Congestive heart failure (CHF) is a major public health concern, affecting more than 4.5 million Americans with 550,000 cases being diagnosed each year. CHF is characterized by neuroimmune activation, including increased levels of proinflammatory cytokines and increased leukocyte activation and adhesion. Depression is the most robust behavioral predictor of premature mortality and morbidity among patients with CHF. A relatively large literature documents neuroimmune and cellular adhesion molecule alterations in patients with major depression, but translation of these observations into clinically relevant outcomes in CHF patients remains incomplete. No studies have examined whether neuroimmune activation is the underlying pathophysiological mechanism through which depression worsens outcomes in patients with CHF. This study will examine BNP levels and neuroimmune (norepinephrine, IL-6, TNF-alpha, IL-1beta, CRP) and cellular adhesion molecule (sICAM-1 and sP-selectin levels, CD11a and CD11b expression on peripheral blood mononuclear cells (PBMC), and PBMC chemotaxis) characteristics in 200 CHF patients with and without major depression and 100 non-CHF controls with and without major depression. CHF patients with and without major depression will be followed in a naturalistic prospective design over 18 months to examine neuroimmune, adhesion molecule contributions to adverse clinical outcomes. The overarching hypothesis of this study is that neuroimmune and adhesion molecule activation constitute an important pathophysiological pathway linking depression to worse outcomes in CHF.
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