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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., (Copyright © 2011 S. Karger AG, Basel.)

Background: Although many studies have focused on post-myocardial infarction (MI) depression, there is limited information about the evolution and determinants of depressive symptoms in the first year post-MI. Therefore we examined (1) the course of depressive symptoms during the first year post-MI and (2) the predictors of these symptom trajectories., Method: To assess depressive symptoms, 287 patients completed the Beck Depression Inventory during hospitalization for MI, and 2, and 12 months post-MI. Personality was assessed with the Type-D scale during hospitalization. We used latent class analysis to examine the evolution of depressive symptoms over a 1-year period and multinomial logit regression analyses to examine predictors of these symptom trajectories., Results: The course of depressive symptoms was stable during the first year post-MI. Four groups were identified and classified as non-depressed [40%, intercept (IC) 2.52], mildly depressed (42%, IC 6.91), moderately depressed (14%, IC 13.73) or severely depressed (4%, IC 24.54). In multivariate analysis, cardiac history (log OR(severe) 2.93, p=0.02; log OR(moderate) 1.81, p=0.02; log OR(mild) 1.46, p=0.01), history of depression (log OR(severe) 4.40, p<0.001; log OR(moderate) 1.97, p=0.03) and Type-D personality (log OR(severe) 4.22, p<0.001; log OR(moderate) = 4.17, p<0.001; log OR(mild) 1.66, p=0.02) were the most prominent risk factors for persistence of depressive symptoms during the first year post-MI., Conclusions: Symptoms of depression tend to persist during the first year post-MI. Cardiac history, prior depression and Type-D personality were identified as independent risk factors for persistence of depressive symptoms. The results of this study strongly argue for routine psychological screening during hospitalization for acute MI in order to identify patients who are at risk for chronicity of depressive symptoms and its deleterious effects on prognosis.

BackgroundWe examined the different trajectories of vital exhaustion (VE) over a 12-month period and their impact on prognosis in a sample of myocardial infarction (MI) and chronic heart failure (CHF) patients.MethodConsecutive MI (n=407) and CHF patients (n=297) were assessed at baseline, and at 3- and 12-month follow-up for symptoms of VE. Latent growth mixture modelling was used to examine the course of VE over time. The combined clinical endpoint was defined as cardiac hospital readmission or death.ResultsFour distinct trajectories for VE were found: low VE, decreasing VE, increasing VE, and severe VE. Sex, marital status, left ventricular ejection fraction, psychotropic medication, sample group (CHF v. MI) and depressive symptoms were associated with VE, varying according to classes. The mean follow-up period was 25.3 months in which 34.7% of the patients experienced an event. Multivariate Cox regression showed that, compared with patients in the low VE class, patients in the increasing VE class [hazard ratio (HR)=1.16, 95% confidence interval (CI) 1.58–3.61, p=0.01], and the severe VE class (HR=1.69, 95% CI 1.31–2.64, p=0.02) had an increased risk for adverse cardiovascular events (i.e. cardiovascular hospital readmission or cardiovascular death). Decreasing VE was not related to adverse cardiovascular events (HR=0.97, 95% CI 0.66–1.69, p=0.81).ConclusionsVE trajectories varied across cardiac patients, and had a differential effect on cardiovascular outcome. Increasing VE and severe VE classes were predictors of poor cardiovascular prognosis. These results suggest that identification of cardiac patients with an increased risk of adverse health outcomes should be based on multiple assessments of VE. [ABSTRACT FROM PUBLISHER]