用600毫克克洛皮多格雷尔在患有冠状动脉疾病的患者中,有或没有慢性克洛皮多格雷尔治疗的负载
Adnan Kastrati1, Nicolas von Beckerath, Alexander Joost
1Deutsches Herzzentrum and 1 Medizinische Klinik rechts der Isar; Technische Universität, Munich, Germany. kastrati@dhm.mhn.de.
Circulation
|July 21, 2004
概括
克洛皮多格雷尔可以进一步抑制血小板,即使在接受维持治疗的患者中也是如此. 一个600毫克的加载剂量显著增强了标准剂量之外的抗血小板作用.
科学领域:
- 心脏病学 心脏病学
- 药理学 药理学是指药理学的学科.
- 血液学 血液学 血液学
背景情况:
- 目前的克洛皮多格雷尔剂量策略可能无法最大限度地抑制血小板功能.
- 评估更高的克洛皮多格雷尔加载剂量的影响对于优化抗血小板治疗至关重要.
研究的目的:
- 为了比较600毫克克洛皮多格雷尔加载剂量的抗血小板作用,在没有先前暴露的患者和慢性克洛皮多格雷尔治疗患者中.
- 为了确定是否可以实现超越既定加载和维护方案的进一步的血小板抑制.
主要方法:
- 涉及接受阿司匹林治疗的患者进行冠状动脉血管造影的前性研究.
- 评估了两组患者:从未服用克洛皮多格雷尔的患者和长期接受75mg/天克洛皮多格雷尔治疗的患者.
- 在600毫克克洛皮多格雷尔负载之前和6小时后分析血小板聚合和受体表达的血液样本.
主要成果:
- 在从未服用克洛皮多格雷尔的患者中,600毫克的加载剂量显著降低了ADP诱导的血小板聚合 (90%至51%).
- 在接受慢性治疗的患者中,600毫克的负载在维持剂量之外提供了进一步显著的抑制 (52%至33%).
- 两组都显示出显著抑制糖蛋白IIb/IIIa和P-选择因子受体表达.
结论:
- 一个600毫克的克洛皮多格雷尔加载剂量可以实现比标准剂量更大的血小板抑制,即使在已经接受维持治疗的患者中.
- 较高的克洛皮多格雷尔剂量可能在临床上有益,因此需要进一步研究疗效和安全性.
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