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Updated: May 12, 2026
10:37
Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
Preserved thrombin-inducible platelet activation in thienopyridine-treated patients
Thomas Gremmel1, Christoph W Kopp, Daniela Seidinger
1Division of Angiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria. thomas.gremmel@meduniwien.ac.at
European Journal of Clinical Investigation
|April 25, 2013
Summary
Patients with cardiovascular disease on dual antiplatelet therapy who do not respond well to thienopyridines show increased platelet activation. Even good responders exhibit significant thrombin-induced platelet activation, suggesting a need for additional therapies.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Hematology
Background:
- Dual antiplatelet therapy (DAPT) is standard for cardiovascular disease patients post-stenting.
- High thrombin generation may drive thromboembolic events despite DAPT.
- Investigating platelet activation in thienopyridine responders vs. non-responders is crucial.
Purpose of the Study:
- To assess platelet activation susceptibility in thienopyridine non-responders versus responders.
- To evaluate the impact of thrombin receptor-activating peptide (TRAP-6) and adenosine diphosphate (ADP) on platelet activation.
- To identify potential therapeutic targets beyond standard antiplatelet agents.
Main Methods:
- 317 cardiovascular disease patients undergoing angioplasty and stenting were studied.
- Thienopyridine response was assessed using vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay and multiple electrode aggregometry (MEA).
- Platelet activation markers including P-selectin, activated glycoprotein IIb/IIIa, and monocyte-platelet aggregates were measured.
Main Results:
- Patients with high on-treatment residual platelet reactivity (HRPR) showed significantly higher P-selectin, GPIIb/IIIa, and MPA formation after TRAP-6 or ADP activation.
- These markers were similar at baseline between HRPR and non-HRPR groups.
- A notable percentage of good responders also exhibited high TRAP-6-inducible platelet activation.
Conclusions:
- Thienopyridine non-responders are more prone to thrombin- and ADP-induced platelet activation.
- Adequate thienopyridine response does not fully prevent thrombin-induced platelet activation.
- Additional strategies like thrombin receptor blockade may benefit patients with residual platelet activation.
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