Abstract 1013: Depression and Heart Failure: A Recipe for Inflammation?

Abstract

Background: Depression is common among HF patients, and is independently associated with morbidity and mortality. Proinflammatory markers, which are elevated in each condition, may adversely affect clinical outcomes in HF patients. Initial studies show that tumor necrosis factor (TNF)-α is related to depression in this population. To date, the relationship of other proinflammatory markers to depression in HF is unclear. Thus, we investigated differences in soluble intracellular adhesion molecule (sICAM)-1, interleukin (IL)-6, and TNF-α between HF patients, with and without depressive symptoms, and controls, with and without depressive symptoms. Methods: Individuals with HF (n = 29, aged 55 ± 8 years, 76% male) and without HF (n = 43, aged 50 ± 7 years, 51% male) were recruited from HF clinics and from the community. Subjects completed the Beck Depression Inventory-II (BDI), were classified as depressed (BDI ≥ 10) or non-depressed (BDI < 10), and underwent phlebotomy. Proinflammatory markers were measured by ELISA. Data were analyzed with linear regression and ANCOVA, using age, gender, BMI, and medications as covariates. Results: Seventeen HF (58%) and 7 controls (16%) were coded as depressed. The depressed HF subgroup differed from the non-depressed controls for each of the inflammatory markers (see Table , p < .05). Additionally, the presence of both HF and depression were independently associated with an increase in sICAM-1 (β = 3.05, p = .003) and IL-6 (β = 2.3, p= .03), but not TNF- α (β = 1.8, p = .07). Conclusion: Increased inflammation in HF results from multiple biomarkers, including sICAM-1 and IL-6. The combination of HF and depression is an independent predictor of increased inflammation. This relationship may partly explain increases in morbidity and mortality associated with comorbid depression and HF. Careful assessment and treatment of depression in HF patients is warranted. Results of ANCOVA for HF and Controls