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Can J Cardiol. 2018 Dec;34(12):1606-1612. doi: 10.1016/j.cjca.2018.08.024. Epub 2018 Aug 20.

Effect of Clopidogrel vs Ticagrelor on Platelet Aggregation and Inflammation Markers After Percutaneous Coronary Intervention for ST-Elevation Myocardial Infarction.

Author information

1
Department of Cardiology, The 1st Hospital of Qiqihar, Qiqihar, China.
2
Department of Cardiology, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, China.
3
Department of Cardiology, The 1st Affiliated Hospital of Harbin Medical University, Harbin, China.
4
Department of Cardiology, Yiwu Central Hospital, Yiwu, China.
5
Department of Cardiology, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, China. Electronic address: jingbohou@163.com.

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.

PMID:
30527148
DOI:
10.1016/j.cjca.2018.08.024

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