Tendera Michal, Wojakowski Wojciech
3rd Division of Cardiology, Silesian School of Medicine, 47 Ziolowa Street, 40-635 Katowice, Poland.
Thromb Res. 2003 Jun 15;110(5-6):355-9. doi: 10.1016/j.thromres.2003.08.003.
Antiplatelet drugs have an established place in the prevention of vascular events in a variety of clinical conditions, such as myocardial infarction, stroke and cardiovascular death. Both European and American guidelines recommend the use of antiplatelet drugs in patients with established coronary heart disease and other atherosclerotic disease. In high-risk patients, such as those with post-acute myocardial infarction (AMI), ischaemic stroke or transient ischaemic attack, and in patients with stable or unstable angina, peripheral arterial occlusive disease or atrial fibrillation, antiplatelet treatment may reduce the risk of a serious cardiovascular event by approximately 25%, including reduction of non-fatal myocardial infarction by 1/6, non-fatal stroke by 1/4 and cardiovascular death by 1/6. Some data indicate that antiplatelet drugs may also have a role in primary prevention. In people who are aged over 65 years, or have hypertension, hypercholesterolaemia, diabetes, obesity or familial history of myocardial infarction at young age, aspirin may reduce both cardiovascular deaths and total cardiovascular events. Aspirin has been studied and used most extensively. It may exert its beneficial effect not only by acting on platelets, but also by other mechanisms, such as preventing thromboxane A2 (TXA2)-induced vasoconstriction or reducing inflammation. Indeed, experimental data show that low-dose aspirin may suppress vascular inflammation and thereby increase the stability of atherosclerotic plaque. Moreover, in human studies, aspirin seems to be most effective in those with elevated C-reactive protein levels. Vascular events, however, do occur despite aspirin administration. This may be due to platelet activation by pathways not blocked by aspirin, intake of drugs that interfere with aspirin effect or aspirin resistance. In the CAPRIE (Clopidogrel vs. Aspirin in Patients at Risk of Ischaemic Events) study, long-term clopidogrel administered to patients with atherosclerotic vascular disease was more effective than aspirin in reducing the combined risk of ischaemic stroke, myocardial infarction or vascular death. In the setting of coronary stenting, a double regimen including aspirin and ticlopidine or clopidogrel has proved more effective in the prevention of in-stent thrombosis than aspirin alone. Chronic oral administration of the inhibitors of platelet membrane receptor GP IIb/IIIa has been largely disappointing.
抗血小板药物在预防多种临床情况下的血管事件中具有既定地位,如心肌梗死、中风和心血管死亡。欧洲和美国的指南均推荐在已确诊冠心病和其他动脉粥样硬化疾病的患者中使用抗血小板药物。在高危患者中,如急性心肌梗死(AMI)后、缺血性中风或短暂性脑缺血发作患者,以及稳定型或不稳定型心绞痛、外周动脉闭塞性疾病或心房颤动患者,抗血小板治疗可使严重心血管事件风险降低约25%,包括非致命性心肌梗死风险降低1/6、非致命性中风风险降低1/4以及心血管死亡风险降低1/6。一些数据表明抗血小板药物在一级预防中也可能发挥作用。在65岁以上人群或患有高血压、高胆固醇血症、糖尿病、肥胖或年轻时有心肌梗死家族史的人群中,阿司匹林可降低心血管死亡和总的心血管事件风险。阿司匹林的研究和应用最为广泛。它不仅可通过作用于血小板发挥有益作用,还可通过其他机制,如预防血栓素A2(TXA2)诱导的血管收缩或减轻炎症。实际上,实验数据表明低剂量阿司匹林可抑制血管炎症,从而增加动脉粥样硬化斑块的稳定性。此外,在人体研究中,阿司匹林似乎对C反应蛋白水平升高的患者最为有效。然而,尽管服用了阿司匹林,血管事件仍会发生。这可能是由于未被阿司匹林阻断的途径导致血小板激活、摄入干扰阿司匹林作用的药物或阿司匹林抵抗。在CAPRIE(氯吡格雷与阿司匹林对缺血事件高危患者的疗效比较)研究中,对动脉粥样硬化性血管疾病患者长期使用氯吡格雷在降低缺血性中风、心肌梗死或血管死亡的综合风险方面比阿司匹林更有效。在冠状动脉支架置入的情况下,包括阿司匹林和噻氯匹定或氯吡格雷的双重治疗方案已被证明在预防支架内血栓形成方面比单独使用阿司匹林更有效。血小板膜受体GP IIb/IIIa抑制剂的长期口服给药效果大多令人失望。