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

BackgroundInflammation increases the risk of thrombosis in coronary artery disease (CAD) patients and affects the antiplatelet efficacy of clopidogrel. C1q interacts with platelets to activate platelets and induce thrombosis by participating in and regulating the inflammatory response. Whether C1q affects adenosine diphosphate (ADP)-induced platelet reactivity during clopidogrel therapy was unclear and our study aimed to explore the issue. MethodWe enrolled 1,334 CAD patients receiving clopidogrel therapy and evaluated the association between C1q level and high residual platelet reactivity (HRPR) using logistic regression and restricted cubic spline (RCS). HRPR was defined as ADP-induced maximum amplitude (MA(ADP)) > 47 mm plus ADP-induced platelet aggregation (ADP(i)) < 50%. ResultsA total of 516 patients (38.7%) performed HRPR. The frequency of HRPR increases with the increase in C1q level (26.3%, 38.4%, 43.2%, and 46.7% for the 1st to 4th quartile of C1q). The result of multivariate logistic regression demonstrated elevated C1q as an independent predictor for HRPR (2(nd) quartile: OR = 1.722, 95% CI 1.215-2.440; 3(rd) quartile: OR = 2.015, 95% CI 1.413-2.874; 4(th) quartile: OR = 2.362, 95% CI 1.631-3.421, compared to the 1st quartile). RCS depicted the nonlinear relationship between C1q and HRPR risk (p for non-linear < 0.05). ConclusionThe current research is the first to explore the association of C1q and ADP-induced platelet reactivity and to demonstrate elevated C1q as an independent risk factor for HRPR in CAD patients during clopidogrel therapy.

Automated summary

This study is the first to explore the association between C1q and ADP-induced platelet reactivity during clopidogrel therapy and demonstrates that elevated C1q is an independent risk factor for high residual platelet reactivity (HRPR) in coronary artery disease (CAD) patients.