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Psychophysiological and Cortisol Responses to Psychological Stress in Depressed and Nondepressed Older Men and Women With Elevated Cardiovascular Disease Risk

From the Departments of Medicine and Psychiatry and Behavioral Sciences, Stanford University, Stanford, California (C.B.T., A.C., E.N., A.D., J.G.-D., W.T.R., R.O., J.C., H.K., D.S.); the Department of Veterans Affairs Health Care System, Palo Alto, California (A.C., W.T.R.); the Institute for Psychology, Department of Clinical Psychology and Psychotherapy, University of Basel, Basel, Switzerland (F.H.W.); and the Department of Psychology, University of Würzburg, Würzburg, Germany (M.A.K.).

Address correspondence and reprint requests to C. Barr Taylor, MD, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Rd., Room 1316, Stanford, CA 94305-5722. E-mail: btaylor{at}stanford.edu

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.

Key Words: depression • cardiovascular risk • psychophysiology • cortisol

Abbreviations: ACTH = adrenocorticotropic hormone; ADH = antidiuretic hormone; ADMA = asymmetric dimethylarginine; ANS = autonomic nervous system; BMI = body mass index; BP = blood pressure; BRC = baroreflex control; CAD = coronary artery disease; CBT = cognitive behavioral therapy; CHD = coronary heart disease; CO = cardiac output; CON = nondepressed control; CPM = cycles per minute; CVD = cardiovascular disease; DBP = diastolic blood pressure; DISH = Depression Interview and Structured Hamilton; ECG = electrocardiogram; FMVD = flow-mediated vasodilation; HDL = high-density lipoprotein; HPA = hypothalamic–pituitary–adrenal axis; HR = heart rate; HRSD = Hamilton Rating Scale of Depression; HRV = heart rate variability; LDL = low-density lipoprotein; MDD = major depressive disorder; MI = myocardial infarction; NO = nitric oxide; PANAS = Positive and Negative Affect Schedule; pCO₂ = partial pressure of carbon dioxide; PEP = preejection period; PSS = Perceived Stress Scale; RSA = respiratory sinus arrhythmia; RSA_TF = transfer function respiratory sinus arrhythmia; SBP = systolic blood pressure; SVR = systemic vascular resistance; TSST = Trier Social Stress Test; VLDL = very-low-density lipoprotein.

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