Borna Catharina, Lazarowski Eduardo, van Heusden Catharina, Ohlin Hans, Erlinge David
Heart & Lung Division, Department of Cardiology, Lund University Hospital, Sweden.
Thromb J. 2005 Jul 26;3:10. doi: 10.1186/1477-9560-3-10.
To be fully activated platelets are dependent on two positive feedback loops; the formation of thromboxane A2 by cyclooxygenase in the platelets and the release of ADP. We wanted to evaluate the effect of aspirin on platelet function in patients with acute coronary syndromes and we hypothesized that increased levels of ADP in patients with acute coronary syndromes could contribute to aspirin resistance.
Platelet activity in 135 patients admitted for chest pain was assessed with PFA-100. An epinephrine-collagen cartridge (EPI-COLL) was used for the detection of aspirin resistance together with an ADP-collagen cartridge (ADP-COLL). ADP was measured with hplc from antecubital vein samples. Three subgroups were compared: chest pain with no sign of cardiac disease (NCD), NonST-elevation myocardial infarction (NSTEMI) and STEMI.
Platelet activation was increased for the STEMI group compared NCD. Aspirin resistance defined as <193 sec in EPI-COLL was 9.7 % in NCD, and increased to 26.0 % (n.s.) in NSTEMI and 83.3 % (p < 0.001) in STEMI. Chronic aspirin treatment significantly reduced platelet aggregation in NCD and NSTEMI, but it had no effect in STEMI. Plasma levels of ADP were markedly increased in STEMI (905 +/- 721 nmol/l, p < 0.01), but not in NSTEMI (317 +/- 245), compared to NCD (334 +/- 271, mean +/- SD). ADP levels correlated with increased platelet activity measured with ADP-COLL (r = -0.30, p < 0.05). Aspirin resistant patients (EPI-COLL < 193 sec) had higher ADP levels compared to aspirin responders (734 +/- 807 vs. 282 +/- 187 nmol/l, mean +/- SD, p < 0.05).
Platelets are activated and aspirin resistance is more frequent in STEMI, probably due to a general activation of platelets. ADP levels are increased in STEMI and correlates with platelet activation. Increased levels of ADP could be one reason for increased platelet activity and aspirin resistance.
血小板要完全激活依赖于两个正反馈回路;血小板中环氧化酶生成血栓素A2以及二磷酸腺苷(ADP)的释放。我们想要评估阿司匹林对急性冠脉综合征患者血小板功能的影响,并且我们推测急性冠脉综合征患者中升高的ADP水平可能导致阿司匹林抵抗。
使用血小板功能分析仪(PFA-100)评估135例因胸痛入院患者的血小板活性。使用肾上腺素-胶原纤维检测卡(EPI-COLL)和ADP-胶原纤维检测卡(ADP-COLL)来检测阿司匹林抵抗。通过高效液相色谱法(hplc)测定肘前静脉样本中的ADP。比较三个亚组:无心脏病迹象的胸痛患者(NCD)、非ST段抬高型心肌梗死(NSTEMI)和ST段抬高型心肌梗死(STEMI)。
与NCD组相比,STEMI组的血小板激活增加。在EPI-COLL检测中,阿司匹林抵抗定义为<193秒,NCD组为9.7%,NSTEMI组升至26.0%(无统计学差异),STEMI组为83.3%(p<0.001)。长期阿司匹林治疗显著降低了NCD组和NSTEMI组的血小板聚集,但对STEMI组无效。与NCD组(334±271,均值±标准差)相比,STEMI组的血浆ADP水平显著升高(905±721 nmol/l,p<0.01),但NSTEMI组(317±245)未升高。ADP水平与用ADP-COLL检测的血小板活性增加相关(r = -0.30,p<0.05)。与阿司匹林反应者相比,阿司匹林抵抗患者(EPI-COLL<193秒)的ADP水平更高(734±807 vs. 282±187 nmol/l,均值±标准差,p<0.05)。
STEMI患者的血小板被激活且阿司匹林抵抗更常见,可能是由于血小板的普遍激活。STEMI患者的ADP水平升高且与血小板激活相关。升高的ADP水平可能是血小板活性增加和阿司匹林抵抗的一个原因。