4.3 Article

Psychophysiological and cortisol responses to psychological stress in depressed and nondepressed older men and women with elevated cardiovascular disease risk

期刊

PSYCHOSOMATIC MEDICINE
卷 68, 期 4, 页码 538-546

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/01.psy.0000222372.16274.92

关键词

depression; cardiovascular risk; psychophysiology; cortisol

资金

  1. NCRR NIH HHS [5 M01 RR000070] Funding Source: Medline
  2. NIA NIH HHS [AG18784] Funding Source: Medline

向作者/读者索取更多资源

Objective: The objective of this study was to compare psychophysiological and cortisol reactions to psychological stress in older depressed and nondepressed patients at risk for cardiovascular disease (CVD). Methods: Forty-eight depressed participants and 20 controls with elevated cardiovascular risk factors underwent a psychological stress test during which cardiovascular variables were measured. Salivary cortisol was collected after each test segment. Traditional (e.g., lipids) and atypical (e.g., C-reactive protein) CVD risk factors were also obtained. Results: At baseline, the groups did not differ on lipid levels, flow-mediated vasodilation, body mass index, or asymmetric dimethylarginine. However, the depressed patients had significantly higher C-reactive protein levels. Contrary to our hypothesis, there were no differences in baseline cortisol levels or diurnal cortisol slopes, but depressed patients showed significantly lower cortisol levels during the stress test (p =.03) and less cortisol response to stress. Compared with nondepressed subjects, depressed subjects also showed lower levels of respiratory sinus arrhythmia (RSA(TF)) during the stress test (p =.02). Conclusions: In this sample, older depressed subjects with elevated risk for CVD, exhibited a hypocortisol response to acute stress. This impaired cortisol response might contribute to chronic inflammation (as reflected in the elevated C-reactive proteins in depressed patients) and in other ways increase CVD risk. The reduced RSA(TF) activity may also increase CVD risk in depressed patients through impaired autonomic nervous system response to cardiophysiological demands.

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