Authors: Nijm, J.; Kristenson, M.¹; Olsson, A. G.²; Jonasson, L.²

Source: Journal of Internal Medicine, Volume 262, Number 3, September 2007 , pp. 375-384(10)

Publisher: Wiley-Blackwell

Abstract:

.  Nijm J, Kristenson M, Olsson AG, Jonasson L (Högland Hospital, Eksjö; and Linköping University, Linköping; Sweden). Impaired cortisol response to acute stressors in patients with coronary disease. Implications for inflammatory activity. J Intern Med 2007; 262: 375-384. Objectives. 

Inflammation is assumed to play a major role in the progress of atherosclerotic disease. We hypothesized that an altered hypothalamic-pituitary adrenal (HPA) axis activity was linked to a disinhibited inflammatory activity in patients with coronary artery disease (CAD). Methods. 

Thirty CAD patients were assessed 12-14 weeks after a first-time acute coronary syndrome. Serum samples were assayed for C-reactive protein (CRP) and interleukin-6. Free cortisol was measured in a 24-h urine sample and in repeated saliva samples 30 min after awakening and at bedtime. The levels of inflammatory markers and cortisol were also determined before and after standardized physical and psychological stress tests. Results. 

The CAD patients had a higher 24-h cortisol secretion and a flattened diurnal slope, resulting from significantly higher cortisol levels at bedtime, compared to clinically healthy controls. The levels of evening cortisol were strongly related to inflammatory markers in serum. When exposed to acute physical and psychological stressors, the CAD patients showed a significantly blunted cortisol response compared to controls. In addition, a stress-induced increase in CRP was only observed in the patient group. Conclusions. 

Patients with CAD exhibited a cortisol pattern that markedly differed from controls. The data indicate that a dysfunctional HPA axis response involves a failure to contain inflammatory activity in CAD patients, thus providing a possible link between stress and inflammation in disease.

Keywords: coronary artery disease; cortisol; inflammation; myocardial infarction; stress

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1365-2796.2007.01817.x

Affiliations: 1: Department of Health and Society, Faculty of Health Sciences, Linköping University, Linköping; Sweden 2: Department of Medicine and Care, Division of Cardiology, Faculty of Health Sciences, Linköping University, Linköping

Publication date: 2007-09-01

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