Similar Inflammatory Biomarkers Reflect Different Platelet Reactivity in Percutaneous Coronary Intervention Patients Treated With Clopidogrel: A Large-Sample Study From China

Abstract

Background: Platelet reactivity is closely associated with adverse events in percutaneous coronary intervention (PCI) patients. Inflammation plays a crucial role in the development of coronary heart disease (CHD).Aim: To investigate the association of inflammatory biomarkers such as leukocyte count and high-sensitivity C reactive proteins (hs-CRP) with platelet reactivity in PCI patients treated with clopidogrel.Method: We examined 10,724 consecutive PCI patients in Fuwai hospital from January 2013 to December 2013. High on-treatment platelet reactivity (HTPR) was defined as adenosine diphosphate (ADP)-induced platelet maximum amplitude [MA(ADP)] of thromboelastogram (TEG) > 47 mm, and low on-treatment platelet reactivity (LTPR) MA(ADP) < 31 mm.Results: Finally, 6,772 PCI patients treated with clopidogrel who had the results of postoperative TEG were enrolled. Among them, 2,070 (30.57%) presented HTPR and 2,568 (37.92%) presented LTPR. As for LTPR, multivariate logistic regression showed that leukocyte count (OR: 1.153, 95% CI 1.117–1.191) and hs-CRP (OR: 0.920, 95% CI 0.905–0.936) were independent predictors, along with diabetes mellites, hemoglobin, platelet count and glucose. As for HTPR, multivariate logistic regression showed that leukocyte count (OR: 0.885, 95% CI 0.854–0.917) and hs-CRP (OR: 1.094, 95% CI 1.077–1.112) were independent predictors, along with sex, hemoglobin, platelet count and glucose.Conclusions: This was the first large real-world study reporting that both leukocyte count and hs-CRP were the independent factors for platelet reactivity in PCI populations treated with clopidogrel, among which higher leukocyte count was associated with more LTPR while higher hs-CRP was associated with more HTPR, providing new insights on individualized antiplatelet therapy.

Inflammation and platelet reactivity during adjunctive colchicine versus aspirin in patients with acute coronary syndrome treated with potent P2Y12 inhibitor

“…Additionally, reduction of residual inflammation by colchicine therapy may impact platelet reactivity, as elevated levels of inflammatory markers like hs-CRP and fibrinogen have been linked to increased platelet reactivity ( 39 , 40 ). Although the present study did not demonstrate a correlation between hs-CRP and PRU measures, a previous study demonstrated that higher hs-CRP levels were associated with greater platelet reactivity in PCI patients treated with clopidogrel ( 41 ). Therefore, the current findings suggest that ticagrelor or prasugrel might be less susceptible to the pro-aggregatory effects of inflammation compared to clopidogrel.…”

Elevated serum C1q is an independent predictor of high residual platelet reactivity in CAD patients receiving clopidogrel therapy

“…Therefore, it is essential to investigate other potential risk factors of HRPR. Contemporary biomedical literature supports that inflammation may play an important role in the progression of atherosclerosis and thrombosis initiated by rupture of atherosclerotic plaques, and a previous study found that inflammatory biomarkers could influence ADP-induced platelet aggregation assessed by platelet function test during clopidogrel treatment (31). As a major participant in innate immune responses and inflammatory processes, the complement system is also involved in the regulation of atherosclerosis.…”

Combined effect of D-dimer, hs-CRP, and Lp(a) on 5-year clinical outcomes after percutaneous coronary intervention: A large real-world study in China

“…It is known that elevated concentrations of these cardiovascular risk biomarkers are associated with many pathological processes; however, the mechanism of how D-dimer, hs-CRP, and Lp(a) predict mortality remains unclear. Previous studies showed that elevated D-dimer was related to thrombosis, 24 plaque necrosis, 24 and infection, 25 whereas elevated hs-CRP was related to high platelet reactivity, 26 smooth muscle cell proliferation, human macrophage polarization, 27 and thromboxane activity. 27 Furthermore, elevated Lp(a) was related to endothelial damage, 28 inflammatory response, 29 and fibrinolytic inhibition.…”