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Mild to moderate levels of depressive symptoms as characterized by Beck Depression Inventory (BDI) scores of > or =10 are associated with decreased survival after acute myocardial infarction (AMI). We investigated whether lower levels of depressive symptoms are also associated with increased mortality risk after AMI. We prospectively studied 285 patients with AMI who survived to discharge for evidence, at the time of hospitalization, of a DSM-IIIR mood disorder (using a structured clinical interview) and for symptoms of depression (using the BDI). The overall mortality rate at 4 months was 6.7%. Multiple logistic regression (chi-square 35.79, p < or =0.001) revealed that the independent predictors of mortality were: age > or =65 years, left ventricular ejection fraction <35%, diabetes mellitus, and any depression (DSM-IIIR mood disorder or BDI > or =10) present at the time of AMI. Among patients > or =65 years old with left ventricular ejection fraction <35%, the 4-month mortality was 12%. However, in this same group, those with any depression at the time of AMI had a 4-month mortality of 50% (relative risk 4.1, p = 0.01). Among patients aged > or =65 years, the mortality according to BDI scale grouping 0 to 3, 4 to 9, and 10+ was 2.6%, 17.1%, and 23.3%, respectively (p <0.002). Highest mortality rates were observed in patients with most severe depressive symptoms. However, compared with those without depression, higher mortality was also observed at very low levels of depressive symptoms (BDI 4 to 9) not generally considered clinically significant and below the level usually considered predictive of increased post-AMI mortality. [ABSTRACT FROM AUTHOR]

Purpose: To measure the effect of long-term clinical hormone replacement therapy on brachial artery vasomotor responses, and to compare these responses in premenopausal and postmenopausal women.Patients and Methods: We studied 23 postmenopausal women, including 18 who were evaluated prior to starting clinically indicated oral hormone replacement therapy. Twelve postmenopausal women received estrogen alone, the other 6 were treated with estrogen/medroxyprogesterone combinations. Eleven premenopausal volunteers served as a comparison group. Change in brachial artery diameter in response to postischemic hyperemic flow and sublingual nitroglycerin was measured by ultrasound.Results: The 18 postmenopausal subjects receiving hormone replacement showed a progressive improvement in their postischemic vasodilation. Mean (+/-SD) postischemic vasodilation was 0.4%+/-7.1% prior to estrogen replacement. There were significant increases in postischemic vasodilation of 4.8%+/-6.6% after 1 month and 8.3%+/-3.4% after 6 months of estrogen replacement. The response to nitroglycerin was similar at all time points studied. Women with the most abnormal responses to hyperemic flow at baseline demonstrated the greatest improvement after 6 months of hormone replacement therapy. Premenopausal and postmenopausal subjects differed in their response to hyperemic flow, with premenopausal women showing 5.8% vasodilatation compared with a 0.6% vasodilation in postmenopausal women (P=0.046).Conclusions: Endothelial function is abnormal in many postmenopausal women compared with premenopausal women, and in some postmenopausal women it can be enhanced by estrogen replacement therapy. This effect may increase with prolonged use. [ABSTRACT FROM AUTHOR]

The bed nucleus of the stria terminalis (BNST) is believed to be a critical relay between the central nucleus of the amygdala (CE) and the paraventricular nucleus of the hypothalamus in the control of hypothalamic-pituitary-adrenal (HPA) responses elicited by conditioned fear stimuli. If correct, lesions of CE or BNST should block expression of HPA responses elicited by either a specific conditioned fear cue or a conditioned context. To test this, rats were subjected to cued (tone) or contextual classical fear conditioning. Two days later, electrolytic or sham lesions were placed in CE or BNST. After 5 days, the rats were tested for both behavioral (freezing) and neuroendocrine (corticosterone) responses to tone or contextual cues. CE lesions attenuated conditioned freezing and corticosterone responses to both tone and context. In contrast, BNST lesions attenuated these responses to contextual but not tone stimuli. These results suggest CE is indeed an essential output of the amygdala for the expression of conditioned fear responses, including HPA responses, regardless of the nature of the conditioned stimulus. However, because lesions of BNST only affected behavioral and endocrine responses to contextual stimuli, the results do not support the notion that BNST is critical for HPA responses elicited by conditioned fear stimuli in general. Instead, the BNST may be essential specifically for contextual conditioned fear responses, including both behavioral and HPA responses, by virtue of its connections with the hippocampus, a structure essential to contextual conditioning. The results are also not consistent with the hypothesis that BNST is only involved in unconditioned aspects of fear and anxiety.