This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. In recent years, a number of studies have demonstrated that depression is a risk factor for atherosclerotic-related cardiovascular medical events. Given the high rate of cardiovascular disease (CVD) and depression in this country, it is important to examine mechanisms by which depression may contribute to cardiac pathophysiology. In this study, 70 older, nonsmoking men and women at high risk for CVD (or with manifest CVD, not on medications, or on medications which can be safely stopped for testing), who are also depressed, will be randomized to a cognitive-behavioral intervention or usual care. At baseline, subjects will be assessed for traditional cardiovascular risk factors (lipids, blood pressure, exercise habits) and nontraditional cardiovascular risk factors (e.g., endothelial dysfunction, urinary nitrogen oxides, platelet reactivity, cell adhesion molecules, asymmetric dimethylarginine). Hypothalamic pituitary axis (HPA) abnormalities [measured with cortisol levels, diurnal cortisol and reactivity] and sympathomedullary/parasympathetic activity (measured with respiratory sinus activity (RSA), baroreflex activity, and presystolic ejection period (PEP) reactivity) will also be assessed. Subjects will be randomized to an intervention (16 weeks of cognitive-behavioral therapy (CBT) for depression) or to a wait-list control (followed by CBT). The above measures will be assessed at baseline, post-treatment and at 6-month follow-up. Thirty non-depressed controls matched for age, gender, and cardiovascular risk level will also be assessed at the pre-treatment time period. We hypothesize that at baseline, compared to controls, depressed subjects will have significantly higher levels of HPA activity, lower RSA, higher endothelial dysfunction, but similar levels of PEP. We hypothesize that subjects in the intervention will demonstrate significant reduction in depressed mood, improved HPA activity, lower endothelial dysfunction, and lower RSA, compared to control subjects and that these changes will be maintained at six-month follow-up. The study is designed to provide new information on how depression might lead to atherosclerosis and affect cardiovascular morbidity and mortality.
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