Abstract
Poor responders to clopidogrel have low levels of circulating active metabolite. However, in vitro experiments have shown that blood platelets from poor responders are fully inhibited by the active metabolite of this prodrug. Impaired platelet inhibition reflects inadequate plasma levels of active metabolites, and not differences in platelet P2Y12 receptor function.
Lingua originale | English |
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pagine (da-a) | 271-272 |
Numero di pagine | 2 |
Rivista | NATURE REVIEWS. CARDIOLOGY |
Volume | 6 |
DOI | |
Stato di pubblicazione | Pubblicato - 2009 |
Pubblicato esternamente | Sì |
Keywords
- Aryl Hydrocarbon Hydroxylases
- Biological Availability
- Biotransformation
- Drug Interactions
- Drug Resistance
- Genetic Variation
- Humans
- Platelet Aggregation Inhibitors
- Platelet Function Tests
- Purinergic P2 Receptor Antagonists
- Receptors, Purinergic P2
- Receptors, Purinergic P2Y12
- Ticlopidine
- Treatment Failure