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Depression, the Autonomic Nervous System, and Coronary Heart Disease

Carney, Robert M. PhD; Freedland, Kenneth E. PhD; Veith, Richard C. MD

doi: 10.1097/01.psy.0000162254.61556.d5
Pathophysiology
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Depression is a risk factor for medical morbidity and mortality in patients with coronary heart disease (CHD). Dysregulation of the autonomic nervous system (ANS) may explain why depressed patients are at increased risk. Studies of medically well, depressed psychiatric patients have found elevated levels of plasma catecholamines and other markers of altered ANS function compared with controls. Studies of depressed patients with CHD have also uncovered evidence of ANS dysfunction, including elevated heart rate, low heart rate variability, exaggerated heart rate responses to physical stressors, high variability in ventricular repolarization, and low baroreceptor sensitivity. All of these indicators of ANS dysfunction have been associated with increased risks of mortality and cardiac morbidity in patients with CHD. Further research is needed to determine whether ANS dysfunction mediates the effects of depression on the course and outcome of CHD, and to develop clinical interventions that improve cardiovascular autonomic regulation while relieving depression in patients with CHD.

ANS = autonomic nervous system; CHD = coronary heart disease; HRV = heart rate variability; MI = myocardial infarction; NE = norepinephrine; SNS = sympathetic nervous system.

From the Department of Psychiatry, Washington University School of Medicine, St. Louis, MO (R.M.C., K.E.F.); and the Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA (R.C.V.).

Address correspondence and reprint requests to Robert M. Carney, PhD, Behavioral Medicine Center, 4625 Lindell Blvd., Suite 420, St. Louis, MO 63108. E-mail: carneyr@bmc.wustl.edu

Received for publication May 5, 2004; revision received August 9, 2004.

In accordance with CME accreditation guidelines, the authors of this article disclosed no real or potential conflicts of interest.

This research was supported in part by grant no. 1UO-1HL58946 from the National Heart, Lung, and Blood Institute, and by the Lewis and Jean Sachs Charitable Lead Trust.

Copyright © 2005 by American Psychosomatic Society
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