Psychobiology of depression/distress in congestive heart failure

Abstract

Heart failure affects millions of Americans and new diagnosis rates are expected to almost triple over the next 30 years as our population ages. Affective disorders including clinical depression and anxiety are common in patients with congestive heart failure. Furthermore, the presence of these disorders significantly impacts quality of life, medical outcomes, and healthcare service utilization. In recent years, the literature has attempted to describe potential pathophysiologic mechanisms relating affective disorders and psychosocial stress to heart failure. Several potential mechanisms have been proposed including autonomic nervous system dysfunction, inflammation, cardiac arrhythmias, and altered platelet function. These mechanisms are reviewed in this article. Additional novel mechanisms such as mental stress-induced myocardial ischemia are also discussed.

Circulating levels of soluble intercellular adhesion molecule-1 (sICAM-1) independently predict depressive symptom severity after 12 months in heart failure patients

“…Heart failure (HF) is a major public health concern associated with both increased incidence of depressive symptoms and clinical depression as well as elevated pro-inflammatory activities indicated by levels of adhesion molecules or inflammatory cytokines (Mari et al, 2002;Parissis et al, 2005;Rutledge et al, 2006;York et al, 2008). Indeed, we and others report cross-sectional associations between inflammation and depressive symptoms or clinical depression in HF patients (Moorman et al, 2007;Parissis et al, 2004;Redwine et al, 2007).…”

2013 ACCF/AHA Guideline for the Management of Heart Failure

“…845 Potential pathophysiologic mechanisms proposed to explain the high prevalence of depression in HF include autonomic nervous system dysfunction, inflammation, cardiac arrhythmias, and altered platelet function, but the mechanism remains unclear. 846 Although remission from depression may improve cardiovascular outcomes, the most effective intervention strategy is not yet known. 842 …”

Psychological vulnerability, ventricular tachyarrhythmias and mortality in implantable cardioverter defibrillator patients: is there a link?

“…An imbalance between the sympathetic and parasympathetic nervous systems is assumed to be one of the primary physiological mechanisms through which distress may influence overall health and predict clinical outcomes in patients with cardiovascular disease [45]. Patients with depression and anxiety tend to have impaired vagally mediated baroflex control of the heart and an increase in sympathetic tone, characterized by an increased level of norepinephrine [46], a decrease in heart rate variability [47,48] and abnormal heart rate turbulence [49].…”

“…Heterogeneities in ventricular repolarization, including QT-dispersion and T-wave alternans, have also been implicated in cardiovascular prognosis and SCD [45]. The QT-interval is the electrocardiographic representation of ventricular repolarization time, and variability in the QT-interval has been consistently linked with depression and emotional stress in patients with a myocardial infarction or acute coronary syndrome [52,53].…”

“…Cortisol, which is the primary glucocorticoid in humans, and corticotrophinreleasing hormone have been found to stimulate proinflammatory cytokine release, which exerts a deleterious effect on the heart due to its implication in plaque ruptures [58] and by suppressing cardiac contractility [58] while impeding cardiac remodeling [57,59]. In addition, excess cortisol can contribute to abdominal obesity, insulin resistance, hypertension, oxidative stress, altered plasma lipoprotein metabolism and vascular tone change, which can all contribute to cardiovascular disease progression [45].…”