Fukushima Kenichi, Kobayashi Yoshio, Kitahara Hideki, Iwata Yo, Nakayama Takashi, Kuroda Nakabumi, Ooyama Masayuki, Nomura Fumio, Komuro Issei
Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Chiba, Japan.
Circ J. 2008 Aug;72(8):1282-4. doi: 10.1253/circj.72.1282.
The loading dose of ticlopidine is 500 mg in both the US and Europe and 200 mg in Japan. A lower loading dose of clopidogrel might achieve adequate platelet inhibition in Japanese patients.
Platelet aggregation was serially measured at baseline, and 2, 4, 6, and 8 h after 150-mg (n=20) and 300-mg (n=20) clopidogrel loading. Platelets were stimulated with 5 and 20 micromol/L adenosine diphosphate (ADP) and aggregation was assessed by optical aggregometry. Pretreatment ADP-induced platelet aggregation in the 150-mg clopidogrel group did not differ from that of the 300-mg group. The administration of 300-mg clopidogrel loading dose resulted in lower platelet aggregation 2 h after the administration (5 micromol/L ADP: 53+/-9% vs 61+/-12%, p<0.05 and 20 micromol/L ADP: 61+/-10% vs 68+/-9%, p<0.05). A lower platelet aggregation induced with 20 micromol/L ADP was still observed 4 h after the 300-mg clopidogrel loading (58+/-10% vs 65+/-9%, p<0.05).
The 150-mg clopidogrel loading does not achieve rapid platelet inhibition. The 300-mg loading dose should be used to suppress platelet function rapidly even in Japanese patients undergoing coronary stent placement.
在美国和欧洲，噻氯匹定的负荷剂量均为500毫克，而在日本为200毫克。较低的氯吡格雷负荷剂量可能在日本患者中实现足够的血小板抑制。
在基线以及氯吡格雷150毫克（n = 20）和300毫克（n = 20）负荷剂量后的2、4、6和8小时连续测量血小板聚集。用5和20微摩尔/升的二磷酸腺苷（ADP）刺激血小板，并通过光学聚集法评估聚集情况。150毫克氯吡格雷组预处理ADP诱导的血小板聚集与300毫克组无差异。给予300毫克氯吡格雷负荷剂量后2小时血小板聚集降低（5微摩尔/升ADP：53±9% 对61±12%，p<0.05；20微摩尔/升ADP：61±10% 对68±9%，p<0.05）。在300毫克氯吡格雷负荷剂量后4小时，仍观察到20微摩尔/升ADP诱导的较低血小板聚集（58±10% 对65±9%，p<0.05）。
150毫克氯吡格雷负荷剂量不能实现快速血小板抑制。即使在接受冠状动脉支架置入的日本患者中，也应使用300毫克负荷剂量来迅速抑制血小板功能。
