Abstract

Abstract Background Platelet reactivity is closely associated with thrombosis and bleeding events in percutaneous coronary intervention (PCI) patients treated with clopidogrel. Inflammation also plays a crucial role in the development of coronary heart disease. How inflammation affects platelet reactivity needs furthrt study. Aim To investigate the association of inflammatory markers including leukocyte count and high-sensitivity C reactive proteins (hs-CRP) with platelet reactivity in PCI patients treated with clopidogrel. Method A total of 6772 PCI patients treated with clopidogrel who have the results of postoperative thromboelastogram (TEG) from January 2013 to December 2013 were enrolled. High on-treatment platelet reactivity (HTPR) was defined as adenosine diphosphate (ADP)-induced platelet maximum amplitude [MA(ADP)] of TEG >47 mm, and low on-treatment platelet reactivity (LTPR) was defined as MA(ADP) <31 mm. Results Among 6772 PCI patients, 2070 (30.57%) presented HTPR and 2568 (37.92%) presented LTPR. As for LTPR, multivariate logistic regression showed that increased leukocyte count (OR 1.153, 95% CI 1.117–1.191) and decreased hs-CRP (OR 0.920, 95% CI 0.905–0.936) were independent predictors, along with diabetes mellites (OR 0.868, 95% CI 0.759–0.993), hemoglobin (OR 1.023, 95% CI 1.019–1.028), platelet count (OR 0.997, 95% CI 0.996–0.998), and glucose (OR 0.962, 95% CI 0.931–0.994). As for HTPR, multivariate logistic regression showed that decreased leukocyte count (OR 0.885, 95% CI 0.854–0.917) and increased hs-CRP (OR 1.094, 95% CI 1.077–1.112) were independent predictors, along with sex (OR 0.636,95% CI 0.537–0.754), hemoglobin (OR 0.972, 95% CI 0.968–0.977), platelet count (OR 1.005, 95% CI 1.004–1.007), and glucose (OR 1.056, 95% CI 1.020–1.092). Conclusions This was the first large real-world study reporting that increased leukocyte count associated with more LTPR while increased hs-CRP associated with more HTPR in PCI populations treated with clopidogrel, which may contribute to understand the potential mechanism of the effect of inflammation on thrombosis and bleeding in patients with PCI. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): National Key Research and Development Program of China; Young and middle-aged talents in the XPCC Science and Technology Project

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