1. Treatment of Depression in Patients with Coronary Heart Disease
W. Victor R. Vieweg, MD, Demetrios A. Julius, MD, Antony Fernandez, MD, Lawson R. Wulsin, MD, Pramod K. Mohanty, MD, Mary Beatty-Brooks, MA, Mehrul Hasnain, MD, Anand K. Pandurangi, MD 
The American Journal of Medicine 
Volume 119, Issue 7, Pages (July 2006)
DOI: /j.amjmed
Copyright © 2006 Elsevier Inc. Terms and Conditions

2. Figure
Neuroendocrine pathways by which major depressive disorder may cause or worsen coronary heart disease. In depression, cortisol levels are commonly increased because of depression-induced increased CRH and ACTH. Glucocorticoids mobilize free fatty acids with resultant inflammation and excessive clotting. Increased cortisol levels may contribute to the metabolic syndrome with complications including increased visceral fat correlating with coronary atherosclerosis, increased triglycerides, hypertension, glucose dysregulation, and dyslipidemia. Depression-associated stress may lead to higher norepinephrine levels further contributing to clot formation by enhancing platelet activity. Also, norepinephrine may induce vasoconstriction. Altered autonomic nervous system function including changes in parasympathetic tone, heart rate variability, and blood pressure variability leave depressed more vulnerable to life-threatening ventricular arrhythmias and sudden cardiac death. Depression appears to increase such inflammatory markers as CRP, IL-6, and ICAM-1. It seems reasonable to conclude that depression itself must contribute to endothelial injury and atherosclerotic plaque formation. CRH = corticotropin-releasing hormone; ACTH = adrenocorticotropic hormone; ICAM-1 = Intercellular adhesion molecule-1; CRP = C-Reactive Protein; IL-6 = Interleukin-6.
The American Journal of Medicine  , DOI: ( /j.amjmed )
Copyright © 2006 Elsevier Inc. Terms and Conditions