阿司匹林减少心血管疾病危险的作用机制,多解释为血小板中小量阿司匹林干扰血栓烷A_2(TMXA_2)生成所必须的环氧化酶的乙酰化位点。过去认为高剂量阿司匹林因抑制血管壁的酶可造成相反倾向。早期研究的规模小,对其有20～30％效应很难肯定。应设计大规模随机试验则有益于取得肯定结果,该文就此加以评论。继发性预防试验由29000病人组成25个预防试验,其中有10个系心肌梗塞的预防,13个系中风或短时脑缺血后预防,以及2个为不稳定型心绞痛的预防。试验测定了阿司匹林、潘生丁和硫氧唑酮单独及合并治疗效应。综合的结果显示:因抗血小板治疗引 The mechanism by which aspirin reduces the risk of cardiovascular disease is mostly explained by the acetylation site of the cyclooxygenase necessary for the small amount of aspirin in the platelet to interfere with the formation of thromboxane A_2 (TMXA_2). In the past that high-dose aspirin inhibition of the walls of the blood vessels can cause the opposite trend. The small size of the early studies, its 20 ~ 30% effect is difficult to be sure. The design of large-scale randomized trials is conducive to obtaining positive results, the article comments on this. The secondary prevention trial consisted of 25 prevention trials of 29,000 patients, 10 of which were prophylactic to prevent myocardial infarction, 13 to prevent post-stroke or transient ischemic attack, and 2 to prevent unstable angina. The effects of aspirin, dipyridamole and thioxazolone alone and in combination therapy were determined. Comprehensive results show that: due to anti-platelet therapy lead