Increased left ventricular mass in hypercortisolemic depressed patients: a hypothesis based on a case series.

BACKGROUND: Hypercortisolemia in depressed patients is known to be related to changes in body composition, especially increased ectopic fat and lowered bone mineral density. Both hypercortisolemia in patients with Cushing's disease and depression in patients undergoing treatment with hemodialysis have been shown to be associated with increased left ventricular mass. HYPOTHESIS: Increased activity of the hypothalamus-pituitary-adrenal (HPA) system in depressed patients is related to high left ventricular mass. EMPIRICAL DATA: To corroborate our hypothesis, we measured left ventricular mass in 5 depressed patients with clear evidence for HPA system activation (nonsuppression in dexamethasone suppression test [DST]; increased 24 h cortisol excretion) and 27 healthy controls. We found increased left ventricular mass in hypercortisolemic depressed patients compared to healthy controls (343±97 vs. 176±57 gr; p=0.007). CONCLUSIONS: Depression is known to be related to an increased risk of cardial morbidity and mortality, although the risk architecture is not completely understood. We hypothesize that hypercortisolemic depression is associated with increased left ventricular mass, which is known to be a strong predictor for cardial mortality. Thus, a potential effect of activated stress-responsive systems on heart morphology may contribute to depressed patients' increased cardiovascular risk.

Do depressed patients without activation of the hypothalamus-pituitary-adrenal (HPA) system have metabolic disturbances?

This study compared features of the metabolic syndrome between healthy controls and depressed patients without activation of the hypothalamus-pituitary-adrenal (HPA) system. After exclusion of non-suppressors to 1mg dexamethasone, we included 20 depressed inpatients and 34 healthy controls in the analyses. We assessed HPA system activity (diurnal saliva cortisol profile, cortisol excretion), normetanephrine excretion as well as fasting glucose, lipid profile and blood pressure. With regard to body composition, we measured waist circumference as well as visceral fat and adrenal volume by magnetic resonance (MR) imaging. Five depressed patients (25%) and five healthy controls (15%) fulfilled the criteria of the metabolic syndrome according NCEP-ATP-III. Depression was significantly related with fasting glucose and negatively associated with mean blood pressure (BP) and, by trend, with low HDL-cholesterol. We conclude that depressed patients may have modest metabolic disturbances even in the complete absence of activation of stress-responsive systems. Hence some metabolic disturbances in depressed patients may not be explicable by HPA activation. Additional factors are required to mediate the link between affective and metabolic disorders.