Net platelet clot strength of thromboelastography platelet mapping assay for the identification of high on-treatment platelet reactivity in post-PCI patients.

Daye Cheng,Yiwen Hao,Shuo Zhao

doi:10.1042/bsr20201346

Daye Cheng, Yiwen Hao + Show 1 more

Open Access

https://doi.org/10.1042/bsr20201346

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Journal: Bioscience reports	Publication Date: Jul 15, 2020
Citations: 5	License type: CC BY 4.0

Affiliation: First Hospital of China Medical University

Abstract

High-on treatment platelet reactivity (HTPR) leads to more prevalence of thrombotic event in patients undergoing percutaneous coronary interventions (PCI). Dual antiplatelet therapy with aspirin in addition to one P2Y12 inhibitor is commonly administrated to reduce HTPR. However, ‘one size fits all’ antiplatelet strategy is widely implemented due to lacking benefits with tailored strategy. One reason for the failure of tailored treatment might be less specificity of the current indicators for HTPR. Therefore, searching for specific indicators for HTPR is critical. Thromboelastograph with platelet mapping (TEGpm) assay has been explored for identifying HTRP. Variables of TEGpm assay, including maximum amplitude (MA) induced by thrombin (MAthrombin), R time, platelet aggregation rate induced by ADP (TEGaradp) and MA induced by ADP (MAadp) have been demonstrated to be able to identify HTPR in post-PCI patients. However, these variables for HTPR might be less specific. Thus, in the present study, a novel variable nMAadp was derived by removing fibrin contribution from MAadp and analyzed for its usefulness in determining HTPR. In addition, MAthrombin, R time, MAadp and TEGaradp were also examined for determining HTPR. In conclusion, nMAadp and TEGaradp were demonstrated to be independent indicators for HTPR; nMAadp had the strongest power to identify HTPR with cutoff value of 26.3 mm; MAthrombin and R time were not significantly different between patients with and without HTPR; combination of TEGaradp and nMAadp further improved the ability to identify HTPR with an AUC of 0.893.

Highlights

Platelet activation and reactivity play pivotal roles in thrombosis [1–3]
Considering of the higher prevalence of High-on treatment platelet reactivity (HTPR) in female might be led by age influence, further analyses were performed through stratifying age variable by gender
A derived Thromboelastograph with platelet mapping (TEGpm) variable, net MAadp (nMAadp) was demonstrated to be as a novel independent risk indicator with more power to identify HTPR in post-percutaneous coronary intervention (PCI) patients and the cutoff value of nMAadp for HTPR was calculated as more than 26.3 mm

Summary

Introduction

Patients with acute coronary syndromes (ACS) and patients undergoing percutaneous coronary intervention (PCI) with higher platelet reactivity on-treatment (HTPR) are at more risk of occurrence of thrombotic events [4–6]. Antiplatelet therapy with aspirin in addition to one P2Y12 pathway inhibitor (dual antiplatelet therapy, DAPT) has been widely introduced to decrease on-treatment platelet reactivity (TPR) aiming to reduce the risk of thrombotic event occurrence in patients after PCI [7]. ‘one size fits all’ antiplatelet strategy is currently administrated without discrimination of individually variable responsiveness to specific antiplatelet drugs and TPR [4,5], which might lead to the reduced efficacy of antiplatelet treatment. Personalized antiplatelet strategy based on assessment of individual responsiveness to antiplatelet medication and TPR should improve the clinical outcome theoretically, despite the multiple studies failing to show benefits from tailored treatment [4,8–10]. A number of PFTs have been introduced, which can be classified into point-of-care test and License 4.0 (CC BY)

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Conclusion