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Whole Blood Multiple Electrode Aggregometry is a Reliable Point-of-Care Test of Aspirin-Induced Platelet Dysfunction

Csilla Jámbor, MD^*, Christian F. Weber, MD, Konstanze Gerhardt, Wulf Dietrich, PhD^*, Michael Spannagl, PhD^*,, Bernhard Heindl, PhD^*, and Bernhard Zwissler, PhD^*

From the *Clinic for Anesthesiology, Department of Transfusion Medicine and Hemostaseology, University of Munich, Germany; and Department of Anesthesiology, Intensive Care and Pain Medicine, Goethe-University Frankfurt am Main, Germany.

Address correspondence and reprint requests to Dr. Csilla Jámbor, Clinic for Anesthesiology, University of Munich, Max-Lebsche-Platz 32, D-81377 Munich, Germany. Address e-mail to csilla.jambor{at}web.de.

Abstract

Background: Aspirin is one of the most commonly ingested over-the-counter drugs. In addition to its analgesic and antiinflammatory actions, it also potently inhibits platelet aggregation. Evaluation of aspirin-induced platelet dysfunction is relevant in various clinical situations, including during complex surgeries with high bleeding risk in individuals who have ingested aspirin. In this study, we examined the suitability of multiple electrode aggregometry (MEA) for time course assessment of the antiplatelet effects of a single oral dose of 500 mg aspirin. We also determined the applicability of this method in the point-of-care (POC) setting by comparing the results of the test after different time intervals after blood sampling.

Method: Twenty-four adult volunteers were enrolled in the study. After blood drawing at baseline, 500 mg aspirin was administered to all volunteers. Blood samples were taken at 4, 24, 56, 80, and 124 h after aspirin ingestion. At each time point, measurements were performed immediately and 30 and 60 min after drawing blood. Whole blood MEA was performed after stimulation with thrombin receptor activating peptide (TRAPtest, 32 µM) and arachidonic acid (ASPItest, 0.5 mM). Repeated measurement analysis of variance with a Bonferroni correction for multiple comparisons was performed to detect differences between time points. Assay imprecision was determined by calculating the coefficient of variation. The level of statistical significance was set to P < 0.05.

Results: Platelet aggregation by ASPItest was markedly decreased 4 h after aspirin intake. From the second day after aspirin intake, ASPItest values recovered with high interindividual variability, and 5 days after aspirin intake, ASPItest values did not differ significantly from baseline. TRAP-induced platelet aggregation (TRAPtest) showed no systematic changes during the study period. The resting time of the sample did not affect TRAPtest or ASPItest values. The coefficients of variation were 10% for the ASPItest and 7% for the TRAPtest.

Conclusions: MEA reliably detected the effects of aspirin. Notably, 500 mg aspirin caused complete inhibition of arachidonic acid-induced platelet aggregation for 2 days in all volunteers. Aggregation returned to baseline values with a wide interindividual variation in time course by day 5. No resting time for the blood sample was required for ASPItest or TRAPtest. These assays can be implemented as real POC tests. The reproducibility of the assays studied here is within the range of modern POC analyzers.