Abstract
Variability of response to clopidogrel and prasugrel is a multifactorial process, with clinical consequences, and drug-drug interactions have been proposed as potential factors. Biological modulation of clopidogrel response has been demonstrated for atorvastatin and omeprazole. However, investigations assessing clinical relevance of these findings have been heterogeneous, and real clinical impact is still debatable. For new P2Y12 blockers, such as prasugrel, with less variability of platelet inhibition, these interactions are not significant; accordingly, no dose adjustment is required. The present review aims to summarize available scientific evidence about CYP-mediated pharmacologic interference with optimal platelet inhibition in patients treated with thienopyridine.
MeSH terms
-
Animals
-
Biotransformation
-
Blood Platelets / drug effects*
-
Blood Platelets / metabolism
-
Cytochrome P-450 Enzyme System / genetics
-
Cytochrome P-450 Enzyme System / metabolism*
-
Drug Interactions
-
Genotype
-
Humans
-
Hydroxymethylglutaryl-CoA Reductase Inhibitors / adverse effects
-
Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacokinetics
-
Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use*
-
Pharmacogenetics
-
Phenotype
-
Platelet Aggregation Inhibitors / adverse effects
-
Platelet Aggregation Inhibitors / pharmacokinetics
-
Platelet Aggregation Inhibitors / therapeutic use*
-
Polymorphism, Genetic
-
Proton Pump Inhibitors / adverse effects
-
Proton Pump Inhibitors / therapeutic use*
-
Risk Assessment
-
Risk Factors
-
Substrate Specificity
-
Treatment Outcome
Substances
-
Hydroxymethylglutaryl-CoA Reductase Inhibitors
-
Platelet Aggregation Inhibitors
-
Proton Pump Inhibitors
-
Cytochrome P-450 Enzyme System