ABSTRACT
BACKGROUND: Depressive disorder after myocardial infarction (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 antidepressant 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 α (TNF-α), the soluble cytokine receptors sIL-6R, sTNF-R1 and sTNF-R2, and the inflammation-sensitive plasma proteins C-reactive protein and neopterin were assessed. RESULTS: Subgroup analyses revealed a highly significant correlation of pronounced sTNF-R1 increase with a decrease in depressive symptoms in antidepressant responders. CONCLUSION: Significant effects on inflammation accompany the therapeutic efficacy of mirtazapine in contrast to the therapeutic efficacy of placebo and the nontherapeutic efficacy of mirtazapine.
Subject(s)
Antidepressive Agents, Tricyclic/therapeutic use , Depression/drug therapy , Depression/immunology , Mianserin/analogs & derivatives , Myocardial Infarction/complications , Myocardial Infarction/immunology , Receptors, Tumor Necrosis Factor, Type I/drug effects , Adult , Aged , Antidepressive Agents, Tricyclic/pharmacology , Depression/blood , Depression/complications , Female , Humans , Inflammation Mediators/blood , Male , Mianserin/pharmacology , Mianserin/therapeutic use , Middle Aged , Mirtazapine , Myocardial Infarction/blood , Myocardial Infarction/drug therapy , Receptors, Tumor Necrosis Factor, Type I/bloodABSTRACT
OBJECTIVE: Lower levels of long-chain omega-3 polyunsaturated fatty acids (n-3 LCPUFAs) and increased inflammation have been associated with both depressive disorder and myocardial infarction (MI). The present study investigated whether patients who develop depression post-MI, have higher arachidonic acid/eicosapentanoic acid (AA/EPA) ratios than non-depressed post-MI patients and whether depressed post-MI patients have signs of increased inflammation as measured by C-reactive protein (CRP). METHOD: Serum AA/EPA ratio and plasma CRP levels were quantified in 50 post-MI patients, of which 29 were depressed and 21 non-depressed. RESULTS: Compared with the non-depressed group, depressed post-MI patients had significantly higher AA/EPA ratios. No significant difference was observed in CRP levels. CONCLUSION: Depressed post-MI patients had lower levels of n-3 LCPUFAs as measured by mean AA/EPA ratio and no signs of increased inflammation as determined by CRP levels.
