CYP2C19 genotype and cardiovascular events [3]

JAMA

Volumn 307, Issue 14, 2012, Pages 1483-1484

  Siasos, Gerasimos ^a   Tousoulis, Dimitris ^a   Stefanadis, Christodoulos ^a  

^a UNIVERSITY OF ATHENS MEDICAL SCHOOL   (Greece)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE DIPHOSPHATE; CLOPIDOGREL; CYTOCHROME P450 3A; DRUG METABOLITE; FIBRINOGEN; PURINERGIC P2Y12 RECEPTOR;

ANTICOAGULANT THERAPY; BODY MASS; CARDIOVASCULAR DISEASE; CARDIOVASCULAR RISK; CLINICAL EVALUATION; CYP2C19 GENE; DIABETES MELLITUS; DRUG ABSORPTION; DRUG EFFECT; DRUG MECHANISM; DRUG METABOLISM; DRUG RESPONSE; DRUG UNDERDOSE; FIBRINOGEN BLOOD LEVEL; GENE; GENETIC ASSOCIATION; GENETIC POLYMORPHISM; GENETIC RISK; GENETIC VARIABILITY; GENOTYPE; HUMAN; LETTER; PATIENT COMPLIANCE; PHARMACOGENETICS; PRIORITY JOURNAL; RECEPTOR BLOCKING;

EID: 84859531156     PISSN: 00987484     EISSN: 15383598     Source Type: Journal    
DOI: 10.1001/jama.2012.445     Document Type: Letter

References (5)

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3. Angiolillo DJ, Fernandez-Ortiz A, Bernardo E, et al. Contribution of gene sequence variations of the hepatic cytochrome P450 3A4 enzyme to variability in individual responsiveness to clopidogrel. Arterioscler Thromb Vasc Biol. 2006; 26(8):1895-1900. (Pubitemid 44305347)
4. Ang L, Palakodeti V, Khalid A, et al. Elevated plasma fibrinogen and diabetesmellitus are associated with lower inhibition of platelet reactivity with clopidogrel. J Am Coll Cardiol. 2008;52(13):1052-1059.
5. Nissen SE. Pharmacogenomics and clopidogrel: irrational exuberance? JAMA. 2011;306(24):2727-2728.