课件：抗血小板药物的作用机理及临床应用全解.ppt

* 该图表示目前主要抗血小板药物的作用机制。阿司匹林是不可逆的把血小板环氧化酶乙酰化，阻止血栓素A2的形成，而它是一个有力的血小板聚集刺激因子。噻吩吡啶类药物是通过抑制P2Y12受体的信号传递，从而抑制通过ADP的血小板激活，并且限制了ADP调节的GP IIb/IIIa构型变化到它的活性形式。GP IIb/IIIa拮抗剂通过对GP IIb/IIIa受体的直接抑制，抑制血小板的激活，阻止血小板聚集的最后通路。这些拮抗剂包括直接阻止纤维蛋白原和VWF与GP IIb/IIIa联结，而无论血小板的刺激。从而阻止了由于血小板与血小板之间相联系的血小板分泌。 * 对相关研究进行荟萃分析（分别为：12项、9项、7项），发现抗血小板治疗分别能使不稳定心绞痛、冠脉血运重建、稳定型心绞痛患者心脑血管事件发生危险显著降低分别达46％、53％、33％，说明阿司匹林能使此类高危人群获益。 * The Antithrombotic Trialists’ Collaboration compared data from 65 aspirin trials to examine the effects of aspirin dose on vascular events in high-risk patients (in some trials, the aspirin dose was used in more than one of the comparisons).1 Serious vascular events (the primary measure of outcome) included nonfatal myocardial infarction, nonfatal stroke, death from vascular causes, and death from unknown causes. They found that all doses of aspirin studied reduced the risk of vascular events. The greatest number of trials (34) examined high aspirin doses (500-1500 mg) and revealed a proportional reduction in vascular events of 19%. Aspirin doses of 160 to 325 mg were associated with a 26% proportional reduction in vascular events, whereas 75 to 150 mg and 75 mg were associated with reductions of 32% and 13%, respectively. References 1 Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002;324:71-86. * 阿司匹林的获益远远大于风险 尽管该荟萃分析统计了部分超大剂量的阿司匹林试验，但是结果仍然显示阿司匹林的获益远远大于其风险，获益为风险的50倍左右。 * What’s More Dangerous, Your Aspirin Or Your Car? Thinking Rationally About Drug Risks (And Benefits) We compare mortality risks of several common drugs with risks related to work, transportation, and recreation. Comparing risks can provide a more intuitive sense of the magnitude of drug risks than stand-alone estimates can, to help inform policy discussions. The drug risks we quantify generally exceed the magnitude of risks for other domains (although aspir