Monitoring ASA and P2Y12-specific platelet inhibition – comparison of conventional (single) and multiple electrode aggregometry

Abstract

Objective. Several platelet function test systems exist for the evaluation of the platelet inhibitory effect in patients on P2Y12 inhibitors and/or acetylsalicylic acid (ASA, aspirin) therapy. Studies comparing different available assays found only a poor correlation. The objective of the present study was to evaluate the correlation and agreement between single electrode (SEA) and multiple electrode (MEA) aggregometry. Methods and results. In whole blood arachidonic acid (AA) and adenosine diphosphate (ADP)-induced platelet aggregation was measured simultaneously using SEA (Chrono-Log) and MEA (Multiplate). We analyzed a total of 226 measurements taken from 58 patients on single ASA therapy or dual antiplatelet therapy with ASA and a thienopyridine. A cut-off value for clopidogrel/prasugrel high on-treatment platelet reactivity (HPR) of > 47 units (U) was chosen for MEA testing using hirudin and > 5 Ohm for SEA with citrate anticoagulated blood samples. The respective cut-off values for ASA HPR were > 30 U for the MEA assay and > 1 Ohm for SEA testing. There was a good correlation of the prevalence of thienopyridine-HPR in both whole blood assays (Spearman rank correlation coefficient r = 0.698) and a good inter-rate accordance (Cohen's Kappa statistic κ = 0.648). For AA-induced aggregation, the correlation of the results obtained was significant (r = 0.536; p < 0.001) and detecting ASA-HPR revealed a moderate (κ = 0.482) correlation between both impedance aggregometry assays. Conclusion. Platelet function testing using SEA and MEA provided both good accordance and correlation and therefore study results obtained by these two assays similarly enabled the detection of HPR of thienopyridine (and ASA) therapy.

Key Words::

• Aspirin
• clopidogrel
• impedance aggregometry
• multiplate
• multiple electrode aggregometry
• platelet function test
• residual platelet reactivity
• whole blood platelet aggregation

Declaration of interest: J-C. Krüger reports receipt of speaker's fees from AstraZeneca and travel grants from Daiichi Sankyo. H. Neubauer received speaker's fees and travel grants from Daiichi Sankyo. None of these parties (or other commercial parties) was involved in the planning and funding of this study. The authors alone are responsible for the content and writing of the paper.

This work was supported by a grant from the FoRUM program of the Ruhr-University Bochum, Germany (FoRUM, F654R-09). We are grateful to Marina Libe for her expert technical assistance.