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Published on: January 12, 2016
Whole blood serotonin and platelet activation in depressed post-myocardial infarction patients
Annique Schins1, Karly Hamulyák, Simon Scharpé
1Department of Psychiatry, University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, The Netherlands.
Insights
Depression post myocardial infarction (MI) is linked to higher serotonin levels, not increased platelet activation. The antidepressant mirtazapine did not significantly alter platelet activation or serotonin in these patients.
Area of Science:
- Cardiology
- Psychiatry
- Hematology
Background:
- Depression is a significant risk factor for mortality following myocardial infarction (MI).
- Altered platelet function and serotonin levels are implicated in the increased cardiovascular risk observed in depressed post-MI patients.
- Previous research suggests a link between depression, platelet activation, and serotonin, but findings are not entirely consistent.
Purpose of the Study:
- To compare markers of platelet activation (beta-thromboglobulin, platelet factor 4, soluble CD40 ligand) and serotonin (5-HT) levels between depressed and non-depressed post-MI patients.
- To evaluate the effect of the antidepressant mirtazapine on platelet activation and serotonin levels in depressed post-MI patients.
Main Methods:
- A study involving 25 depressed post-MI patients treated with mirtazapine or placebo for 8 weeks.
- A control group of 22 non-depressed post-MI patients, matched for key demographic and clinical factors.
- Measurement of plasma beta-thromboglobulin (betaTG), platelet factor 4 (PF4), soluble CD40 ligand (sCD40L), and serotonin (5-HT) levels before and after treatment.
Main Results:
- Depressed post-MI patients exhibited significantly higher whole blood and platelet serotonin (5-HT) levels compared to non-depressed controls.
- No statistically significant differences were found in plasma betaTG, PF4, or sCD40L levels between the depressed and non-depressed groups.
- Mirtazapine treatment led to non-significant reductions in betaTG, PF4, and platelet 5-HT levels, and a non-significant trend towards decreased platelet activation.
Conclusions:
- Depression in post-MI patients is associated with elevated serotonin levels, but not with increased markers of platelet activation.
- Treatment with mirtazapine did not significantly reduce platelet activation or serotonin levels in this cohort.
- Further research is needed to clarify the role of serotonin and platelet function in cardiovascular risk associated with depression post-MI.
Abstract:
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. Some but not all studies showed changes in blood serotonin level. Increased platelet activation and blood serotonin level have been associated with increased risk of cardiac events in patients with MI. The goal of this study was to investigate whether 1) depressed post-MI patients have higher markers of platelet activation as measured by plasma levels of beta-thromboglobulin (betaTG), platelet factor 4 (PF4) and soluble CD40 ligand (sCD40L) and higher serotonin (5-HT) levels than non-depressed post-MI patients and 2) treatment with the antidepressant mirtazapine decreases platelet activation. In this study, 25 depressed post-MI patients were asked for blood collection before start as well as after 8 weeks treatment with mirtazapine or placebo. The control group (n=22) consisted of non-depressed post-MI patients, matched for age, gender and time elapsed since MI. Plasma levels of betaTG, PF4 and sCD40L were not statistically different between the groups, but 5-HT levels were significantly higher in depressed patients. Treatment with mirtazapine resulted in a non-significant decrease in betaTG and PF4 and platelet 5-HT levels. Platelet and whole blood 5-HT, but not platelet activation was significantly increased in depressed post-MI patients. Treatment with mirtazapine showed a non-significant decrease in platelet activation and platelet 5-HT.
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