题[M].北京:人民卫生出版社,心脏病学实践.2004.380-385.
600mg氯吡格雷治疗的基础上,加用阿昔单抗在术后30d
内并未显示出额外的益处[19]。
[9]
WangTH,BhattDL,TopolEJ.Aspirinandclopidogrelresis-tance:anemergingclinicalentity[J].EurHeartJ,2006,27:647-654.
5.3避免药物相互作用
最近,一项荟萃分析[20]综合4项临床研究发现,氯吡
格雷和他汀类药物合用可以产生有益的协同作用,且但是CYP3A4代谢和非CYP3A4代谢的他汀比较没有差异。部分体外实验则显示,当同时服用氯吡格雷和阿托伐他[10]MorelO,OhlmannP,JeselL.Variableextentofplateletre-
sponsivenesstoclopidogrelinhibition:"clopidogrelresis-tance"[J].AnnCardiolAngeiol,2005,54:194-200.
[11]MatetzkyS,ShenkmanB,GuettaV.Clopidogrelresistanceis
汀,在体内达到等克分子浓度时,氯吡格雷代谢被抑制>
90%。因此他们建议应用不经CYP3A4代谢的他汀类药物
和氯吡格雷的相互影响可能会更小、临床应用也相对安全。虽然CYP3A4诱导剂可以减少CR发生,但临床上尚无报道。
5.4防治动脉粥样硬化
氯吡格雷反应的个体差异性可能与心绞痛的分级、
糖尿病等有关,而妇女、
糖尿病及肥胖患者更容易出现双重抵抗,均反映了血小板聚集和激活增加。因此,个体化抗血小板治疗还应包括针对预防动脉粥样硬化、稳定粥样斑块、改变血小板活性的常规治疗,其中包括抗栓治疗、血脂的达标、有效控制血压、严格控制血糖等一系列措施。
6
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