Letter to the Editors-in-ChiefIdentification, Evaluation and Treatment of Prasugrel Low-Response after Coronary Stent Implantation – A Preliminary Study
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Conflict of Interest Statement
None declared.
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Cited by (19)
Assessment of Platelet REACtivity After Transcatheter Aortic Valve Replacement: The REAC-TAVI Trial
2019, JACC: Cardiovascular InterventionsHigh residual platelet reactivity after switching from clopidogrel to low-dose prasugrel in Japanese patients with end-stage renal disease on hemodialysis
2019, Journal of CardiologyCitation Excerpt :In contrast to the rate of HPR under clopidogrel in the present study, which is consistent with the results of Western studies, the rate of HPR under 3.75 mg prasugrel in Japanese patients seems to be much higher than with 10 mg prasugrel in Western patients [24]. Previously, Neubauer et al. showed that doubling of the 10 mg prasugrel was effective with adequate platelet inhibition without bleeding events in all 4 patients with prasugrel resistance [33]. Since the antiplatelet effect of prasugrel is dose-dependent [34], higher doses might be needed in order to obtain adequate platelet inhibition in Japanese HD patients.
Repetitive stent thrombosis in a patient who had resistance to both clopidogrel and prasugrel
2016, Journal of Cardiology CasesCitation Excerpt :In patients 75 years or older, the median PRU values were 164 (IQR, 105–216) [7]. Neubauer et al. demonstrated that doubling of the maintenance dose of 10 mg prasugrel was effective with an adequate platelet inhibitory effect and without bleeding events in all four patients with prasugrel resistance [8]. In the present case, we did not double the maintenance dose of 3.75 mg prasugrel because it is not allowed in Japan.
ADP-receptor inhibitors in the perioperative period: The good, the bad, and the ugly
2013, Journal of Cardiothoracic and Vascular AnesthesiaCitation Excerpt :As compared to clopidogrel, prasugrel has a stronger, faster, and more consistent IPA. Possible mechanisms responsible for prasugrel resistance include poor patient compliance, drug absorption disturbances, drug interactions (the concomitant use of CYP3A4 inhibitors), drug underdosing, increased platelet turnover and P2Y12-receptor polymorphism.95-97 However, overall prasugrel is less susceptible to resistance because multiple CYP enzymes are responsible for drug conversion to the active metabolite, and inhibition of one pathway has not been shown to reduce the drug plasma concentrations.24
Ticagrelor versus prasugrel in acute coronary syndrome patients with high on-clopidogrel platelet reactivity following percutaneous coronary intervention: A pharmacodynamic study
2012, Journal of the American College of CardiologyCitation Excerpt :By contrast, PR reduction by prasugrel was less apparent, particularly in patients originated from the upper quartile of baseline PR. A tentative explanation for the stronger antiplatelet action of ticagrelor would be that although prasugrel pharmacodynamic action has been reported not to be affected by CYP2C19 and CYP2C9 polymorphism, we cannot exclude the existence of other polymorphisms or intrahepatic abnormalities affecting the extent of prasugrel active metabolite in patients with HTPR, while leaving unaffected the non–hepatic-dependent ticagrelor action (20,21). Ticagrelor and prasugrel were very effective in eliminating HTPR while on clopidogrel.