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Pharmacologic Treatment of Depression in Patients With Heart Disease

Roose, Steven P. MD; Miyazaki, Marissa BA

doi: 10.1097/01.psy.0000163455.43226.bf
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The relationship between depression and cardiovascular disease is complex and multifaceted. There is a growing body of evidence that depression significantly and adversely affects cardiovascular health. Perhaps the most prominent finding is the documented increase in mortality rate in patients with depression after myocardial infarction. The critical questions of interest to both the clinician and researcher are whether there are safe and effective treatments for depression in patients with heart disease and whether treatment of depression reduces the increased risk of cardiac morbidity and mortality. Although the data are limited and are primarily from open or comparator trials, the tricyclics (TCAs) and selective serotonin reuptake inhibitors (SSRI) are effective for treatment of depression in patients with ischemic heart disease (IHD), and response rates are comparable with those reported in depressed patients without heart disease. In terms of safety, the TCAs are associated with documented adverse cardiovascular effects, including increases in heart rate, orthostatic hypotension, and conduction delays. Use of TCAs in patients with IHD carries a proven increased risk of cardiac morbidity and perhaps of mortality as well. The SSRI appear to be relatively safe and effective in the treatment for depression in patients with comorbid IHD.

TCA = tricyclic antidepressant; MI = myocardial infarction; IHD = ischemic heart disease; CAST = Cardiac Arrhythmia Suppression Trial; SADHART = Sertraline Antidepressant Heart Attack Randomized Trial; HRSD = Hamilton Rating Scale for Depression; SSRI = selective serotonin reuptake inhibitor.

From the College of Physicians and Surgeons, Columbia University, New York, New York (S.P.R.); and Neuropsychiatry Research Clinic, New York State Psychiatric Institute, New York, New York (M.M.).

Address correspondence and reprint requests to Steven P. Roose, MD, New York State Psychiatric Institute, 1051 Riverside Drive, Unit 98, New York, NY 10032. E-mail: spr2@columbia.edu

Received for publication April 16, 2004; revision received July 27, 2004.

In accordance with CME accreditation guidelines, author Steven Roose disclosed that he has received research support from and served as a consultant for Forest Lab and Wyeth. The other author of this article disclosed no real or potential conflicts of interest.

Copyright © 2005 by American Psychosomatic Society
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