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Depression is associated with flatter cortisol rhythms in patients with coronary artery disease
Mimi R Bhattacharyya1, Gerard J Molloy, Andrew Steptoe
1Department of Epidemiology and Public Health, University College London, London, UK. m.bhattacharyya@ucl.ac.uk
Insights
Depressed patients with coronary artery disease (CAD) exhibit flatter cortisol rhythms, potentially worsening atherosclerosis. This study links depressive symptoms to altered daily cortisol patterns in individuals with suspected CAD.
Area of Science:
- Endocrinology
- Cardiology
- Psychiatry
Background:
- Depression is linked to coronary heart disease (CHD), but mechanisms remain unclear.
- Cortisol plays a role in coronary artery disease (CAD) development.
- Limited evidence directly connects depression, cortisol, and CAD in patients.
Purpose of the Study:
- To evaluate daily cortisol output in patients with suspected CAD.
- To assess the relationship between depressive symptoms and cortisol patterns in these patients.
Main Methods:
- Eighty-eight patients with suspected CAD provided saliva samples over a day.
- Depressive mood was measured using the Beck Depression Inventory.
- Actigraphy objectively determined waking times.
Main Results:
- A flatter daily cortisol slope was observed in more depressed patients with CAD (P<.001), not in those without CAD (P=.68).
- This flatter rhythm resulted from lower morning and higher evening cortisol levels in depressed CAD patients.
- Higher cortisol upon waking was noted in CAD patients versus non-CAD patients (P=.04), unrelated to depression.
Conclusions:
- Altered cortisol rhythms in depressed patients with CAD may contribute to coronary atherosclerosis progression.
Objective:
Depression is associated with coronary heart disease, but the underlying mechanisms are not fully understood. Cortisol is involved in the development of coronary artery disease (CAD), but evidence directly linking depression with cortisol in patients with CAD is limited. This study evaluated cortisol output over the day in patients with suspected CAD in relation to depressive symptoms.
Methods:
Eighty-eight patients who were being investigated for suspected CAD (defined by clinical symptoms plus positive exercise tests or myocardial perfusion scans) took eight saliva samples over the day and evening. Depressed mood was assessed with the Beck Depression Inventory. Actigraphy was used to define time of waking objectively.
Results:
The cortisol awakening response and cortisol rhythm over the remainder of the day and evening were analyzed separately. Fifty-two (61.9%) patients were later found to have definite CAD on angiography, while the remainder did not. The cortisol slope over the day was flatter in more depressed patients with CAD (P<.001) but was not related to depression in patients without CAD (P=.68). This effect was due to the combination of lower cortisol early in the day and higher cortisol in the evening in more depressed CAD patients, independent of age, gender, medication, and times of waking and sleeping (P=.003). Additionally, cortisol measured on waking and 15 and 30 min after waking was greater in CAD than in non-CAD patients (P=.04), but was not related to depression.
Conclusions:
The flatter cortisol rhythms of more depressed CAD patients may contribute to the progression of coronary atherosclerosis.
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