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 patients in group B received 75 mg/d clopidogrel in addition to ASA 100 mg for 4 weeks. In the first group A the patients were treated with 100 mg acetylsalicylic acid (ASA) and additional placebo for 4 weeks. This study examined the effect of clopidogrel on platelet reactivation and the release of inflammatory chemokines in patients with PAD.Ĥ0 patients with PAD were randomized into two groups. Whether a treatment with clopidogrel is associated with an inhibition of systemic inflammation in patients with PAD has not been thoroughly explored. Clopidogrel inhibits and thus reduces platelet reactivity. RANTES and sCD40L are chemokines which are stored in the alpha-granules of platelets. The reactivity of platelets is increased in patients with peripheral artery disease (PAD).
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