reactivity was associated with reduced hippocampus volume. In contrast, no associations between diastolic blood pressure, mean arterial blood pressure, stroke volume, or total peripheral resistance reactivity with amygdala or hippocampus volumes were apparent. Comparison analyses examining insula volume found no significant associations. Some indicators of greater stressor‐evoked cardiovascular reactivity associate with reduced amygdala and hippocampus gray matter volume, but the mechanisms of this association warrant further study.
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spelling pubmed-68495912019-11-15 Increased stressor‐evoked cardiovascular reactivity is associated with reduced amygdala and hippocampus volume Trotman, Gavin P. Gianaros, Peter J. Veldhuijzen van Zanten, Jet J. C. S. Williams, Sarah E. Ginty, Annie T. Psychophysiology Original Articles Exaggerated cardiovascular reactivity to acute psychological stress is associated with an increased risk of developing cardiovascular disease. The amygdala and hippocampus have been implicated in centrally mediating stressor‐evoked cardiovascular reactivity. However, little is known about the associations of amygdala and hippocampus morphology with stressor‐evoked cardiovascular reactivity. Forty (M (age) = 19.05, SD = 0.22 years) healthy young women completed two separate testing sessions. Session 1 assessed multiple parameters of cardiovascular physiology at rest and during a validated psychological stress task (Paced Auditory Serial Addition Test), using electrocardiography, Doppler echocardiography, and blood pressure monitoring. In Session 2, 1 year later, structural MRI was conducted. Brain structural volumes were computed using automated segmentation methods. Regression analyses, following Benjamini‐Hochberg correction, showed that greater heart rate and cardiac output reactivity were associated with reduced amygdala and hippocampus gray matter volume. Systolic blood pressure reactivity was associated with reduced hippocampus volume. In contrast, no associations between diastolic blood pressure, mean arterial blood pressure, stroke volume, or total peripheral resistance reactivity with amygdala or hippocampus volumes were apparent. Comparison analyses examining insula volume found no significant associations. Some indicators of greater stressor‐evoked cardiovascular reactivity associate with reduced amygdala and hippocampus gray matter volume, but the mechanisms of this association warrant further study. John Wiley and Sons Inc. 2018-08-22 2019-01 /pmc/articles/PMC6849591/ /pubmed/30132921 http://dx.doi.org/10.1111/psyp.13277 Text en © 2018 The Authors. Psychophysiology published by Wiley Periodicals, Inc. on behalf of Society for Psychophysiological Research This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Trotman, Gavin P.
Gianaros, Peter J.
Veldhuijzen van Zanten, Jet J. C. S.
Williams, Sarah E.
Ginty, Annie T.
Increased stressor‐evoked cardiovascular reactivity is associated with reduced amygdala and hippocampus volume
title Increased stressor‐evoked cardiovascular reactivity is associated with reduced amygdala and hippocampus volume
title_full Increased stressor‐evoked cardiovascular reactivity is associated with reduced amygdala and hippocampus volume
title_fullStr Increased stressor‐evoked cardiovascular reactivity is associated with reduced amygdala and hippocampus volume
title_full_unstemmed Increased stressor‐evoked cardiovascular reactivity is associated with reduced amygdala and hippocampus volume
title_short Increased stressor‐evoked cardiovascular reactivity is associated with reduced amygdala and hippocampus volume
title_sort increased stressor‐evoked cardiovascular reactivity is associated with reduced amygdala and hippocampus volume
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6849591/
https://www.ncbi.nlm.nih.gov/pubmed/30132921
http://dx.doi.org/10.1111/psyp.13277
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