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The Role of Immune System Parameters in the Relationship Between Depression and Coronary Artery Disease

From the Uniformed Services University of the Health Sciences, Bethesda, MD (W.J.K.); and the Division of Cardiology, University of Maryland Hospital, Baltimore, MD (J.S.G.).

Address correspondence and reprint requests to Willem J. Kop, PhD, Department of Medical and Clinical Psychology, Uniformed Services University, 4301 Jones Bridge Road, Bethesda MD 20814. E-mail: WJKOP{at}USUHS.MIL

The relationship between depressive symptoms and coronary artery disease (CAD) is mediated in part by immune system parameters. This review describes research on the psychoneuroimmunological pathways accounting for the association between depression and CAD, and addresses conceptual and methodological issues. Relationships between central nervous system correlates of depression and immune system parameters are bidirectional and are mediated via neurohormonal and parasympathetic pathways. Evidence suggests that these associations can be affected by a) the clinical characteristics of depression (e.g., typical depression versus atypical depression and exhaustion), b) the duration and severity of depressive symptoms, and c) the stage of underlying CAD. Depressive symptoms are hypothesized to affect primarily the transition from stable CAD to acute coronary syndromes via plaque activation and prothrombotic processes, and may play an additional role in the response to injury at early stages of coronary atherosclerosis.

Key Words: depression • cytokines • coronary artery disease • myocardial infarction • exhaustion • immune system • stress • risk factors

Abbreviations: CAD = coronary artery disease; CRP = C-reactive protein; TNF- = tumor necrosis factor ; IL-6 = interleukin-6; HPA = hypothalamic-pituitary-adrenal.

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