National Clinical Research Center for Cardiovascular Diseases, State Key Laboratory of Cardiovascular Disease, Fu Wai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, China.
Clin Appl Thromb Hemost. 2024 Jan-Dec;30:10760296241280711. doi: 10.1177/10760296241280711.
Recently, the effect of Lipoprotein(a) [Lp(a)] on thrombogenesis has aroused great interest, while inflammation has been reported to modify the Lp(a)-associated risks through an unidentified mechanism.
This study aimed to evaluate the association between platelet reactivity with Lp(a) and high-sensitivity C-reactive protein (hs-CRP) levels in percutaneous intervention (PCI) patients treated with clopidogrel.
Data were collected from 10,724 consecutive PCI patients throughout the year 2013 in Fuwai Hospital. High on-treatment platelet reactivity (HTPR) and low on-treatment platelet reactivity (LTPR) were defined as thrombelastography (TEG) maximum amplitude of adenosine diphosphate-induced platelet (MA) > 47 mm and < 31 mm, respectively.
6615 patients with TEG results were finally enrolled. The mean age was 58.24 ± 10.28 years and 5131 (77.6%) were male. Multivariable logistic regression showed that taking Lp(a) < 30 mg/dL and hs-CRP < 2 mg/L as the reference, isolated Lp(a) elevation [Lp(a) ≥ 30 mg/dL and hs-CRP < 2 mg/L] was not significantly associated with HTPR (= 0.153) or LTPR (= 0.312). However, the joint elevation of Lp(a) and hs-CRP [Lp(a) ≥ 30 mg/dL and hs-CRP ≥ 2 mg/L] exhibited enhanced association with both HTPR (OR:1.976, 95% CI 1.677-2.329) and LTPR (OR:0.533, 95% CI 0.454-0.627).
The isolated elevation of Lp(a) level was not an independent indicator for platelet reactivity, yet the concomitant elevation of Lp(a) and hs-CRP levels was significantly associated with increased platelet reactivity. Whether intensified antiplatelet therapy or anti-inflammatory strategies could mitigate the risks in patients presenting combined Lp(a) and hs-CRP elevation requires future investigation.
最近，脂蛋白(a) [Lp(a)]对血栓形成的影响引起了极大的兴趣，而炎症已被报道通过一种未知的机制来改变与 Lp(a)相关的风险。
本研究旨在评估经皮冠状动脉介入治疗 (PCI) 患者中氯吡格雷治疗后血小板反应性与高敏 C 反应蛋白 (hs-CRP) 水平之间的关系。
本研究于 2013 年全年从阜外医院的 10724 例连续 PCI 患者中收集数据。高反应性血小板 (HTPR)和低反应性血小板 (LTPR)定义为血栓弹力图 (TEG) 二磷酸腺苷诱导血小板最大振幅 (>47mm)和(<31mm)。
最终纳入了 6615 例 TEG 结果的患者。患者平均年龄为 58.24±10.28 岁，5131 例(77.6%)为男性。多变量 logistic 回归显示，以 Lp(a)<30mg/dL 和 hs-CRP<2mg/L 为参考，孤立的 Lp(a)升高[Lp(a)≥30mg/dL 和 hs-CRP<2mg/L]与 HTPR(=0.153)或 LTPR(=0.312)无显著相关性。然而，Lp(a)和 hs-CRP 的联合升高[Lp(a)≥30mg/dL 和 hs-CRP≥2mg/L]与 HTPR(OR：1.976，95%CI 1.677-2.329)和 LTPR(OR：0.533，95%CI 0.454-0.627)均呈显著相关性。
孤立的 Lp(a)水平升高不是血小板反应性的独立指标，但 Lp(a)和 hs-CRP 水平的同时升高与血小板反应性增加显著相关。在伴有 Lp(a)和 hs-CRP 升高的患者中，强化抗血小板治疗或抗炎策略是否能降低风险，还需要进一步研究。
