Comparison between urinary 11-dehydrothromboxane B2 detection and platelet Light Transmission Aggregometry (LTA) assays for evaluating aspirin response in elderly patients with coronary artery disease

Liu, Tengfei; Zhang, Jingwei; Chen, Xiahuan; Feng, Xinglei; Fu, Sidney W.; McCaffrey, Timothy A.; Liu, Meilin

doi:10.1016/j.gene.2015.06.045

Cited by 3 publications

(3 citation statements)

References 24 publications

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“…26 Furthermore, based on our previous data, cardiovascular events occurred more frequently in aspirin hyporesponsiveness patients who were diagnosed by LTA-AA test. 27 We have extensive experience in LTA-AA detection demonstrated by our prior studies. 25,27 Therefore, LTA-AA test was employed to evaluate aspirin response in the present study.…”

Section: Discussionmentioning

confidence: 97%

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miR-34b-3p May Promote Antiplatelet Efficiency of Aspirin by Inhibiting Thromboxane Synthase Expression

et al. 2019

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Aspirin has been widely used for the prevention of cardiovascular diseases, but its antiplatelet efficiency varies between individuals. The present study aimed to evaluate response to aspirin based on gene profiles as well as potential regulating pathways using human blood samples and cell lines. Platelet function in patients 50 years or older with coronary artery disease on 100 mg/day aspirin was measured by light transmission aggregometry (LTA) of arachidonic acid (AA)-induced platelet aggregation. The expression of eight candidate genes—PTGS1/COX1, PLA2G4A, PLA2G6, PLA2G7, TBXAS1, TBXA2R, PTGIR, and ITGA2B—and the ingredients involved in AA metabolism were analyzed. Our data showed that the expressions of thromboxane A synthase 1 (TBXAS1), thromboxane synthase (TXS), and thromboxane B2 (TXB2) were increased in the upper quartile of platelet aggregation (LTA-AA_Q4) group compared with the lower quartile of platelet aggregation (LTA-AA_Q1) group. Our bioinformatics analysis suggested that TBXAS1 was targeted by miR-34b-3p via binding to its 3′-UTR, which was subsequently verified experimentally. Although overexpression of miR-34b-3p exhibited no apparent effect on cell proliferation, inhibition of miR-34b-3p promoted megakaryocyte viability. Our data demonstrated that the expression of TBXAS1 was higher in the aspirin hyporesponsiveness group than that in the hyperresponsiveness group, suggesting that high expression of TBXAS1 may be associated with aspirin hyporesponsiveness. miR-34b-3p may regulate the platelet and aspirin response by suppressing TBXAS1 expression and megakaryocyte proliferation.

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Section: Discussionmentioning

confidence: 97%

“…27 We have extensive experience in LTA-AA detection demonstrated by our prior studies. 25,27 Therefore, LTA-AA test was employed to evaluate aspirin response in the present study.…”

Section: Discussionmentioning

confidence: 97%

miR-34b-3p May Promote Antiplatelet Efficiency of Aspirin by Inhibiting Thromboxane Synthase Expression

et al. 2019

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“…Therefore, the measurement of TX formation is the pharmacologic most specific assay to evaluate platelet inhibition by aspirin. Different studies have now applied the measurement of TXB2 formation in the evaluation of aspirin antiplatelet effects [4,6,17]. However, a consensual cut-off level in the definition of HTPR to aspirin has not been reported.…”

Section: Discussionmentioning

confidence: 99%

Thromboxane Formation Assay to Identify High On-Treatment Platelet Reactivity to Aspirin

Mohring

Piayda²,

Dannenberg³

et al. 2017

Pharmacology

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Platelet inhibition by aspirin is indispensable in the secondary prevention of cardiovascular events. Nevertheless, impaired aspirin antiplatelet effects (high on-treatment platelet reactivity [HTPR]) are frequent. This is associated with an enhanced risk of cardiovascular events. The current gold standard to evaluate platelet hyper-reactivity despite aspirin intake is the light-transmittance aggregometry (LTA). However, pharmacologically, the most specific test is the measurement of arachidonic acid (AA)-induced thromboxane (TX) B2 formation. Currently, the optimal cut-off to define HTPR to aspirin by inhibition of TX formation is not known. Therefore, in this pilot study, we aimed to calculate a TX formation cut-off value to detect HTPR defined by the current gold standard LTA. We measured platelet function in 2,507 samples. AA-induced TX formation by ELISA and AA-induced LTA were used to measure aspirin antiplatelet effects. TX formation correlated nonlinearly with the maximum of aggregation in the AA-induced LTA (Spearman's rho R = 0.7396; 95% CI 0.7208-0.7573, p < 0.0001). Receiver operating characteristic analysis and Youden's J statistics revealed 209.8 ng/mL as the optimal cut-off value to detect HTPR to aspirin with the TX ELISA (area under the curve: 0.92, p < 0.0001, sensitivity of 82.7%, specificity of 90.3%). In summary, TX formation ELISA is reliable in detecting HTPR to aspirin. The calculated cut-off level needs to be tested in trials with clinical end points.

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Establishment of 11-dehydro-thromboxane B2 time-resolved immunoassay and application in membranous nephropathy

Hui

Zhang

et al. 2023

Analytical Biochemistry

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Comparison between urinary 11-dehydrothromboxane B2 detection and platelet Light Transmission Aggregometry (LTA) assays for evaluating aspirin response in elderly patients with coronary artery disease

Cited by 3 publications

References 24 publications

miR-34b-3p May Promote Antiplatelet Efficiency of Aspirin by Inhibiting Thromboxane Synthase Expression

miR-34b-3p May Promote Antiplatelet Efficiency of Aspirin by Inhibiting Thromboxane Synthase Expression

Thromboxane Formation Assay to Identify High On-Treatment Platelet Reactivity to Aspirin

Establishment of 11-dehydro-thromboxane B2 time-resolved immunoassay and application in membranous nephropathy

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