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Published on: March 2, 2015
Antiplatelet effects of antidepressant treatment: a randomized comparison between escitalopram and nortriptyline
Anne Flöck1, Astrid Zobel, Gerhard Bauriedel
1Department of Internal Medicine II - Cardiology, University of Bonn, Germany.
Insights
Major depressive disorder is linked to increased platelet aggregation, a potential cardiovascular risk factor. Antidepressant treatment with escitalopram or nortriptyline significantly reduced platelet aggregation in responders after three months.
Area of Science:
- Cardiology
- Psychiatry
- Pharmacology
Background:
- Depressive disorders are recognized as independent risk factors for coronary heart disease.
- Elevated platelet aggregation in depressed individuals may contribute to increased cardiovascular morbidity.
Purpose of the Study:
- To compare platelet function in depressed patients versus healthy controls.
- To analyze changes in platelet aggregation during 3 months of antidepressant treatment.
- To assess differential effects of escitalopram and nortriptyline on platelet aggregation.
Main Methods:
- Whole blood aggregometry was used to analyze blood samples from 91 major depressed patients and 91 healthy controls.
- Depressed patients were randomized to receive either escitalopram (n=47) or nortriptyline (n=44).
- Platelet aggregation was measured at multiple time points in response to adenosine diphosphate (ADP) and collagen.
Main Results:
- Platelet aggregation induced by ADP was significantly higher in depressed patients compared to controls (26%, p=0.006).
- Early changes in platelet aggregation were similar between escitalopram and nortriptyline groups.
- After 84 days, responders showed significant reductions: escitalopram decreased ADP and collagen-induced aggregation by 23% (p=0.03) and 15% (p=0.03), respectively; nortriptyline reduced ADP-induced aggregation by 29% (p=0.046).
Conclusions:
- Depressed patients exhibit heightened ex vivo platelet aggregation, potentially increasing cardiovascular risk.
- Three months of antidepressant treatment with escitalopram or nortriptyline led to significant reductions in platelet aggregation among responders.
- The observed reduction in platelet aggregation was independent of the specific antidepressant medication used.
Introduction:
Depressive disorders have been identified as independent risk factors for coronary heart disease. The present study (i) compared platelet function of depressed patients with that of healthy controls, (ii) analysed possible aggregability changes during 3 months of treatment with antidepressants, and (iii) sought to assess different effects of escitalopram and nortriptyline on platelet aggregation.
Methods:
Blood samples of 91 major depressed patients and 91 healthy controls were analysed with whole blood aggregometry in a case-control setting. Depressed patients were randomized to two groups treated either with escitalopram (n=47) or nortriptyline (n=44). Platelet aggregation was studied on days 0, 1, 3, 7, 14, 21, 84 of continuing medication and was determined in response to adenosine diphosphate (ADP) and collagen.
Results:
Platelet aggregation induced by ADP was increased among depressive patients compared with that of healthy controls (26%, p=0.006). With antidepressant treatment, changes in platelet aggregation remained comparable in both groups at early time points (d1 to 21). In contrast, at day 84, patients with antidepressive response revealed significant differences in both medication groups: Patients receiving escitalopram showed a 23% decrease of ADP induced aggregation (p=0.03) and a 15% decrease of collagen induced aggregation (p=0.03). With nortriptyline the increase in impedance was reduced by 29% after ADP induction (p=0.046).
Conclusion:
Depressed patients have higher ex vivo platelet aggregation that may contribute to increased cardiovascular morbidity. After three months of antidepressant treatment with either escitalopram or nortriptyline, platelet aggregation was significantly reduced in antidepressant responders, irrespective of the antidepressant medication type.
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