Prasugrel
Ticagrelor
Prodrug—requires conversion to active
metabolite that irreversibly blocks P2Y12
receptor. Conversion to active metabolite occurs
more rapidly and to a greater degree than with
clopidogrel.
Parent compound is active and no
biotransformation is required for reversible
inhibition of P2Y12 receptor.
Onset of antiplatelet effect is faster and extent of inhibition of aggregation is greater than with
clopidogrel (a significant antiplatelet effect was observed within 30 min of loading).
Conservative
Invasive
Conservative
Invasive
Generally not
recommended for
precatheterization use
in UA/NSTEMI.
60 mg at time of PCI
180 mg
180 mg
Initiate as soon as
coronary anatomy is
known and decision is
made to proceed with
PCI.
Initiate on
presentation.
Initiate as soon as
possible before or at
the time of PCI.
10 mg
Consider reduction
to 5 mg in patients
weighing <60 kg. The
efficacy (or benefit)
of prasugrel in those
age ≥75 y is uncertain.
Contraindicated in
patients with a history
of stroke or TIA.
90 mg twice daily
(The recommended maintenance dose of ASA
to be used with ticagrelor is 81 mg daily.)
≥12 mo for patients
receiving DES
≤12 mo for patients
receiving BMS
Ideally ≤12 mo
≥12 mo for patients
receiving DES
≤12 mo for patients
receiving BMS
Less than with clopidogrel. Impact of genotype and concomitant medications appears less than with
clopidogrel.
Clinical utility not rigorously established but less likely to be necessary given lesser degree of
variation in response.
Risk of spontaneous, instrumented, and fatal
bleeds higher with prasugrel compared with
standard-dose clopidogrel.
Risk of non-CABG bleeds higher with
ticagrelor compared with standard-dose
clopidogrel.
Wait 7 d after last dose.
Wait 5 d after last dose.
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