Cortisol responses to mental stress and the progression of coronary artery calcification in healthy men and women.

BACKGROUND:Psychosocial stress is a risk factor for coronary heart disease (CHD). The mechanisms are incompletely understood, although dysfunction of the hypothalamic pituitary adrenal (HPA) axis might be involved. We examined the association between cortisol responses to laboratory-induced mental s...

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Main Authors: Mark Hamer, Romano Endrighi, Shreenidhi M Venuraju, Avijit Lahiri, Andrew Steptoe
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3273460?pdf=render
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spelling doaj-0b5bfbc2fca0434db9cbd1df632853ca2020-11-25T02:12:54ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0172e3135610.1371/journal.pone.0031356Cortisol responses to mental stress and the progression of coronary artery calcification in healthy men and women.Mark HamerRomano EndrighiShreenidhi M VenurajuAvijit LahiriAndrew SteptoeBACKGROUND:Psychosocial stress is a risk factor for coronary heart disease (CHD). The mechanisms are incompletely understood, although dysfunction of the hypothalamic pituitary adrenal (HPA) axis might be involved. We examined the association between cortisol responses to laboratory-induced mental stress and the progression of coronary artery calcification (CAC). METHODS AND RESULTS:Participants were 466 healthy men and women (mean age = 62.7±5.6 yrs), without history or objective signs of CHD, drawn from the Whitehall II epidemiological cohort. At the baseline assessment salivary cortisol was measured in response to mental stressors, consisting of a 5-min Stroop task and a 5-min mirror tracing task. CAC was measured at baseline and at 3 years follow up using electron beam computed tomography. CAC progression was defined as an increase >10 Agatston units between baseline and follow up. 38.2% of the sample demonstrated CAC progression over the 3 years follow up. There was considerable variation in the cortisol stress response, with approximately 40% of the sample responding to the stress tasks with an increase in cortisol of at least 1 mmol/l. There was an association between cortisol stress reactivity (per SD) and CAC progression (odds ratio = 1.27, 95% CI, 1.02-1.60) after adjustments for age, sex, pre-stress cortisol, employment grade, smoking, resting systolic BP, fibrinogen, body mass index, and use of statins. There was no association between systolic blood pressure reactivity and CAC progression (odds ratio per SD increase = 1.03, 95% CI, 0.85-1.24). Other independent predictors of CAC progression included age, male sex, smoking, resting systolic blood pressure, and fibrinogen. CONCLUSION:Results demonstrate an association between heightened cortisol reactivity to stress and CAC progression. These data support the notion that cortisol reactivity, an index of HPA function, is one of the possible mechanisms through which psychosocial stress may influence the risk of CHD.http://europepmc.org/articles/PMC3273460?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Mark Hamer
Romano Endrighi
Shreenidhi M Venuraju
Avijit Lahiri
Andrew Steptoe
spellingShingle Mark Hamer
Romano Endrighi
Shreenidhi M Venuraju
Avijit Lahiri
Andrew Steptoe
Cortisol responses to mental stress and the progression of coronary artery calcification in healthy men and women.
PLoS ONE
author_facet Mark Hamer
Romano Endrighi
Shreenidhi M Venuraju
Avijit Lahiri
Andrew Steptoe
author_sort Mark Hamer
title Cortisol responses to mental stress and the progression of coronary artery calcification in healthy men and women.
title_short Cortisol responses to mental stress and the progression of coronary artery calcification in healthy men and women.
title_full Cortisol responses to mental stress and the progression of coronary artery calcification in healthy men and women.
title_fullStr Cortisol responses to mental stress and the progression of coronary artery calcification in healthy men and women.
title_full_unstemmed Cortisol responses to mental stress and the progression of coronary artery calcification in healthy men and women.
title_sort cortisol responses to mental stress and the progression of coronary artery calcification in healthy men and women.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2012-01-01
description BACKGROUND:Psychosocial stress is a risk factor for coronary heart disease (CHD). The mechanisms are incompletely understood, although dysfunction of the hypothalamic pituitary adrenal (HPA) axis might be involved. We examined the association between cortisol responses to laboratory-induced mental stress and the progression of coronary artery calcification (CAC). METHODS AND RESULTS:Participants were 466 healthy men and women (mean age = 62.7±5.6 yrs), without history or objective signs of CHD, drawn from the Whitehall II epidemiological cohort. At the baseline assessment salivary cortisol was measured in response to mental stressors, consisting of a 5-min Stroop task and a 5-min mirror tracing task. CAC was measured at baseline and at 3 years follow up using electron beam computed tomography. CAC progression was defined as an increase >10 Agatston units between baseline and follow up. 38.2% of the sample demonstrated CAC progression over the 3 years follow up. There was considerable variation in the cortisol stress response, with approximately 40% of the sample responding to the stress tasks with an increase in cortisol of at least 1 mmol/l. There was an association between cortisol stress reactivity (per SD) and CAC progression (odds ratio = 1.27, 95% CI, 1.02-1.60) after adjustments for age, sex, pre-stress cortisol, employment grade, smoking, resting systolic BP, fibrinogen, body mass index, and use of statins. There was no association between systolic blood pressure reactivity and CAC progression (odds ratio per SD increase = 1.03, 95% CI, 0.85-1.24). Other independent predictors of CAC progression included age, male sex, smoking, resting systolic blood pressure, and fibrinogen. CONCLUSION:Results demonstrate an association between heightened cortisol reactivity to stress and CAC progression. These data support the notion that cortisol reactivity, an index of HPA function, is one of the possible mechanisms through which psychosocial stress may influence the risk of CHD.
url http://europepmc.org/articles/PMC3273460?pdf=render
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