Author + information
- Ryo Yoshioka1,
- Atsushi Hirohata1,
- Keizo Yamamoto1,
- Kiyotaka Tohgi1,
- Toshinobu Yoshida1 and
- Toru Yoshioka1
Prasugrel, a third-generation thienopyridine antiplatelet drug, is purported to rapidly and potently inhibit platelet aggregation with less pharmacological variability among CYP2C19 genotypes than other thienopyridines. However, there are no data comparing platelet function at the very early phase after thienopyridine-loading, especially in Japanese.
110 patients with acute myocardial infarction were randomly assigned to receive either 20 mg Prasugrel (n=54) or 300 mg Clopidogrel (n=27) as a loading dose before the emergency coronary intervention. Platelet aggregation with P2Y12 reaction units (PRU) using verify now assay was measured before and 1, 4 and 8-hours after administration of the study medication. Secondary endpoints were clinical events until 30 days.
Patient characteristics were similar between the 2 groups. Baseline PRU (293 ± 54.0 vs. 284 ± 65.7) were similar between the 2 groups. PRU levels after 1-hour, after 4 and 8-hours were significantly lower in the prasugrel group compared with the clopidogrel group (258 ± 77.2 vs. 279.5 ± 52.7, p<0.05, 140.8 ± 38.6 vs. 250.4 ± 62.7, p<0.05, 129.1 ± 96.5 vs. 264.1 ± 58.8, p<0.01, respectively). Although 42% of patients in the prasugrel group showed more than 10% inhibition of PRU levels from baseline, only 8% of patients in the clopidogrel group achieved more than 10% inhibition of PRU from baseline to 1-hour. There was no difference in hospital clinical events between the 2 groups.
Loading doses of prasugrel rapidly and potently inhibited platelet aggregation compared with clopidogrel at 1, 4 and 8-hours. Compared with a baseline of PRU, Prasugrel inhibited platelet aggregation significantly even at 1-hour. PRU≧179 at 8 hours were one of a predictor of cardiac events until day 30 or hospital discharge.