Inhibition of platelet function with clopidogrel is associated with a reduction of inflammation in patients with peripheral artery disease
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Updated: Mar 21, 2026
Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Alexander Meyer1, Alice Weithaeuser1, Daniel Steffens1
1Department of Cardiology, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12203 Berlin, Germany.
Insights
Clopidogrel treatment significantly reduced platelet activation and RANTES chemokine release in peripheral artery disease (PAD) patients. This suggests clopidogrel may mitigate systemic inflammation associated with PAD.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Pharmacology
Background:
- Peripheral artery disease (PAD) is linked to heightened platelet reactivity.
- Platelets store inflammatory chemokines like RANTES and sCD40L.
- The anti-inflammatory effects of clopidogrel in PAD patients remain underexplored.
Purpose of the Study:
- To investigate clopidogrel's impact on platelet reactivation in PAD patients.
- To assess clopidogrel's effect on the release of inflammatory chemokines (RANTES, sCD40L) from platelets.
Main Methods:
- A randomized trial involving 40 PAD patients.
- Group A received aspirin (ASA) + placebo; Group B received aspirin (ASA) + clopidogrel.
- Platelet activation markers (CD63, CD62p, TSP) and chemokine levels (RANTES, sCD40L) were measured at baseline, day 7, and day 28.
Main Results:
- Clopidogrel treatment significantly reduced platelet activation markers (CD62p, CD63) and RANTES levels.
- No significant changes were observed in TSP expression or sCD40L levels.
Conclusions:
- Clopidogrel effectively reduces platelet reactivity in PAD patients.
- Clopidogrel decreases RANTES release from platelets, potentially impacting systemic inflammation in PAD.
Background:
The reactivity of platelets is increased in patients with peripheral artery disease (PAD). RANTES and sCD40L are chemokines which are stored in the alpha-granules of platelets. Clopidogrel inhibits and thus reduces platelet reactivity. Whether a treatment with clopidogrel is associated with an inhibition of systemic inflammation in patients with PAD has not been thoroughly explored. This study examined the effect of clopidogrel on platelet reactivation and the release of inflammatory chemokines in patients with PAD.
Methods:
40 patients with PAD were randomized into two groups. In the first group A the patients were treated with 100mg acetylsalicylic acid (ASA) and additional placebo for 4weeks. The patients in group B received 75mg/d clopidogrel in addition to ASA 100mg for 4weeks. After obtaining blood at days 0, 7 and 28 the platelet activation was determined by measuring the surface protein expression of CD63, CD62p and thrombospondin (TSP) after stimulation with TRAP and ADP. The release of the chemokines RANTES and sCD40L from platelets was analyzed by ELISA.
Results:
Platelet activation markers (CD62p and CD63) and chemokine RANTES were significantly reduced in patients with PAD after 7 and 28days after treatment with clopidogrel. No alterations were found in TSP expression and sCD40L during the treatment.
Conclusion:
The treatment with clopidogrel leads to a reduction of platelet reactivity and release of RANTES from the platelets of patients with PAD.
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