Division of Angiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
J Atheroscler Thromb. 2013;20(7):630-45. doi: 10.5551/jat.17665. Epub 2013 Jun 4.
Inflammation has been postulated to modify the platelet response to aspirin treatment, thereby causing high on-treatment residual platelet reactivity (HRPR). Both high levels of inflammatory markers and HRPR have been linked to adverse cardiovascular events. We aimed to study the impact of inflammation on residual arachidonic acid (AA)-inducible platelet reactivity.
In 288 patients receiving dual antiplatelet therapy, residual AA-inducible platelet reactivity was assessed using light transmission aggregometry (LTA), the VerifyNow assay, multiple electrode aggregometry (MEA) and the Impact-R. The levels of urinary 11-dehydro-thromboxane B2 (D-TXB2), serum thromboxane B2 (TXB2), interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hsCRP) were determined using immunoassays.
The IL-6 level was found to be an independent predictor of platelet reactivity as determined according to LTA and D-TXB2 using a multiple linear regression analysis. Accordingly, patients with supramedian IL-6 levels exhibited significantly higher platelet reactivity than patients with inframedian IL-6 levels when determined according to LTA and D-TXB2 (both p ≤0.02). High IL-6 levels were associated with a 3.6-fold (95%CI 2.1-6.4) increased risk of HRPR, as defined according to D-TXB2, and a 3.4-fold (95%CI 1.4-8.3) increased risk of HRPR, as defined according to MEA. The HsCRP level was found to be an independent predictor of platelet reactivity when determined according to LTA, D-TXB2, the Impact-R and TXB2 using a multiple linear regression analysis. High hsCRP levels were associated with a 3.6-fold (95%CI 1.3-10) increased risk of HRPR, as defined according to LTA, and a 2.5-fold (95%CI 1.3-4.6) increased risk of HRPR, as defined according to TXB2.
Increased levels of inflammatory markers are independently associated with residual AA-inducible platelet reactivity in patients receiving dual antiplatelet treatment.
炎症被认为可以改变血小板对阿司匹林治疗的反应，从而导致治疗后残留血小板反应性高（HRPR）。高炎症标志物水平和 HRPR 均与不良心血管事件相关。我们旨在研究炎症对残留花生四烯酸（AA）诱导的血小板反应性的影响。
在 288 名接受双联抗血小板治疗的患者中，使用光传输聚集仪（LTA）、VerifyNow 测定、多电极聚集仪（MEA）和 Impact-R 测定评估残留 AA 诱导的血小板反应性。使用免疫测定法测定尿 11-脱氢血栓素 B2（D-TXB2）、血清血栓素 B2（TXB2）、白细胞介素-6（IL-6）和高敏 C 反应蛋白（hsCRP）的水平。
多元线性回归分析显示，IL-6 水平是 LTA 和 D-TXB2 测定血小板反应性的独立预测因子。因此，根据 LTA 和 D-TXB2，IL-6 水平高于中位数的患者的血小板反应性明显高于 IL-6 水平低于中位数的患者（均 p≤0.02）。高 IL-6 水平与 D-TXB2 定义的 HRPR 风险增加 3.6 倍（95%CI 2.1-6.4）相关，与 MEA 定义的 HRPR 风险增加 3.4 倍（95%CI 1.4-8.3）相关。多元线性回归分析显示，hsCRP 水平是 LTA、D-TXB2、Impact-R 和 TXB2 测定血小板反应性的独立预测因子。高 hsCRP 水平与 LTA 定义的 HRPR 风险增加 3.6 倍（95%CI 1.3-10）相关，与 TXB2 定义的 HRPR 风险增加 2.5 倍（95%CI 1.3-4.6）相关。
炎症标志物水平升高与接受双联抗血小板治疗的患者残留 AA 诱导的血小板反应性独立相关。
