Abstract
Background
Patients with acute coronary syndrome show an inflammatory response that is known
to affect platelet aggregation. We aimed to clarify the relationship between the inflammation
severity and the effect of antiplatelet therapy after percutaneous coronary intervention
(PCI) for ST-elevation myocardial infarction (STEMI).
Methods
This retrospective, single-center study included 203 patients with STEMI who underwent
primary PCI and were stratified on the basis of the antiplatelet therapy on admission
(clopidogrel vs ticagrelor). Inflammation levels were defined as low, intermediate,
and high, based on the tertiles of the distribution of high-specificity C-reactive
protein levels pre-PCI. Platelet aggregation function during hospitalization and follow-up
was quantified as residual adenosine diphosphate–induced platelet reactivity on light
transmittance aggregometry. Inflammation markers were measured on admission and at
1 year post-PCI.
Results
At intermediate and high levels of inflammation, residual adenosine diphosphate–induced
platelet aggregation was significantly higher among clopidogrel users than among ticagrelor
users. In the clopidogrel group, statistically significant differences in platelet
aggregation function were observed among the 3 levels of inflammation. At 1 year post-PCI,
ticagrelor users had significantly lower levels of interleukin-1β and higher levels
of interleukin-35 and transforming growth factor-β.
Conclusion
At different inflammation levels, ticagrelor provides more potent platelet inhibition
than clopidogrel, suggesting that ticagrelor might exert a more stable antiplatelet
effect at higher levels of systemic inflammation. Furthermore, ticagrelor is associated
with reduced indices of inflammation on follow-up after PCI, suggesting that anti-inflammatory
effects might play a role in the clinical benefit observed with antiplatelet therapy,
which would provide an additional rationale for using ticagrelor in patients with
STEMI undergoing primary PCI.
Résumé
Contexte
Chez les patients atteints du syndrome coronarien aigu, on observe une réaction inflammatoire
reconnue pour avoir une incidence sur l’agrégation plaquettaire. L’objectif de notre
étude était de préciser le lien entre la gravité de l’inflammation et l’effet d’un
traitement antiplaquettaire après une intervention coronarienne percutanée (ICP) effectuée
chez des patients ayant eu un infarctus du myocarde avec élévation du segment ST (STEMI).
Méthodologie
Cette étude rétrospective monocentrique portait sur 203 patients ayant eu un STEMI
et subi une ICP primaire, qui ont été stratifiés en fonction du traitement antiplaquettaire
reçu lors de leur admission à l’hôpital (clopidogrel vs ticagrélor). L’intensité de
l’inflammation était considérée comme faible, modérée ou élevée selon les tertiles
de la distribution des taux de protéine C-réactive (mesurés par une méthode à haute
spécificité) avant l’ICP. Pendant les périodes d’hospitalisation et de suivi, la fonction
d’agrégation plaquettaire a été évaluée par la réactivité plaquettaire résiduelle
induite par l’adénosine diphosphate, mesurée par agrégométrie optique (mesure de la
variation de la transmission lumineuse). Les marqueurs de l’inflammation ont été mesurés
lors de l’admission et un an après l’ICP.
Résultats
À des degrés d’inflammation modéré et élevé, l’agrégation plaquettaire résiduelle
induite par l’adénosine diphosphate a été significativement plus importante chez les
patients ayant reçu le clopidogrel que chez ceux traités par le ticagrélor. Dans le
groupe clopidogrel, des différences statistiquement significatives quant à la fonction
d’agrégation plaquettaire ont été observées entre les trois degrés d’inflammation.
Un an après l’ICP, les patients traités par le ticagrélor continuaient à présenter
des taux significativement plus faibles d’interleukine-1β et des taux plus élevés
d’interleukine-35 et de facteur de croissance transformant β.
Conclusions
À différents degrés d’inflammation, le ticagrélor assure une inhibition de l’agrégation
plaquettaire plus marquée que le clopidogrel, ce qui laisse croire que cet agent pourrait
exercer un effet antiplaquettaire plus stable à des degrés d’inflammation systémique
plus élevés. De plus, le ticagrélor est associé à une diminution des signes d’inflammation
lors du suivi d’une ICP, ce qui amène à croire que les effets anti-inflammatoires
pourraient jouer un rôle dans les bienfaits cliniques du traitement antiplaquettaire
qui ont été observés. Une telle possibilité viendrait renforcer encore le bien-fondé
du traitement par le ticagrélor des patients subissant une ICP primaire après un STEMI.
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Article info
Publication history
Published online: August 20, 2018
Accepted:
August 14,
2018
Received:
April 9,
2018
Footnotes
See page 1611 for disclosure information.
Identification
Copyright
© 2018 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
