2006
DOI: 10.1016/j.jacc.2005.12.078
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Metyrapone Improves Endothelial Dysfunction in Patients With Treated Depression

Abstract: Inhibition of cortisol production by metyrapone ameliorates the endothelial dysfunction seen in depression, suggesting that the mechanism of the endothelial dysfunction may involve cortisol.

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Cited by 61 publications
(40 citation statements)
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“…[31][32][33] Endothelial function is also impaired during and after episodes of depression, 34 -37 even among patients with CAD, 38 perhaps via effects of depression on cortisol release. 39 Depression could indirectly alter control of other atherosclerotic risk factors through its effects on weight, smoking, alcohol use, and exercise, and the present results suggested that addition of these factors might indeed account for a portion of the observed association of depressive symptoms with atherosclerosis.…”
Section: Discussionsupporting
confidence: 52%
“…[31][32][33] Endothelial function is also impaired during and after episodes of depression, 34 -37 even among patients with CAD, 38 perhaps via effects of depression on cortisol release. 39 Depression could indirectly alter control of other atherosclerotic risk factors through its effects on weight, smoking, alcohol use, and exercise, and the present results suggested that addition of these factors might indeed account for a portion of the observed association of depressive symptoms with atherosclerosis.…”
Section: Discussionsupporting
confidence: 52%
“…ACTH stimulates secretion and growth of zona fasciculate and zona reticularis of adrenal gland and stimulates the secretion of cortisol. Therefore, there is an increase in plasma cortisol level (22). However, the results showed that the level of serum glucose was approximately same in both groups after noise exposure.…”
Section: Control Groupmentioning
confidence: 79%
“…The model predicts that standard depression treatments will probably be ineffective for somatic depressions because of their atypical etiology and underlying neurophysiology. Standard depression treatments must lead to significant improvement in CAD risk factors in order to normalize atherosclerosis- and CAD-associated abnormalities, including increased systemic inflammation, platelet activation (except selective serotonin reuptake inhibitors), endothelial dysfunction, reduced heart rate variability, and baroreceptor sensitivity [117]. If most depressions in ACS patients consist of the somatic type, screening seems problematic since somatic depression has no clearly effective treatment yet.…”
Section: Discussionmentioning
confidence: 99%