Fax +41 61 306 12 34 E-Mail karger@karger.ch www.karger.com Original Paper Neuropsychobiology 2011;63:169–176 DOI: 10.1159/000321624 Antidepressive Effect of Mirtazapine in Post-Myocardial Infarction Depression Is Associated with Soluble TNF-R1 Increase: Data from the MIND-IT D.M. Tulner   a O.R.F. Smith   i A. Schins   c P. de Jonge   e M. Quere   b J.R. Delanghe   j H.J. Crijns   d J.A. den Boer   f J. Korf   f A. Honig   g, h Departments of a  Psychiatry and b  Cardiology, Medical Centre Leeuwarden, Leeuwarden, c  Department of Psychiatry, University Hospital Maastricht, and d  Department of Cardiology, University Hospital Maastricht, Maastricht, e  Internal Medicine and Psychiatry, and f  Department of Biological Psychiatry, University Medical Centre Groningen, Groningen, g  Department of Psychiatry, St. Lucas Andreas Hospital, and h  Department of Psychiatry, Free University of Amsterdam, Amsterdam, The Netherlands; i  Department of Health Promotion and Development, Faculty of Psychology, University of Bergen, Bergen, Norway; j  Department of Clinical Chemistry, Ghent University, Ghent, Belgium sponders. Conclusion: Significant effects on inflammation accompany the therapeutic efficacy of mirtazapine in con- trast to the therapeutic efficacy of placebo and the nonther- apeutic efficacy of mirtazapine. Copyright © 2011 S. Karger AG, Basel Introduction The prevalence of depressive symptoms during hospi- talization in the post-myocardial infarction (MI) period varies from 8 to 30% depending on the assessment meth- od [1]. Several studies have addressed the issue whether antidepressant treatment (ADT) alleviates post-MI de- pression [2–5]. Most of these studies demonstrated effects among more severe and recurrent post-MI major depres- sive disorders. In minor post-MI depression, ADT dem- onstrated little difference in effect compared to placebo. The Myocardial Infarction and Depression Intervention Trial (MIND-IT) showed that an incomplete response to ADT of post-MI depression is associated with increased cardiac events [6]. Key Words Myocardial infarction Inflammation Depression Mirtazapine Abstract Background: Depressive disorder after myocardial infarc- tion (MI) is associated with increased cardiac morbidity and mortality. Immune activity such as inflammation might be implicated as an underlying mechanism. The purpose of this study is to investigate whether the response to an antide- pressant in post-MI depression is associated with changes of inflammatory markers in serum. Methods: In a double-blind placebo-controlled study with mirtazapine 30 mg/day (50 patients), the antidepressive effect was related to immune activation parameters. The cytokines interleukin 6 (IL-6) and tumor necrosis factor (TNF- ), the soluble cytokine recep- tors sIL-6R, sTNF-R1 and sTNF-R2, and the inflammation-sen- sitive plasma proteins C-reactive protein and neopterin were assessed. Results: Subgroup analyses revealed a highly sig- nificant correlation of pronounced sTNF-R1 increase with a decrease in depressive symptoms in antidepressant re- Received: November 19, 2009 Accepted after revision: September 27, 2010 Published online: January 13, 2011 D.M. Tulner, MD Medisch Centrum Leeuwarden PO Box 888 NL–8901 BR Leeuwarden (The Netherlands) E-Mail dmtulner  @  home.nl © 2011 S. Karger AG, Basel 0302–282X/11/0633–0169$38.00/0 Accessible online at: www.karger.com/nps