ArticleThe American journal of cardiology2014
Platelet response to serotonin in patients with stable coronary heart disease.
Article in The American journal of cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Role of Serotonin on Gene Expression and Physiology in Human Cytotrophoblasts and Placenta.Endocrinology · 2025Article
- Membrane Transporter of Serotonin and Hypercholesterolemia in Children.International journal of molecular sciences · 2024Article
- A Signature for Smoking Status of Coronary Heart Disease Patients through Weighted Gene Coexpression Network Analysis.Computational and mathematical methods in medicine · 2022Article
- The intriguing relationship between coronary heart disease and mental disorders.Dialogues in clinical neuroscience · 2018Review
- 5-Hydroxytryptamine Changes under Different Pretreatments on Rat Models of Myocardial Infarction and/or Depression.Chinese medical journal · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p=0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression.
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