Acute Myocardial Necrosis and Depression: Antiplatelet Effect of Reuptake Inhibition of Serotonin (ANDROS)
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|ClinicalTrials.gov Identifier: NCT02463110|
Recruitment Status : Terminated (Investigator's decision)
First Posted : June 4, 2015
Last Update Posted : May 3, 2016
To evaluate the evolution in time of the antiaggregant platelet effect of sertraline (SSRI) compared to placebo in depressive patients with ACS (Acute Coronary Syndrome) and treated as recommended by a double antiplatelet therapy, aspirin and clopidogrel.
The benefits of SSRIs observed in depressive patients with ACS are related to an antiplatelet effect.
|Condition or disease||Intervention/treatment||Phase|
|Depression Coronary Artery Disease||Drug: Sertraline Drug: No treatment Drug: Placebo||Phase 4|
40% of patients hospitalized for acute coronary syndrome (ACS) present depressive symptoms. The increase in cardiovascular morbidity and mortality at 6 months (hazard ratio = 3.5) could partly be explained by an alteration of the platelet parameters in patients with depression.
Sertraline is a potent inhibitor of the selective serotonin reuptake (SSRI). At the platelet level, it decreases the secretion induced by collagen and causes the inhibition of serotonin reuptake and platelet activation, wider than the simple anti-serotonergic effect. Its efficacy on depression of patients with ACS has been demonstrated (-20% of ischemic events at 24 weeks vs placebo), partly independent of the correction of depressive symptoms, and with a wide safety action. Antiplatelet, anti-inflammatory and endothelial function effects of sertraline are demonstrated in healthy volunteers, in stable patients and in patients with heart failure, but have never been explored in ACS .
Multicenter, randomized, double-blind, controlled trial comparing SSRI and placebo in depressive patients with ACS.
A control (non depressive) ACS group will also do the clinical and laboratory follow-up at the same time (without drug administration), to constitute a reference for platelet parameters and to allow a comparison with the depressive ACS group treated with placebo.
Randomization and initiation of the treatment at the end of the hospitalization for ACS (possibly after reperfusion and stabilization of cardiac medication)
|Study Type :||Interventional (Clinical Trial)|
|Actual Enrollment :||2 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||Double (Participant, Investigator)|
|Official Title:||Acute Myocardial Necrosis and Depression: Antiplatelet Effect of Reuptake Inhibition of Serotonin: The ANDROS Study|
|Study Start Date :||July 2015|
|Actual Primary Completion Date :||February 2016|
|Actual Study Completion Date :||February 2016|
Experimental: 1: Sertraline
Sertraline one capsule (50mg per day), which can be increased up to 200mg per day (maximum dose) for 6 months.
Placebo Comparator: 2: Placebo
Other Name: Placebo one capsule, which can be increased up to 4 capsules per day (maximum dose) for 6 months.
ACS, no depression, no treatment
Drug: No treatment
- Time dependent pattern of changes in platelet reactivity under sertraline compared to placebo within a time Frame of 6 months of treatment [ Time Frame: 0 day, 1 day, 6 weeks, 24 weeks, 28 weeks ]
To evaluate the time variation of the level of platelet reactivity (ADP induced residual aggregation) under sertraline compared to placebo within a time Frame of 6 months of treatment.
T0 = before starting treatment with sertraline T1 = at discharge from the hospital = J1 after introduction of treatment with sertraline T2 = 6 weeks of treatment with sertraline T3 = 24 weeks of treatment with sertraline = end of treatment with sertraline T4 = 4 weeks after the end of treatment with sertraline (biological and psychiatric rebound)
- Time dependent pattern of changes in platelet activation [ Time Frame: 0 day, 1 day, 6 weeks, 24 weeks, 28 weeks ]Maximal platelet aggregation (ADP, Arachidonic Acid, Collagen), markers of platelet activation (betaTG, CD40s)
- Time dependent pattern of changes in inflammation markers [ Time Frame: 0 day, 1 day, 6 weeks, 24 weeks, 28 weeks ]Dosage of inflammation markers (IL-6, CRP, Fg, myeloperoxydase)
- Time dependent changes in Depression [ Time Frame: 0 day, 1 day, 6 weeks, 24 weeks, 28 weeks ]Beck Depression Inventory (BDI)
- Time dependent changes in Tobacco addiction [ Time Frame: 0 day, 1 day, 6 weeks, 24 weeks, 28 weeks ]Fargenström test
- Time dependent changes in Bleeding risk [ Time Frame: 0 day, 1 day, 6 weeks, 24 weeks, 28 weeks ]Dosage of hemoglobin, hematocrit and follow-up of hemorrhage
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT02463110
|ACTION Group - Pitié-Salpêtrière University Hospital (APHP)|
|Paris, France, 75013|
|Principal Investigator:||Johanne SILVAIN, MD, PhD||Assistance Publique - Hôpitaux de Paris|