Abstracts
Detection of drug-induced platelet inhibition with sonic estimation of elasticity via resonance using the QuantraTM
Inhoud:

    Auteur(s):

    Jan Krumeich1, Rachel Chin Kwie Joe2,  Marc Buise3, Iwan van der Horst4, Gerardus Kuiper3, Yvonne Henskens5

     

    1Deparment of Intensive Care Medicine, Maastricht University Medical Centre+, Maastricht University, Maastricht, the Netherlands

    2Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, the Netherlands

    3Department of Anesthesiology, Maastricht University Medical Centre+, Maastricht University, Maastricht, the Netherlands

    4Department of Acute and Critical care, Maastricht University Medical Centre+, Maastricht University, Maastricht, the Netherlands

    5Department of Central Diagnostic Laboratory, Maastricht University Medical Centre+, Maastricht University, the Netherlands
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    Abstracts

    Detection of drug-induced platelet inhibition with sonic estimation of elasticity via resonance using the QuantraTM

    Teaser: Er is een nieuwe test, de QuantraTM, die door visco-elasticiteit van volbloed middels sonische resonantie te meten mogelijk beter medicijn-geïnduceerde plaatjesremming kan quantificeren dan klassieke testen zoals ROTEM of TEG. Om dit te onderzoeken werd volbloed van 16 vrijwilligers getest met de QuantraTM voor en na spiken met trombocytenaggregatieremmers. Helaas lijkt ook de QuantraTM medicijn-geïnduceerde plaatjesremming niet te kunnen quantificeren.

     

    Background: Viscoelastic tests (VETs) based on rotational thromboelastometry give insight into coagulation. However, current VETs cannot reliably detect drug-induced platelet inhibition (DIPI). A new test, “QuantraTM” is a VET based on sonic resonance. QuantraTM measures clot elasticity more directly than other VETs, therefore, it is suggested it can detect DIPI. If so, it could be useful for guiding perioperative management. This study aims to investigate whether the QuantraTM can detect DIPI in vitro.

     

    Methods: Whole blood samples of 16 healthy volunteers were collected. The QuantraTM was used to determine Clot Stiffness (CS), Platelet Contribution to Clot Stiffness (PCS), and Fibrinogen Contribution to Clot Stiffness (FCS) expressed in hectopascal (hPa). Samples were measured before and after spiking with aspirin or ticagrelor. The difference was determined for each sample and paired samples t-tests were used to test for statistical significance (primary endpoint). Additionally, samples were tested using multiple electrode aggregometry (MEA) to check if spiking did indeed inhibit platelet aggregation.

    Results: Samples of 4 volunteers were excluded because of missing parameters, test errors, or no inhibition detected with MEA. Samples of 5 volunteers were spiked with aspirin and 7 with ticagrelor. MEA detected DIPI in all but one sample. Aspirin spiking did not show significant differences in CS, PCS and FCS. Ticagrelor spiking did show a significant increase in CS (from 18.3 hPa to 20.7 hPa; p=0.020) and PCS (from 16.7 hPa to 19.0 hPa; p=0.020).

    Conclusion: The QuantraTM could not detect DIPI after spiking with aspirin. Moreover, while a decrease was expected after ticagrelor spiking, significant increases were seen for the parameters CS and PCS. Inhibitory effects were detected with MEA. It is, therefore, unlikely that the QuantraTM can detect and quantify DIPI.