Depressive symptoms and the regulation of proinflammatory cytokine expression in patients with coronary heart disease

Objective: Depressive symptoms increase the risk of morbidity and mortality in patients with coronary heart disease (CHD). Mounting evidence indicates that inflammatory processes may underlie this association. This study examined whether depressive symptoms are associated with the dysregulation of inflammatory cytokine production in response to an in vitro infectious challenge. Methods: Forty-one patients with CHD were enrolled 3 months or more after an acute myocardial infarction or revascularization procedure. Depressive symptoms were assessed through self-report and interviewer ratings. Cytokine production was measured after white blood cells were cultured in vitro with endotoxin in the presence of varying concentrations of dexamethasone. Results: Depressive symptoms were not associated with the quantity of in vitro inflammatory cytokine production. However, to the extent that they reported symptoms of depression, patients showed greater sensitivity to the anti-inflammatory properties of glucocorticoids. This was manifested by increased suppression of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) production by dexamethasone. Conclusions: Increased sensitivity to glucocorticoid inhibition could render depressed patients vulnerable to latent infections and inflammatory processes that accelerate the progression of cardiac disease.