Treatment
Table 5. Comparisons Among Orally Effective P2Y12 Inhibitors
Clopidogrel
Pharmacology
Prodrug—requires conversion to active metabolite that
irreversibly blocks P2Y12 receptor.
Effect on platelet aggregation
There is a delay of several hours before maximal antiplatelet effect
is seen.
Management strategy
Conservative
Invasive
Loading dose
300 mg
600 mg
Timing
Initiate on presentation.
Initiate as soon as possible
before or at the time of PCI.
Maintenance dose
75 mg
Optimal approach to dosing
in individual patients based
on genotype and individual
antiplatelet effects not
rigorously established.
75 mg
Optimal individual dose not
rigorously established (see
comment to left).
(150 mg for first 6 d is an
alternative.)
Duration
Ideally ≤12 mo
≥12 mo for patients receiving
DES
≤12 mo for patients receiving
BMS
Additional considerations
Variability of response
Greater than with prasugrel or ticagrelor. Factors affecting response
in some patients may include genetic predisposition to convert
parent compound to active metabolite and drug interactions (eg,
PPIs).
Platelet function testing
Clinical utility not rigorously established. May be useful in selected
patients with ischemic/thrombotic events while compliant with a
clopidogrel regimen.
Genotyping
Identifies patients with diminished (CYP2C19*2, *3) or enhanced
(CYP2C17) allele to form active metabolite. Role of genotyping in
clinical management not rigorously established.
Risk of bleeding
Standard dosing with clopidogrel is associated with less bleeding
than with prasugrel and ticagrelor. Higher doses of clopidogrel
are associated with greater risk of bleeding than standard-dose
clopidogrel.
Transition to surgery
Wait 5 d after last dose.
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