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Impaired cortisol response to acute stressors in patients with coronary disease. Implications for inflammatory

J Nijm1, M Kristenson, A G Olsson

  • 1Department of Medicine, Högland Hospital, Eksjö, and Department of Medicine and Care, Division of Cardiology, Faculty of Health Sciences, Linköping University, Linköping, Sweden. johnny@nijm.se

Journal of Internal Medicine
|August 19, 2007
PubMed

Insights

Coronary artery disease patients show abnormal cortisol patterns and a weakened stress response, suggesting a link between stress, inflammation, and HPA axis dysfunction in cardiovascular disease.

Area of Science:

  • Endocrinology
  • Cardiovascular Medicine
  • Immunology

Background:

  • Inflammation is a key factor in atherosclerotic disease progression.
  • The hypothalamic-pituitary-adrenal (HPA) axis regulates stress response and inflammation.
  • Altered HPA axis activity may contribute to heightened inflammation in coronary artery disease (CAD).

Purpose of the Study:

  • To investigate the relationship between HPA axis activity and inflammatory markers in patients with CAD.
  • To determine if CAD patients exhibit altered cortisol secretion patterns and stress responses compared to healthy controls.

Main Methods:

  • Assessed 30 CAD patients post-acute coronary syndrome for serum C-reactive protein (CRP) and interleukin-6.
  • Measured 24-h urinary free cortisol and salivary cortisol (awakening, bedtime).
  • Evaluated cortisol and inflammatory marker responses to standardized physical and psychological stress tests.

Main Results:

  • CAD patients displayed higher 24-h cortisol secretion and a flattened diurnal rhythm with elevated bedtime cortisol.
  • Evening cortisol levels correlated significantly with serum inflammatory markers.
  • CAD patients showed a blunted cortisol response to acute stressors, with stress-induced CRP increase observed only in this group.

Conclusions:

  • CAD patients exhibit distinct HPA axis dysfunction characterized by altered cortisol patterns and blunted stress responses.
  • This HPA axis dysfunction may impair the containment of inflammatory activity in CAD.
  • Findings suggest a potential link between stress, inflammation, and cardiovascular disease via HPA axis dysregulation.
Abstract

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