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The Relationship of Depression to Cardiovascular Disease:  Epidemiology, Biology, and Treatment

Dominique L. Musselman, MD; Dwight L. Evans, MD; Charles B. Nemeroff, MD, PhD
Arch Gen Psychiatry. 1998;55(7):580-592. doi:10.1001/archpsyc.55.7.580.
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This article reviews the burgeoning literature on the relationship of mood disorders and heart disease. Major depression and depressive symptoms, although commonly encountered in medical populations, are frequently underdiagnosed and undertreated in patients with cardiovascular disease (CVD). This is of particular importance because several studies have shown depression and its associated symptoms to be a major risk factor for both the development of CVD and death after an index myocardial infarction. This review of the extant literature is derived from MEDLINE searches (1966-1997) using the search terms "major depression," "psychiatry," "cardiovascular disease," and "pathophysiology." Studies investigating pathophysiological alterations related to CVD in depressed patients are reviewed. The few studies on treatment of depression in patients with CVD are also described. Treatment of depression in patients with CVD improves their dysphoria and other signs and symptoms of depression, improves quality of life, and perhaps even increases longevity. Recommendations for future research are proposed.

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Figure 1.

Hypothetical schema of pathophysiologic alterations associated with depression that likely contribute to increased vulnerability to cardiovascular disease (CVD). Autonomic nervous system innervation of the heart via parasympathetic vagus (X) and sympathetic (postganglionic efferents from cervical and upper thoracic paravertebral ganglia) nerves is shown. CRF indicates corticotropin-releasing factor; ACTH, corticotropin; TNF-α, tumor necrosis factor α; IL-1, interleukin 1; IL-6, interleukin-6; HRV, heart rate variability; and HPA, hypothalamic-pituitary-adrenocortical axis.

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Figure 2.

Platelet adhesion to collagen exposed within the denuded area of vascular endothelium has stimulated platelet activation. Activation is accompanied by extrusion of platelet storage granule contents, which recruits other platelets, causes irreversible platelet-platelet aggregation, and forms a fused platelet thrombus. Ca++ indicates intracellular free calcium concentrations; PF4, platelet factor 4; β-TG, β-thromboglobulin; ADP, adenosine diphosphate; and 5HT, serotonin. Adapted from R&D Systems, Minneapolis, Minn. Used with permission.

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The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
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