Related Experiment Video
Updated: Jun 22, 2026

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function
Published on: March 15, 2022
Effect of long-term clopidogrel treatment on platelet function and inflammation in patients undergoing coronary
Mark J Antonino1, Elisabeth Mahla, Kevin P Bliden
1Sinai Center for Thrombosis Research, Baltimore, Maryland, USA.
Insights
Long-term clopidogrel therapy significantly reduces platelet reactivity and inflammation markers in patients undergoing stenting. This maintenance therapy demonstrates a notable anti-inflammatory effect beyond its antiplatelet action.
Area of Science:
- Cardiology
- Pharmacology
- Inflammation Research
Background:
- Clopidogrel loading dose during stenting reduces inflammation.
- The anti-inflammatory impact of clopidogrel maintenance therapy is less understood.
Purpose of the Study:
- To investigate the anti-inflammatory effects of long-term clopidogrel maintenance therapy.
- To compare platelet reactivity and inflammation markers in patients on long-term clopidogrel versus clopidogrel-naive patients before stenting.
Main Methods:
- Studied 110 patients undergoing non-emergent stenting, including 41 on long-term clopidogrel (>6 months) and 69 clopidogrel-naive patients.
- Measured platelet reactivity to adenosine diphosphate (ADP) using turbidimetric aggregometry.
- Assessed inflammation markers and platelet activation (P-selectin, activated glycoprotein IIb/IIIa) via flow cytometry and multianalyte profiling.
Main Results:
- Patients on long-term clopidogrel showed significantly lower ADP-induced platelet aggregation, P-selectin, and activated glycoprotein IIb/IIIa expression.
- Lower levels of selected inflammation markers were observed in the long-term clopidogrel group.
- Strong correlations were found between platelet aggregation measurements and inflammation markers.
Conclusions:
- Long-term clopidogrel therapy markedly reduces platelet reactivity to ADP.
- Maintenance clopidogrel therapy is associated with a significant anti-inflammatory effect in patients undergoing stenting.
Abstract:
A clopidogrel loading dose administered during stenting attenuates inflammation marker release. However, less is known of the anti-inflammatory effect of clopidogrel maintenance therapy. Platelet reactivity to adenosine diphosphate and inflammation markers were measured in 110 consecutive patients (69 clopidogrel-naive patients and 41 patients receiving long-term clopidogrel therapy for >6 months) before nonemergent stenting by turbidimetric aggregometry and flow cytometry and multianalyte profiling, respectively. All patients were treated with aspirin. Prestenting adenosine diphosphate-induced platelet aggregation, P-selectin, and activated glycoprotein IIb/IIIa expression were lower in patients receiving long-term clopidogrel therapy compared with the clopidogrel-naive group (p <0.001), accompanied by lower levels of selected inflammation markers (p < or = 0.05). Additionally, there were strong correlations between platelet aggregation and flow cytometric measurements (p < or = 0.04) and between specific inflammation markers (p < or = 0.02). In conclusion, in addition to markedly lowering platelet reactivity to adenosine diphosphate, long-term clopidogrel therapy is associated with an anti-inflammatory effect.
Related Concept Videos
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Peripheral Artery Disease III: Interprofessional Care
Coronary Artery Disease V: Interprofessional Care
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Acute Coronary Syndrome IV: Interprofessional Care
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
