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• W2022911171 abstract "In a large cohort of out-hospital cardiac arrest (OHCA) patients treated by primary percutaneous coronary intervention (PCI) and mild therapeutic hypothermia (MTH), Ibrahim et al. showed that in vitro platelet inhibition was more pronounced with new P2Y12 inhibitors (ticagrelor and prasugrel) than with clopidogrel.1Ibrahim K. Christoph M. Schmeinck S. et al.High rates of prasugrel and ticagrelor non-responder in patients treated with therapeutic hypothermia after cardiac arrest.Resuscitation. 2014; 85: 649-656https://doi.org/10.1016/j.resuscitation.2014.02.004Abstract Full Text Full Text PDF PubMed Scopus (97) Google Scholar This could explain the higher incidence of definite acute or subacute stent thrombosis (ST) in our OHCA population of patients treated with clopidogrel, recently published in this journal.2Joffre J. Varenne O. Bougouin W. et al.Stent thrombosis: an increased adverse event after angioplasty following resuscitated cardiac arrest.Resuscitation. 2014; https://doi.org/10.1016/j.resuscitation.2014.02.013Abstract Full Text Full Text PDF PubMed Scopus (62) Google Scholar Indeed, antiplatelet effect of clopidogrel is reduced by delayed absorption and altered pharmacological transformation of the non-active prodrug into active compounds during MTH, as shown by Bjelland et al. using a vasodilator stimulated phosphoprotein phosphorylation (VASP-P) test.3Bjelland T.W. Hjertner Ø. Klepstad P. et al.Antiplatelet effect of clopidogrel is reduced in patients treated with therapeutic hypothermia after cardiac arrest.Resuscitation. 2010; 81: 1627-1631https://doi.org/10.1016/j.resuscitation.2010.07.002Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar In a cohort of 20 consecutive OHCA patients included in our hospital, we compared antiplatelet efficacy of clopidogrel and ticagrelor with a point of care system (VerifyNow®) at different time points after primary PCI. We confirmed that residual platelet activity was higher with clopidogrel than with ticagrelor, expressed as platelet reaction units, 4 h (day 0) after loading dose (297 ± 76 vs. 122 ± 54, p < 0.001), during MTH (293 ± 63 vs. 83 ± 99, p < 0.01) but also after MTH up to day 7, (273 ± 89 vs. 43 ± 38, p < 0.001) (Fig. 1). To the best of our knowledge, this is the first report to demonstrate that the lack of efficacy of clopidogrel was persisting many days after MTH, suggesting that MTH is not solely responsible for its poor biological efficacy. Furthermore, despite a good in vitro efficacy, two ticagrelor-treated patients experienced a definite subacute ST. Although we cannot make definitive clinical conclusions because of the small number of patients studied, our results emphasize that ST is a multifactorial phenomenon which is clearly not only driven by clopidogrel lack of efficacy during MTH. Haemodynamic failure, associated sepsis and postresuscitation syndrome are frequent and are often associated with immunologic and coagulation disorders which could represent a much higher risk factor for ST.4Adrie C. Monchi M. Laurent I. et al.Coagulopathy after successful cardiopulmonary resuscitation following cardiac arrest: implication of the protein C anticoagulant pathway.J Am Coll Cardiol. 2005; 46: 21-28https://doi.org/10.1016/j.jacc.2005.03.046Abstract Full Text Full Text PDF PubMed Scopus (165) Google Scholar Then, if new P2Y12 inhibitors or intravenous antiplatelet agent like cangrelor seem to be an attractive option in this population to obtain optimal antiplatelet efficacy, in OHCA patients and MTH, the “illusion of optimal antiplatelet therapy” is actual. There is no relationship with industry. There is no conflict of interest and relationship with industry for any authors." @default.
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• W2022911171 date "2015-05-01" @default.
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• W2022911171 title "Optimal antiplatelet therapy in out-hospital cardiac arrest patients treated by primary percutaneous coronary intervention" @default.
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• W2022911171 doi "https://doi.org/10.1016/j.resuscitation.2015.02.030" @default.
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