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.

Thrombosis Research
|June 18, 2010
PubMed

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.
Abstract

Related Concept Videos

Antidepressant Drugs: Tricyclics, SSRIs, and SNRIs01:28

Antidepressant Drugs: Tricyclics, SSRIs, and SNRIs

Tricyclic Antidepressants (TCAs), including Desipramine (Norpramin), Imipramine (Tofranil), Clomipramine (Anafranil), and Amitriptyline (Elavil), inhibit serotonin and norepinephrine reuptake and also block other receptors. They are used for depression, pain conditions, and insomnia. Common adverse effects include anticholinergic effects, sedation, orthostatic hypotension, and weight gain. They have a narrow therapeutic window and so require plasma-level monitoring. Abrupt discontinuation can...
Antidepressant Drugs: MAOIs and Other Agents01:23

Antidepressant Drugs: MAOIs and Other Agents

Atypical antidepressants, including bupropion (Wellbutrin), mirtazapine (Remeron), nefazodone (Serzone), trazodone (Desyrel), and vilazodone (Viibryd), offer unique mechanisms of action. Bupropion weakly inhibits dopamine and norepinephrine reuptake, aiding depression treatment and smoking cessation, with a low risk of sexual dysfunction. Mirtazapine enhances serotonin and norepinephrine neurotransmission, leading to sedation, increased appetite, and weight gain. As a result, it helps treat...
Antidepressant Drugs: Overview01:25

Antidepressant Drugs: Overview

Antidepressant drugs are a class of medications primarily used for treating various mood disorders, including major depression, anxiety disorders, and other related conditions. These medicines work by modulating the neurotransmitter balance within the brain, alleviating depressive symptoms. Antidepressants can be broadly categorized into several groups according to their mechanism of action and chemical structure: Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin-Norepinephrine...
Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists01:23

Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists

Serotonin, a crucial neurotransmitter synthesized by enterochromaffin cells, plays a cardinal role in regulating gastrointestinal (GI) motility. With over 90% of the body's total serotonin in the GI tract, its influence on digestive processes is profound. Serotonin is swiftly released upon various stimuli, such as food boluses or certain drugs, triggering intrinsic sensory neurons in the myenteric plexus and extrinsic vagal and spinal sensory neurons. This leads to the activation of the...
Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
Electroconvulsive Therapy01:30

Electroconvulsive Therapy

Electroconvulsive therapy (ECT), or shock therapy, remains a critical biomedical intervention for severe, treatment-resistant depression. While its origins can be traced back to Hippocrates' observations that malaria-induced convulsions alleviated mental illness, modern ECT has evolved significantly from its earlier, more primitive applications. First introduced in 1938 by Ugo Cerletti and his colleagues, ECT involves inducing controlled seizures using electrical currents. In its early years,...