Evaluation of platelet function in aspirin treated patients with CAD

Evaluation of platelet function in aspirin treated patients with CAD
复制标题

DOI:
10.1007/s11239-006-6968-4
复制
发表时间:
2006-06-01
影响因子:
4
通讯作者:
Bush, DE
Bush, DE
中科院分区:
医学4区
文献类型:
--
作者:
Williams, MS;Kickler, TS;Bush, DE

文献摘要

被引文献

相似文献

背景:对急性冠脉综合征(ACS)患者血小板功能的研究表明,血小板活化水平既有升高,也有无变化。为了更好地了解阿司匹林治疗背景下冠心病患者的血小板功能,我们对ACS患者进行了血小板功能检测,并将结果与非CAD患者进行了比较。研究方法:我们检测了80例年龄和性别匹配的住院患者(40例ACS,40例非心源性胸痛(NCCP))对ADP和肾上腺素的血小板聚集和活化反应。所有受试者均接受阿萨(81-325 mg)。使用标准光透射在富血小板血浆中进行血小板聚集,并通过流式细胞术分析测量活化。我们还研究了血小板功能分析仪(PFA-100)测定的高剪切率下的血小板功能。结果:ASA对花生四烯酸引起的血小板聚集反应有抑制作用。与NCCP患者相比,ACS患者的血小板对肾上腺素的聚集水平显著更高(p = 0.001)。血小板功能的其他指标,包括ADP聚集、P选择素、活化糖蛋白IIb/IIIa表达和PFA-100,在两组之间没有变化。结论:我们发现ACS患者的血小板功能检测结果相互矛盾。具体而言,ACS患者的阿司匹林治疗可有效抑制血小板释放反应,并可有效部分抑制血小板聚集;然而,尽管使用阿司匹林,但与年龄和性别匹配的无CAD对照组相比,ACS患者似乎对肾上腺素能刺激的血小板聚集增加。在一些研究中,由于ACS患者对肾上腺素能刺激的反应增强,这可能被解释为阿司匹林抵抗。我们的研究表明,根据用于确定阿司匹林抵抗的试验,并非所有具有该标签的患者都对阿司匹林的生物学作用具有抵抗力,但他们可能对肾上腺素能刺激具有高于正常基线的血小板敏感性。
Background: Studies of platelet function in the acute coronary syndrome (ACS) have revealed both increased and unchanged platelet activation. To obtain a better understanding of platelet function in coronary artery disease in the setting of aspirin therapy, we performed platelet functional testing in patients with ACS and compared results to patients without CAD. Methods: We measured platelet aggregation and activation in response to ADP and epinephrine in 80 age and gender matched hospitalized patients (40 with ACS, 40 with non-cardiac chest pain (NCCP)). All subjects received ASA (81-325 mg). Platelet aggregation was performed using standard light transmission in platelet-rich plasma and activation was measured via flow cytometric analyses. We also studied platelet function under high shear rates measured by the platelet function analyzer (PFA-100). Results: ASA effect was found to be present in all subjects by blunted platelet aggregation in response to arachidonic acid. Patients with ACS showed significantly higher levels of platelet aggregation to epinephrine compared to patients with NCCP (p = 0.001). Other measures of platelet function including ADP aggregation, Pselectin, activated glycoprotein IIb/IIIa expression, and PFA-100 were unchanged between the two groups. Conclusions: We have found conflicting results of platelet functional testing in ACS. Specifically aspirin therapy in patients with ACS is effective in suppressing the platelet release response and is effective in the partial suppression of platelet aggregation; however, it appears that ACS patients have increased platelet aggregation to adrenergic stimuli when compared to age and gender matched controls without CAD despite the use of aspirin. In some studies, because ACS patients have an accentuated response to adrenergic stimuli this might be interpreted as aspirin resistance. Our study suggests that depending on the assay used to determine aspirin resistance, not all patients with this label are resistant to the biological effects of aspirin but they may have higher than normal baseline platelet sensitivity to adrenergic stimuli.