Kuliczkowski Wiktor, Kobusiak-Prokopowicz Malgorzata, Prajs Iwona, Karolko Bozena, Mazurek Walentyna
Department of Cardiology, Wroclaw Medical University, Pasteur 4 Street, 50-367 Wroclaw, Poland.
Thromb Res. 2007;119(6):679-86. doi: 10.1016/j.thromres.2006.05.003. Epub 2006 Jun 14.
The aspirin failure (resistance) is a still discussed and highly studied problem. This phenomenon is observed in rest, but could be precipitated by an exercise. The aspirin resistance was also linked with the inflammatory process which is a key event for the atherosclerosis development. Platelets seem to play an important role also in that setting, probably by the CD40-CD40L axis. The aim of the study was to assess the frequency of the aspirin failure induced by the exercise and the role of sCD40L in that regard.
The study included 40 patients with established coronary artery disease. The control group consisted of 10 patients without coronary artery disease matched for age. All patients and controls were on 75 mg of aspirin for at least 30 days and had treadmill testing and blood collected for measurement of sCD40L and optical platelet aggregation with ADP, collagen and arachidonic acid. Aspirin resistance was defined as a maximal aggregation with ADP and collagen exceeding 70%.
There were 15 aspirin-resistant patients in the studied group (37%). There were significantly higher concentration of sCD40L (ng/ml) in aspirin-resistant patients in comparison with aspirin-sensitive ones before testing (7,9 +/- 2,5 vs. 5,1 +/- 3,5, p < 0,05) and on the top of it (8,1 +/- 2,9 vs. 4,5 +/- 3,9, p < 0,05). There were 3 persons who become resistant on the top of the exercise which was connected with the significant increase of sCD40L concentration in that group (from 7,6 +/- 1,9 before exercise to 10,1 +/- 2,9 on the top of the exercise, p < 0,05). There was also a positive correlation between the sCD40L level before and on the top of the exercise in an aspirin-resistant group (r = 0,48 for both, p < 0,05). Patients who were aspirin-resistant at rest had also significant elevation of platelet aggregation on the top of the exercise (ADP (%) from 90,5 +/- 8,6 to 95,0 +/- 6,5, p < 0,05 and collagen (%) from 87,8 +/- 8,7 to 92,1 +/- 8,0, p < 0,05).
阿司匹林抵抗（失效）仍是一个备受讨论且深入研究的问题。这种现象在静息状态下即可观察到，但运动可能会促使其出现。阿司匹林抵抗还与炎症过程相关，而炎症过程是动脉粥样硬化发展的关键事件。在这种情况下，血小板似乎也发挥着重要作用，可能是通过CD40 - CD40L轴。本研究的目的是评估运动诱导的阿司匹林抵抗的发生率以及可溶性CD40L（sCD40L）在这方面的作用。
本研究纳入了40例确诊为冠心病的患者。对照组由10例年龄匹配的无冠心病患者组成。所有患者和对照均服用75毫克阿司匹林至少30天，并进行了平板运动试验，同时采集血液以测定sCD40L以及用二磷酸腺苷（ADP）、胶原和花生四烯酸检测光学血小板聚集情况。阿司匹林抵抗定义为ADP和胶原诱导的最大聚集率超过70%。
研究组中有15例阿司匹林抵抗患者（37%）。与阿司匹林敏感患者相比，阿司匹林抵抗患者在运动试验前（7.9±2.5对5.1±3.5，p<0.05）以及运动试验高峰时（8.1±2.9对4.5±3.9，p<0.05）sCD40L（纳克/毫升）浓度显著更高。有3例患者在运动试验高峰时出现抵抗，且该组sCD40L浓度显著升高（从运动前的7.6±1.9升至运动试验高峰时的10.1±2.9，p<0.）。阿司匹林抵抗组运动试验前和运动试验高峰时的sCD40L水平之间也存在正相关（两者r = 0.48，p<0.05）。静息时阿司匹林抵抗的患者在运动试验高峰时血小板聚集也显著升高（ADP诱导的聚集率从90.5±8.6升至95.0±6.5，p<0.05；胶原诱导的聚集率从87.8±8.7升至92.1±8.0，p<0.05）。
