Pettersen A A, Arnesen H, Seljeflot I
Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital, Ullevaal, Norway; Department of Medicine, Vestre Viken HF, Ringerike Hospital, Hønefoss, Norway.
Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital, Ullevaal, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway.
Vascul Pharmacol. 2015 Apr-Jun;67-69:6-9. doi: 10.1016/j.vph.2015.03.018. Epub 2015 Apr 11.
Although aspirin is effective in secondary prevention in coronary heart disease, new thromboembolic events in patients on aspirin are frequently seen. In trials on aspirin-treated patients, platelet function tests have revealed large variability in platelet aggregation. This phenomenon has been named aspirin resistance, aspirin non-responsiveness or high-on-aspirin residual platelet reactivity. The mechanism of aspirin antiplatelet effect is due to the inhibition of cyclooxygenase-1 enzyme in platelets. In some trials, almost all patients on aspirin have a very low level of serum thromboxane B2, indicating that the measured platelet reactivity in aspirin-treated patients might be due to platelet activation via other pathways, such as ADP or thrombin. The prevalence of real aspirin resistance seems to be very low, and probably the term "high-on-aspirin residual platelet reactivity" should be preferred to describe this phenomenon.
尽管阿司匹林在冠心病二级预防中有效,但服用阿司匹林的患者仍经常出现新的血栓栓塞事件。在对服用阿司匹林患者的试验中,血小板功能测试显示血小板聚集存在很大差异。这种现象被称为阿司匹林抵抗、阿司匹林无反应或高剂量阿司匹林残留血小板反应性。阿司匹林抗血小板作用的机制是由于抑制血小板中的环氧化酶-1酶。在一些试验中,几乎所有服用阿司匹林的患者血清血栓素B2水平都非常低,这表明在服用阿司匹林的患者中测得的血小板反应性可能是由于其他途径(如ADP或凝血酶)导致的血小板活化。真正的阿司匹林抵抗的发生率似乎非常低,也许用“高剂量阿司匹林残留血小板反应性”来描述这种现象更合适。