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Observational Study
. 2016 Nov;82(5):1343-1350.
doi: 10.1111/bcp.13053. Epub 2016 Jul 24.

Abciximab as a bridging strategy to overcome morphine-prasugrel interaction in STEMI patients

Jolanta M Siller-Matula  1 , Simon Specht  2 , Jacek Kubica  3 , Dimitrios Alexopoulos  4 , Raffaele De Caterina  5 , Eva-Luise Hobl  6 , Bernd Jilma  6 , Günter Christ  7 , Irene M Lang  2
Affiliations
Observational Study

Abciximab as a bridging strategy to overcome morphine-prasugrel interaction in STEMI patients

Jolanta M Siller-Matula et al. Br J Clin Pharmacol. 2016 Nov.

Abstract

Objective: The present study investigated whether the glycoprotein (GP)IIb/IIIa receptor blocker abciximab might be a successful bridging strategy to achieve adequate levels of platelet inhibition rapidly in cases where prasugrel is used in morphine-pretreated ST-elevation myocardial infarction (STEMI) patients.

Methods: In a prospective observational cohort study, 32 patients presenting with STEMI were given prasugrel at a loading dose of 60 mg. Patients were stratified into four groups, according to morphine and/or abciximab use. Adenosine diphosphate (ADP)-induced platelet aggregation was measured at four time points: at baseline, and at 2 h, 1 day and 2 days after prasugrel loading.

Results: Morphine use was associated with a three-fold higher level of ADP-induced platelet aggregation 2 h after prasugrel loading compared with no morphine/no abciximab (P = 0.019). However, when abciximab was infused in the catheterization laboratory, the effect of morphine on ADP-induced platelet aggregation disappeared (P = 0.884). This interaction was also seen in the presence of high on-treatment platelet reactivity (HTPR) at 2 h; while HTPR was seen in 88% of morphine users/no abciximab users, it was found in only 17-20% in the three other groups (P = 0.003). The effect of morphine disappeared by day 1 - 2.

Conclusion: The infusion of the GPIIb/IIIa receptor blocker abciximab allows immediate and efficient platelet inhibition in STEMI patients concomitantly receiving the oral ADP receptor blocker prasugrel and morphine.

Keywords: abciximab; morphine; platelet; prasugrel.

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Figures

Figure 1
Figure 1
Study design. (A) Time points of drug administration and blood sampling. (B) Flow of participants in the study. ACS, acute coronary syndrome; d, day; NSTE‐ACS, non ST‐elevation ACS
Figure 2
Figure 2
Adenosine diphosphate (ADP)‐induced platelet aggregation assessed by multiple electrode aggregometry in relation to the time of prasugrel loading. d, day
Figure 3
Figure 3
Adenosine diphosphate (ADP)‐induced platelet aggregation values stratified by morphine and abciximab administration, measured 2 h after prasugrel loading
Figure 4
Figure 4
The proportion of patients with high on‐treatment platelet reactivity (HTPR) stratified by morphine and abciximab administration, measured 2 h after prasugrel loading
Figure 5
Figure 5
Adenosine diphosphate (ADP)‐induced platelet aggregation stratified by morphine and abciximab administration, measured at various time points after prasugrel loading. HTPR, high on‐treatment platelet reactivity. The P values given are for the comparison between baseline and other time points
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