von Lewinski Friederike, Riggert Joachim, Paulus Walter
Department of Clinical Neurophysiology, Georg-August University of Göttingen, Göttingen, Germany.
J Stroke Cerebrovasc Dis. 2009 Mar-Apr;18(2):111-5. doi: 10.1016/j.jstrokecerebrovasdis.2008.09.010.
The recurrence of ischemic cerebrovascular events despite treatment with aspirin (ASA) and/or clopidogrel remains a serious problem. Although there is increasing evidence that clinical failure may at least partially result from the nonresponsiveness of platelets to medication, the adjustment of the therapy according to ex vivo platelet responses is not yet common in clinical practice. Here, we compare two commonly used ex vivo platelet function tests under different treatment conditions. Blood samples from 142 patients with cerebrovascular disease receiving either ASA, clopidogrel, or a combined treatment, and 51 controls were evaluated by the platelet function analyzer (PFA)-100 (collagen/epinephrine cartridge), as well as collagen and ADP-induced aggregometry. The tests all demonstrated the interindividual heterogeneity of platelet aggregation inhibition, but the fractions of nonresponsiveness differed considerably with 58-62% of patients being nonresponsive to ASA by PFA-100 compared with 27-33% by collagen-induced aggregation. The clopidogrel nonresponsiveness was 44% by ADP-induced aggregation. The agreement of the test values between PFA-100 and collagen-induced aggregometry was weak (correlation coefficient r= -0.1 to -0.3). Only about half of the patients were consistently identified as either ASA responsive or nonresponsive by both tests. Under dual therapy conditions, the unspecificity of aggregometric tests prevented reliable measurements of platelet responses. In conclusion, there are currently considerable limitations in platelet aggregation monitoring. Nevertheless, we encourage prospective trials to improve the predictive value of platelet aggregation testing and to prove whether a systematic strategy of "platelet aggregation-adapted treatment" will improve the clinical outcome of patients with cerebrovascular events.
尽管使用阿司匹林（ASA）和/或氯吡格雷进行治疗，但缺血性脑血管事件仍会复发，这仍然是一个严重的问题。虽然越来越多的证据表明，临床治疗失败可能至少部分是由于血小板对药物无反应所致，但根据体外血小板反应调整治疗方案在临床实践中并不常见。在此，我们比较了两种常用的体外血小板功能测试在不同治疗条件下的情况。对142例接受ASA、氯吡格雷或联合治疗的脑血管疾病患者以及51例对照者的血样，采用血小板功能分析仪（PFA）-100（胶原/肾上腺素检测盒）以及胶原和ADP诱导的凝集试验进行评估。所有测试均显示出血小板聚集抑制的个体间异质性，但无反应的比例差异很大，PFA-100检测显示58%-62%的患者对ASA无反应，而胶原诱导聚集试验的这一比例为27%-33%。ADP诱导聚集试验显示氯吡格雷无反应的比例为44%。PFA-100与胶原诱导凝集试验的测试值之间的一致性较弱（相关系数r = -0.1至-0.3）。两种测试一致判定为对ASA有反应或无反应的患者仅约占一半。在双重治疗条件下，凝集试验的非特异性使得无法可靠测量血小板反应。总之，目前血小板聚集监测存在相当大的局限性。尽管如此，我们鼓励进行前瞻性试验，以提高血小板聚集检测预测价值，并证明“根据血小板聚集调整治疗”的系统策略是否能改善脑血管事件患者的临床结局。
