Inflammation
Combined elevation of Lp(a) and hs-CRP, not Lp(a) alone, raises platelet reactivity on clopidogrel in 6,615 PCI patients (Clin Appl Thromb Hemost 2024)
Original title: Elevated High-Sensitivity C-Reactive Protein Level Enhances the Impact of Lipoprotein(a) on Platelet Reactivity in PCI Patients Treated with Clopidogrel
Among 6,615 patients undergoing percutaneous coronary intervention with clopidogrel therapy at Fuwai Hospital (mean age 58.24 years, 77.6% men), platelet reactivity was assessed by thromboelastography. Isolated elevation of Lp(a) (>=30 mg/dL) with normal hs-CRP (<2 mg/L) was not significantly associated with high or low on-treatment platelet reactivity. However, joint elevation of Lp(a) (>=30 mg/dL) and hs-CRP (>=2 mg/L) was associated with both high on-treatment platelet reactivity (OR 1.976, 95% CI 1.677-2.329) and low on-treatment platelet reactivity (OR 0.533, 95% CI 0.454-0.627) relative to patients with both markers low. The findings suggest inflammation modifies the thrombotic impact of Lp(a), raising the question of whether intensified antiplatelet or anti-inflammatory therapy could help this subgroup.
Original abstract
Background: 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.
Purpose: 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.
Methods: 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 (MAADP) > 47 mm and < 31 mm, respectively.
Results: 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 (P = 0.153) or LTPR (P = 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).
Conclusions: 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.
inflammationmechanismsthrombosis
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.