Antidepressive effect of mirtazapine in post-myocardial infarction depression is associated with soluble TNF-R1 increase: data from the MIND-IT.

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.

Treatment of post-myocardial infarction depressive disorder: a randomized, placebo-controlled trial with mirtazapine.

Objective: To examine the antidepressant efficacy of a dual-acting antidepressant (mirtazapine) in patients with post-myocardial infarction (MI) depressive disorder. Antidepressants used in post MI trials with a randomized, double-blind, placebo-controlled design have been restricted to selective serotonin reuptake inhibitors (SSRIs). Antidepressant effects have been limited.

Nonresponse to treatment for depression following myocardial infarction: association with subsequent cardiac events.

Objective: Depression following myocardial infarction is associated with an increased risk of cardiac events, but attempts to alter cardiovascular prognosis by providing antidepressive treatment have not been successful. This may be because of the limited effects of antidepressive treatment on depression itself. The authors assessed whether nonresponse to treatment of post-myocardial infarction depression is associated with new cardiac events.

Effects of antidepressant treatment following myocardial infarction.

Background: Depression following myocardial infarction is associated with poor cardiac prognosis. It is unclear whether antidepressant treatment improves long-term depression status and cardiac prognosis.

Aims: To evaluate the effects of antidepressant treatment compared with usual care in an effectiveness study.

Altered omega-3 polyunsaturated fatty acid status in depressed post-myocardial infarction patients.

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.

Increased cerebral serotonin-2A receptor binding in depressed patients with myocardial infarction.

Serotonin (5-HT) has been implicated in the pathophysiology of depression. It is not known whether depression in post-myocardial infarction (MI) patients is also serotonin-mediated. In somatically healthy depressed persons, increased brain 5-HT(2A) receptor binding has been reported in some studies.

Inflammatory markers in depressed post-myocardial infarction patients.

Background: Depressive disorder in the post-myocardial infarction (MI) period has been associated with increased cardiac morbidity and mortality. Possible pathophysiological mechanisms behind this association are not clear. Major depression in physically healthy subjects has been related to immune abnormalities including increased plasma levels of interleukin-6 (IL-6), tumor necrosis factor alfa (TNF-alpha) and C-reactive protein (CRP).

Whole blood serotonin and platelet activation in depressed post-myocardial infarction patients.

Depression is an independent risk factor for post myocardial infarction (MI) mortality. Abnormalities in platelet function have been proposed as one of the mechanisms involved in increased cardiovascular risk among patients with depression post-MI. Depression in somatically healthy patients has been associated with increased platelet activation.

Increased coronary events in depressed cardiovascular patients: 5-HT2A receptor as missing link?

Objective: Major depressive disorder and depressive symptoms have been identified as independent risk factors for cardiac morbidity and mortality in patients with ischemic heart disease. Increased susceptibility to platelet activation has been proposed as one of the mechanisms by which depression acts as a significant risk factor for thrombotic events. In this review, data on platelet activation and platelet aggregation measures in depressed patients with or without concomitant cardiovascular disease are given.