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Published on: January 12, 2016
Antidepressant in treating myocardial infarction complicated with depression via 5-HT/inflammation from heart to
Lijun Zhang1, Meiyan Liu1, Haiyang Chen1
1Department of Psycho-cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
Insights
Inflammation and serotonin (5-HT) link myocardial infarction (MI) and depression. Treatments like fluoxetine show promise in improving cardiac function and reducing depressive symptoms by targeting inflammation.
Area of Science:
- Cardiovascular Medicine
- Neuroscience
- Psychiatry
Background:
- Myocardial infarction (MI) and depression frequently co-occur, suggesting shared underlying mechanisms.
- Inflammation and altered serotonin (5-HT) pathways are implicated in both conditions.
Purpose of the Study:
- To explore the mechanistic link between inflammation, 5-HT, and the comorbidity of MI and depression.
- To evaluate the therapeutic efficacy of fluoxetine and SN50 in preclinical models.
Main Methods:
- Recruited coronary artery disease (CAD) patients, assessed depressive symptoms and inflammatory markers.
- Administered fluoxetine and SN50 to MI mice, SERT knockout mice, and H9C2 cells.
Main Results:
- CAD patients with depression exhibited elevated inflammatory markers (TNF-α, IL-4, IL-17, IFN-α, IFN-γ).
- Selective serotonin reuptake inhibitor (SSRI) treatment in CAD patients with depression correlated with fewer cardiac events.
- Fluoxetine and SN50 improved cardiac function, autonomic regulation, and reduced depressive behaviors in mice, mediated by the macrophages/TNF-α/TNFR/NF-κB pathway.
Conclusions:
- Inflammation, autonomic dysfunction, and 5-HT are key mechanisms in MI + depression.
- Antidepressant therapy offers dual benefits for cardiac and neurological health.
- Anti-inflammatory strategies present a promising therapeutic avenue for MI complicated by depression.
Objective:
Exploring the potential mechanism by which inflammation and 5-HT linking myocardial infarction (MI) and depression, and to evaluate therapeutic effect of fluoxetine and SN50.
Methods:
Patients with coronary artery disease (CAD) were recruited; depressive symptoms were evaluated, inflammatory factors were detected, and the effects of selective serotonin reuptake inhibitors (SSRIs) for CAD patients with depression were recorded. Furthermore, fluoxetine and SN50 were administrated separately for treatment in MI mice, SERT knockout mice, and H9C2 cell experiments.
Results:
CAD patients with depression had higher value of TNF-α, IL-4, IL-17, IFN-α, and IFN-γ (P < 0.05) compared to those without depression. CAD + depression patients were followed up for 2 years, those who received SSRIs treatment experienced lower cardiac events [1 events (3.7 %) vs. 14 events (11.8 %)] than those who did not. The animal experiment showed that MI surgery induced cardiac dysfunction and autonomic nerves injury which were exacerbated by excessive inflammatory response. Moreover, MI mice exhibited depressive behaviors, possibly due to autonomic nerves injury and inflammation in the cortex and hippocampus. Furthermore, fluoxetine and SN50 contributed to improving cardiac function, regulating cardiac vegetative nervous, relieving depressive behaviors, and reducing inflammation via macrophages/TNF-α/TNFR/NF-κB signaling pathway. SERT knockout mice experiment further revealed the association between 5-HT and inflammation. In addition, the H9C2 cell experiment presented demonstrated the anti-inflammatory effect of fluoxetine.
Conclusion:
This study identified inflammation, autonomic nerves dysfunction/5-HT as critical mechanisms of MI + depression. Antidepressant treatment would benefit both heart and brain. Moreover, anti-inflammation would be a promising approach for treating MI complicated with depression.
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