Meyer Alexander, Weithaeuser Alice, Steffens Daniel, Bobbert Peter, Hassanein Adel, Ayral Yunus, Schultheiss Heinz-Peter, Rauch Ursula
Department of Cardiology, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12203 Berlin, Germany.
Department of Cardiology, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12203 Berlin, Germany.
Cardiovasc Revasc Med. 2016 Apr-May;17(3):169-75. doi: 10.1016/j.carrev.2016.01.010. Epub 2016 Mar 9.
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.
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.
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.
The treatment with clopidogrel leads to a reduction of platelet reactivity and release of RANTES from the platelets of patients with PAD.
外周动脉疾病（PAD）患者血小板反应性增加。调节激活正常T细胞表达和分泌的趋化因子（RANTES）和可溶性CD40配体（sCD40L）是储存在血小板α颗粒中的趋化因子。氯吡格雷具有抑制作用，从而降低血小板反应性。氯吡格雷治疗是否与PAD患者全身炎症的抑制有关尚未得到充分研究。本研究探讨了氯吡格雷对PAD患者血小板再激活及炎性趋化因子释放的影响。
40例PAD患者随机分为两组。第一组A组患者接受100mg阿司匹林（ASA）治疗，并额外服用安慰剂4周。B组患者除接受100mg ASA治疗外，还接受75mg/d氯吡格雷治疗4周。在第0、7和28天采集血液后，通过测量用凝血酶受体激活肽（TRAP）和二磷酸腺苷（ADP）刺激后血小板表面蛋白CD63、CD62p和血小板反应蛋白（TSP）的表达来确定血小板活化情况。通过酶联免疫吸附测定（ELISA）分析血小板中趋化因子RANTES和sCD40L的释放情况。
氯吡格雷治疗7天和28天后，PAD患者的血小板活化标志物（CD62p和CD63）和趋化因子RANTES显著降低。治疗期间TSP表达和sCD40L未发现变化。
氯吡格雷治疗可降低PAD患者血小板反应性，并减少血小板中RANTES的释放。
