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. 2019 Jun;49(6):e13102.
doi: 10.1111/eci.13102. Epub 2019 Mar 29.

Platelet reactivity patterns in patients treated with dual antiplatelet therapy

Max-Paul Winter  1 , Theresia Schneeweiss  1 , Rolf Cremer  1 , Benedikt Biesinger  1 , Christian Hengstenberg  1 , Florian Prüller  2 , Markus Wallner  3 , Ewald Kolesnik  3 , Dirk von Lewinski  3 , Irene M Lang  1 , Jolanta M Siller-Matula  1
Affiliations

Platelet reactivity patterns in patients treated with dual antiplatelet therapy

Max-Paul Winter et al. Eur J Clin Invest. 2019 Jun.

Abstract

Aim: The aim of the present study was to investigate the patterns of platelet reactivity and discriminators of therapeutic response to dual antiplatelet therapy (DAPT) with aspirin and ticagrelor or prasugrel in patients with acute coronary syndrome (ACS).

Design: In this multicentre prospective observational study, 492 patients with ACS were enrolled. Platelet aggregation was determined by multiple electrode aggregometry after stimulation with adenosine diphosphate (ADP) or arachidonic acid (AA) as agonists in the maintenance phase of treatment with prasugrel or ticagrelor.

Results: Age emerged as the strongest variable influencing aspirin response status: The mean AA-induced platelet aggregation in patients <49 years of age was 49% higher than in those >49 years (13.1 U vs 8.8 U; P = 0.011). The second strongest discriminator of aspirin response was sex: Male patients had a 40% higher AA-induced platelet aggregation values than female patients (9.5 U vs 6.8 U; P = 0.026). Platelet count emerged as the only variable influencing ADP antagonists response status showing that patients with platelet count >320 g/L displayed higher ADP-induced platelet aggregation. About 12% of patients had high on-treatment platelet reactivity (HTPR) to aspirin, 3% and 4% a HTPR to prasugrel and ticagrelor, respectively, and only 2% displayed HTPR to dual antiplatelet therapy.

Conclusion: When potent platelet inhibitors as prasugrel and ticagrelor are administered with aspirin, HTPR to DAPT plays only a marginal role.

Keywords: ACS; HTPR; LTPR; MEA; platelets; prasugrel; ticagrelor.

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Conflict of interest statement

DvL received honoraria for advisory boards from AstraZeneca and Daiichi Sankyo. JSM received lecture or consultant fees from Daaichi, Eli Lilly, Bayer, Roche and Astra Zeneca. All other authors report no conflict of interests.

Figures

Figure 1
Figure 1
Patient flow
Figure 2
Figure 2
Adenosine diphosphate (ADP)‐ and arachidonic acid (AA)‐induced platelet aggregation assessed by multiple electrode aggregometry (MEA) in patients treated with ticagrelor or prasugrel and aspirin
Figure 3
Figure 3
A, Adenosine diphosphate (ADP)‐ and (B): arachidonic acid (AA) ‐ induced platelet aggregation assessed by multiple electrode aggregometry (MEA) in patients treated with ticagrelor and prasugrel according to the clinical presentation: ST‐elevation myocardial infarction (STEMI) vs. none ST‐elevation acute coronary syndrome (ACS) during the hospital stay after the maintenance dose administration
Figure 4
Figure 4
Scatter plot showing distribution of adenosine diphosphate (ADP)‐ induced platelet aggregation values in relation to high on‐treatment platelet reactivity (HTPR), moderate on treatment platelet reactivity (MTPR) and low on treatment platelet reactivity (LTPR) in patients treated with ticagrelor and prasugrel
Figure 5
Figure 5
Scatter plot showing the correlation between arachidonic acid (AA) and adenosine diphosphate (ADP) – induced aggregation assessed by multiple electrode aggregometry (MEA) in ticagrelor (A) and prasugrel treated patients (B). HTPR: high on treatment platelet reactivity
Figure 6
Figure 6
Chi‐squared automatic interaction detection (CHAID) analysis for the discriminators of arachidonic acid (AA) and adenosine diphosphate (ADP) – induced aggregation assessed by multiple electrode aggregometry (MEA)
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