Department of Cardiology, Medical University of Warsaw, Poland.
Cardiol J. 2013;20(5):545-51. doi: 10.5603/CJ.2013.0045.
The aim of the study was to compare the effects of 2 strategies of antiplatelet treatment (i.e., 150 mg ASA vs. 75 mg clpoidogrel) on plasma level of inflammatory markers in type 2 diabetes mellitus (T2DM) patients with high platelet reactivity (HPR).
Study cohort consisted of 304 T2DM patients on chronic ASA therapy (75 mg per day) participating in the Aspirin Versus/Or Clopidogrel in Aspirin-resistant Diabetics inflammation Outcomes (AVOCADO) study. Patients with HPR defined as Platelet Function Analyzer (PFA)-100 collagene/epinephrine closure time (CEPI-CT) < 193 s (n = 80) were randomized to 150 mg of ASA or 75 mg of clopidogrel in 2:3 ratio, respectively. Concentrations of the selected inflammatory markers, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, solubleCD40 ligand (sCD40L), and high sensitivity C-reactive protein (hsCRP), were measured and compared in both treatment groups before and after 8 weeks of treatment in both groups.
Out of 234 patients included into final analysis, the total of 34.2% (n = 80) patients displayed HPR, of which 14.1% (n = 33) were randomized into 150 mg of ASA group and 20.1% (n = 47) into 75 mg of clopidogrel group. Treatment with clopidogrel was a positive predictor (stepwise multiple regression analysis) of reduction of sCD40L concentration (odds ratio [OR] 4.15; p = 0.013), while treatment with 150 mg ASA was a positive predictor of reduction of IL-6 concentration (OR 4.38; p = 0.033). There was no statistically significant differences between clopidogrel and ASA 150 mg treatment in respect to predictive value for decreased hsCRP concentrations or increased TNF-α concentrations.
Increasing the dose of ASA from 75 mg to 150 mg daily or switching ASA 75 mg to clopidogrel 75 mg daily may reduce concentrations of some inflammatory markers (in particular hsCRP, IL-6 and CD40L) in T2DM patients with HPR treated previously with 75 mg of ASA.
本研究旨在比较两种抗血小板治疗策略(即 150 mg ASA 与 75 mg 氯吡格雷)对伴有高血小板反应性(HPR)的 2 型糖尿病(T2DM)患者血浆炎症标志物水平的影响。
研究队列由 304 例接受慢性 ASA 治疗(每天 75 mg)的 T2DM 患者组成,他们参加了阿司匹林与氯吡格雷在抗阿司匹林抵抗的糖尿病炎症结局(AVOCADO)研究。高血小板反应性定义为血小板功能分析仪(PFA)-100 胶原/肾上腺素闭合时间(CEPI-CT)<193 s(n=80)。这些患者随机分为 ASA 150 mg 或氯吡格雷 75 mg 组,两组比例为 2:3。分别在两组治疗 8 周前后测量并比较两组患者的选定炎症标志物(包括肿瘤坏死因子-α、白细胞介素-6、可溶性 CD40 配体和高敏 C 反应蛋白)的浓度。
在最终分析的 234 例患者中,共有 34.2%(n=80)的患者存在 HPR,其中 14.1%(n=33)被随机分配到 ASA 150 mg 组,20.1%(n=47)被随机分配到氯吡格雷 75 mg 组。氯吡格雷治疗是 sCD40L 浓度降低的正预测因子(逐步多元回归分析;比值比 [OR] 4.15;p=0.013),而 150 mg ASA 治疗是白细胞介素-6 浓度降低的正预测因子(OR 4.38;p=0.033)。氯吡格雷和 ASA 150 mg 治疗在预测 hsCRP 浓度降低或 TNF-α浓度增加方面无统计学差异。
将 ASA 剂量从 75 mg 增加到 150 mg 每日,或将 ASA 75 mg 转换为氯吡格雷 75 mg 每日,可能会降低以前接受 75 mg ASA 治疗的 HPR T2DM 患者某些炎症标志物(特别是 hsCRP、白细胞介素-6 和 CD40L)的浓度。