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The extent to which depression impairs health-related quality of life (HRQoL) in the physically ill has not been clearly established.
To quantify the adverse influence of depression and anxiety assessed at the time of first myocardial infarction and 6 months later, on the physical aspect of HRQoL 12 months after the infarction.
In all, 260 in-patients, admitted following first myocardial infarction, completed the Hospital Anxiety and Depression Scale and the Medical Outcomes Study SF–36 assessment before discharge and at 6- and 12-month follow-up.
Depression and anxiety 6 months after myocardial infarction predicted subsequent impairment in the physical aspects of HRQoL (attributable adjusted R2=9%, P<0.0005). These negative effects of depression and anxiety on outcome were mediated by feelings of fatigue. Depression and anxiety present before myocardial infarction did not predict HRQoL 12 months after myocardial infarction.
Detection and treatment of depression and anxiety following myocardial infarction improve the patient's health-related quality of life.
Social adversity may be a risk factor for depression, by increasing Cortisol secretion, which impairs serotonin (5-HT) neurotransmission.
To examine this causal pathway in a community setting.
Women who were currently ICD–10 depressed (n=94), vulnerable to depression but not depressed (n=166) and non-vulnerable controls (n=177) were recruited. We assessed social adversity and vulnerability (Life Eventsand Difficulties Schedule; Self Evaluation and Social Support Scales) and psychiatric state (Schedules for Clinical Assessment in Neuropsychiatry). Salivary cortisol concentrations were measured at 09.00 and 23.00 h. Serotonin function was assessed using prolactin responses to dexfenfluramine.
Cortisol concentrations were not increased in the depressed or vulnerable. Morning salivary and serum cortisol were reduced in depression. Evening cortisol was increased after recent life events. Life events and depression were associated with increased prolactin responses.
The hypothalamic–pituitary–adrenal axis is sensitive to social stress but does not mediate vulnerability to depression. Exaggerated 5-HT2 receptor responsiveness to stress may play a role in the evolution of depression.
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