A Potential Shift From Adaptive Immune Activity to Nonspecific Inflammatory Activation Associated With Higher Depression Symptoms in Chronic Heart Failure Patients

Abstract

Background: Chronic heart failure (CHF) patients with elevated depression symptoms are at greater risk of morbidity and mortality. The mechanisms linking symptoms of depression with disease progression in CHF are unclear. However, research studies have found evidence of alterations in immune activity associated with depression symptoms that may influence heart function. The present study sought to determine the relationship between depression symptoms and chemotaxis of peripheral blood mononuclear cells (PBMCs) in CHF patients, both at rest and in response to moderate exercise. Methods and Results: Sixty-five patients diagnosed with CHF (mean age, 59.8 6 14.5 years) and 45 non-CHF control subjects (mean age, 52.1 6 11.6) completed the Beck Depression Inventory (BDI) before undergoing a moderate 20-minute bicycle exercise task. Chemotaxis of PBMCs was examined in vitro to a bacterial peptide f-met leu phe (fMLP) and a physiologic chemokine, stromal cell derived factor-1 (SDF-1) immediately before and after exercise. CHF patients had reduced chemotaxis to SDF-1 (P 5 .025) compared with non-CHF subjects. Higher BDI scores were associated with reduced baseline chemotaxis to SDF-1 in both CHF and non-CHF subjects (P 5 .027). In contrast, higher BDI scores were associated with increased chemotaxis to fMLP (P 5 .049) and SDF-1 (P 5 .018) in response to exercise in the CHF patients. Conclusion: The present study suggests a shift in immune cell mobility in CHF patients with greater depression symptom severity, with reduced chemotaxis to a physiologically specific chemokine at rest but increased chemotaxis to both nonspecific and specific chemical attractants in response to physical activity. This could have implications for cardiac repair and remodeling in CHF patients and therefore may affect disease progression.

Cognitive/affective and somatic/affective symptom dimensions of depression are associated with current and future inflammation in heart failure patients

“…When analyzing both subcomponents and their change over time in a single analysis, only baseline cognitive/affective depression remained a covariate-independent associate of sTNFR2. This is in concurrence with two previous studies in HF patients (Ferketich, et al, 2005;Redwine et al, 2009), although it should be emphasized that these studies were crosssectional, had small sample sizes (n ≤ 56), and did not evaluate the link between depressive symptoms and soluble TNF receptors, nor the association with somatic/affective symptoms of depression. Most previous studies on depression and inflammation in HF were small (Andrei et al, 2007;Ferketich, et al, 2005;Parissis, et al, 2004;Redwine et al, 2007), except one study (n = 129) (Moorman, et al, 2007), such that adjustment for confounders was often not feasible.…”

Depression as a Potential Modulator of Beta-Adrenergic–Associated Leukocyte Mobilization in Heart Failure Patients

“…Indeed, depression is associated with increased leukocyte sensitivity to stress hormones (15), and greater pro-inflammatory responses to stress and physical exertion (2,3). Our research suggests that HF patients with elevated depression symptoms also exhibit augmented immune migration processes to exercise (16,17). While the clinical relevance of these findings remains to be elucidated, excessive leukocyte mobilization can elicit leukocyte infiltration into myocardial interstitium, which can underlie injury to the cardiovascular system (4,5).…”

Psychiatric Comorbidity and Mortality Among Veterans Hospitalized for Congestive Heart Failure

“…8 There may also be direct biological influences of mental illness, such as changes in immune system response. 9 Individuals with severe mental illness tend to delay cardiac care 10 and those with mental disorders have been found to under use evidence-based cardiovascular services. 11 …”