Abstract
Disturbances of HPA axis functioning as represented by cortisol awakening reaction (CAR) belong to the mediating pathways linking psychosocial distress and cardiovascular risk. Both depression and anxiety have been confirmed as independent risk factors for coronary artery disease (CAD). However, data on anxiety and cortisol output in CAD patients are scarce. Based on previous data, we hypothesized that anxiety would be associated with higher cortisol output and a more pronounced morning increase in moderately depressed CAD patients. 77 patients (60 y, 79% male) underwent saliva sampling (+0, +30, +45, +60 min after awakening, midday and late-night sample). Anxiety was measured using the Hospital Anxiety and Depression Scale (HADS) and patients were grouped into anxious versus non anxious subjects based upon the recommended score (≥11). A repeated measures ANOVA yielded a significant time and quadratic time effect referring to the typical CAR. Anxious patients showed a significantly steeper 30 min increase, higher AUCi, lower waking and late-night cortisol levels. The steeper cortisol increase in the anxious group is in line with previous data and may be interpreted as a biological substrate of affect regulation. The lower basal and late-night levels coupled with greater AUCi mirror a more dynamic reactivity pattern compared to depressed subjects without anxiety.
Highlights
Coronary artery disease (CAD) represents a major cause of morbidity and mortality worldwide [1]
Most of them were on beta blockers, statins and ACE-inhibitors, and most had a history of myocardial infarction (MI)
There were no significant differences in AUCg or AUCi with regard to NYHA class, hypertension, diabetes, history of MI, smoking, beta blockers, statins, antidepressants, marital status, socio-economic status (SES), employment status, nor Type D
Summary
Coronary artery disease (CAD) represents a major cause of morbidity and mortality worldwide [1]. Both depression [2,3,4] and anxiety [5,6] have been posited as independent risk factors for both incidence and prognosis of CAD. Altered functioning of the hypothalamic pituitary adrenal (HPA) axis are thought to be among the mediating pathways involved in CAD as well as in depression and anxiety [7,8], promoting hypertension, procoagulant activity, and other cardiac risk factors [9,10,11]. Waller et al [14] reported blunted cortisol reactivity to a psychosocial stress test (Trier Social Stress Test, TSST) in depressed CAD but not in depressed non-CAD patients
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