Depressive symptoms and inflammation among heart failure patients

Psychological depression has been linked to heart failure, both an antecedent to and as a risk factor for poor outcomes among patients with existing heart failure. Elevated levels of proinflammatory cytokines have been proposed as a possible physiological link between the 2 conditions. The objective of this study was to examine the proinflammatory cytokines interleukin (IL)-6, IL-1beta, and tumor necrosis factor-alpha (TNFalpha) in heart failure patients with and without elevated symptoms of depression.

Thirty-two heart failure patients were recruited from an outpatient heart failure clinic. Depressive symptoms were measured with the Beck Depression Inventory (BDI), and a patient was classified as having elevated symptoms of depression if he/she scored > or = 10. The cognitive-affective subscale score of the BDI, which measures depressed mood independent of physical symptoms, was also examined.

In the multiple linear regression models controlling for age, sex, smoking, and antidepressant medication use, there was no relation between BDI score and IL-6 (P = .7612) or IL-1beta (P = .8261). However, there was a statistically significant positive relation between BDI score and TNFalpha (P = .0374). There was also a significant relation between an elevated cognitive-affective score and TNFalpha (P = .0322) but no association with IL-6 (P = .8593) or IL-1beta (P = .3737).

The association between TNFalpha and the cognitive-affective subscale, which eliminates the physical signs and symptoms that are shared by depression and heart failure, demonstrates a depression-specific activation of proinflammatory cytokines that may promote disease progression and mortality in patients with heart failure.