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

Abstract

Background Clinical outcomes are worse for heart failure (HF) patients presenting with symptoms of depression. Sympathetically modulated immune dysregulation associated with depression may be one mechanism leading to worse prognosis. Objectives We sought to determine whether depressive symptoms are related to alterations in sensitivity of peripheral blood mononuclear cells (PBMC) to β-adrenergic agonists in HF patients by measuring in vitro chemotaxis (CTX) to isoproterenol (ISO) at rest and following acute exercise in HF patients and controls. Methods 80 HF patients and 44 controls (mean age ± SEM: 56.4 ± 1.3 years) completed the Beck Depression Inventory (BDI) and a 15 minute mild graded exercise task on a stationary bicycle. Exercise intensity was kept relative to fitness levels for all participants by gradually increasing resistance to reach a Borg scale subjective rating of 12 –13, “somewhat hard”. Plasma norepinephrine (NE) and epinephrine (EPI) levels were measured in plasma before and after exercise. Chemotaxis to ISO (CTX-I) was determined by measuring in vitro PBMC migration through a modified Boyden chamber. Results In HF patients, depressive symptom severity was associated with greater CTX following exercise (p = .001). Higher resting NE in HF patients was also associated with increased CTX to exercise (p = .03). Conclusion HF patients with higher depression symptoms and NE exhibited increased PBMC CTX-I to mild exercise, suggesting greater β-adrenergic sensitivity. Increased immune migration in HF patients having elevated depression symptoms could be associated with cardiac remodelling and HF disease progression.

Relationship between depression and subclinical left ventricular changes in the general population

“…Treatment adherence, lifestyle factors, platelet reactivity, dysregulation of the autonomic nervous system, dysregulated hypothalamic-pituitary-adrenal axis activity, and altered immune/inflammation responses were suggested as possible biobehavioural links 30–35. Among these factors, altered immune/inflammation responses are considered a leading mechanism of worse cardiovascular outcomes associated with depression, and increased serum CRP concentration, an independent risk factor for CAD, was also demonstrated in subjects with depression 30 34 35. However, in our study, serum hsCRP concentration was comparable among study groups, and no interaction was identified between LV function and serum hsCRP concentration.…”

Pathophysiological Relationships Between Heart Failure and Depression and Anxiety

“…Increased β-adrenergic sensitivity is postulated to be associated with cardiac remodeling and progression of heart failure. 72 Anxiety reduces compliance with medications, resulting in shorter event-free survival. 73 No published studies on the combination of anxiety, epinephrine, and heart failure are available.…”

Heart Rate Response to Dypiridamole Stress in Relation to Perfusion and Function during Gated Technetium Tc99 M Sestamibi Spect Study

“…Dysfunctional autonomic nervousactivity may underlie both progressions of inflammation as well as elevated resting heart rate [14]. Elevated sympathetic activity modifies the inflammatory processand thereby promotes endothelial dysfunction and subsequent at hero progression [15]. So, The European Society of Hypertension/European Society of Cardiology guidelines recently proposed the inclusion of elevated heart rate when evaluating the cardiovascular risk profile of an individual [16].…”