Relation of cytochrome P450 2C19 loss-of-function polymorphism to occurrence of drug-eluting coronary stent thrombosis.

[1]  A. Gori,et al.  Incidence and clinical impact of dual nonresponsiveness to aspirin and clopidogrel in patients with drug-eluting stents. , 2008, Journal of the American College of Cardiology.

[2]  K. Kim,et al.  The Effect of CYP2C19 Polymorphism on the Pharmacokinetics and Pharmacodynamics of Clopidogrel: A Possible Mechanism for Clopidogrel Resistance , 2008, Clinical pharmacology and therapeutics.

[3]  M. Fromm,et al.  Cytochrome P450 2C19 681G>A polymorphism and high on-clopidogrel platelet reactivity associated with adverse 1-year clinical outcome of elective percutaneous coronary intervention with drug-eluting or bare-metal stents. , 2008, Journal of the American College of Cardiology.

[4]  P. Morange,et al.  Effect of cytochrome p450 polymorphisms on platelet reactivity after treatment with clopidogrel in acute coronary syndrome. , 2008, The American journal of cardiology.

[5]  Matthew J Price,et al.  Prognostic significance of post-clopidogrel platelet reactivity assessed by a point-of-care assay on thrombotic events after drug-eluting stent implantation. , 2008, European heart journal.

[6]  Dominique Mottier,et al.  Influence of omeprazole on the antiplatelet action of clopidogrel associated with aspirin: the randomized, double-blind OCLA (Omeprazole CLopidogrel Aspirin) study. , 2008, Journal of the American College of Cardiology.

[7]  M. Gawaz,et al.  The Residual Platelet Aggregation after Deployment of Intracoronary Stent (PREDICT) score , 2007, Journal of thrombosis and haemostasis : JTH.

[8]  B. Giusti,et al.  Role of glycoprotein Ia gene polymorphisms in determining platelet function in myocardial infarction patients undergoing percutaneous coronary intervention on dual antiplatelet treatment. , 2008, Atherosclerosis.

[9]  M. Fromm,et al.  Cytochrome P 450 2 C 19 681 G > A Polymorphism and High On-Clopidogrel Platelet Reactivity Associated With Adverse 1-Year Clinical Outcome of Elective Percutaneous Coronary Intervention With Drug-Eluting or Bare-Metal Stents , 2008 .

[10]  B. Giusti,et al.  Cytochrome P450 2C19 loss-of-function polymorphism, but not CYP3A4 IVS10+12G/A and P2Y12 T744C polymorphisms, is associated with response variability to dual antiplatelet treatment in high-risk vascular patients , 2007, Pharmacogenetics and genomics.

[11]  S. Iturria,et al.  Common polymorphisms of CYP2C19 and CYP2C9 affect the pharmacokinetic and pharmacodynamic response to clopidogrel but not prasugrel , 2007, Journal of thrombosis and haemostasis : JTH.

[12]  J. Hulot,et al.  Influence of CYP2C19 and CYP3A4 gene polymorphisms on clopidogrel responsiveness in healthy subjects , 2007, Journal of thrombosis and haemostasis : JTH.

[13]  A. Gori,et al.  Impact of platelet reactivity after clopidogrel administration on drug-eluting stent thrombosis. , 2007, Journal of the American College of Cardiology.

[14]  K. Bairy,et al.  Aspirin resistance. , 2007, Indian journal of physiology and pharmacology.

[15]  A. Gori,et al.  Usefulness of aspirin resistance after percutaneous coronary intervention for acute myocardial infarction in predicting one-year major adverse coronary events. , 2006, The American journal of cardiology.

[16]  M. Gilard,et al.  Influence of omeprazol on the antiplatelet action of clopidogrel associated to aspirin , 2006, Journal of thrombosis and haemostasis : JTH.

[17]  Harald Langer,et al.  Low response to clopidogrel is associated with cardiovascular outcome after coronary stent implantation. , 2006, European heart journal.

[18]  A. Bura,et al.  2 C 19 loss-of-function polymorphism is a major determinant of clopidogrel responsiveness in healthy subjects , 2006 .

[19]  C. Lau,et al.  Relation of aspirin resistance to coronary flow reserve in patients undergoing elective percutaneous coronary intervention. , 2005, The American journal of cardiology.

[20]  D. Baruch,et al.  Enhanced shear-induced platelet aggregation in patients who experience subacute stent thrombosis: a case-control study. , 2005, Journal of the American College of Cardiology.

[21]  J. Diodati,et al.  Resistance to clopidogrel: a review of the evidence. , 2005, Journal of the American College of Cardiology.

[22]  Deepak L. Bhatt,et al.  Variability in platelet responsiveness to clopidogrel among 544 individuals. , 2005, Journal of the American College of Cardiology.

[23]  O. Hess,et al.  Stent thrombosis is associated with an impaired response to antiplatelet therapy. , 2005, Journal of the American College of Cardiology.

[24]  杨靓,et al.  Aspirin resistance , 2004 .

[25]  C. Lau,et al.  Aspirin resistance is associated with a high incidence of myonecrosis after non-urgent percutaneous coronary intervention despite clopidogrel pretreatment. , 2004, Journal of the American College of Cardiology.

[26]  P. Watkins,et al.  Contribution of Hepatic Cytochrome P450 3A4 Metabolic Activity to the Phenomenon of Clopidogrel Resistance , 2004, Circulation.

[27]  M. Maftouh,et al.  Structure and stereochemistry of the active metabolite of clopidogrel. , 2002, Drug metabolism and disposition: the biological fate of chemicals.

[28]  S. Yusuf,et al.  Aspirin-Resistant Thromboxane Biosynthesis and the Risk of Myocardial Infarction, Stroke, or Cardiovascular Death in Patients at High Risk for Cardiovascular Events , 2002, Circulation.

[29]  S. Anand.  Aspirin-resistant thromboxane biosynthesis and the risk of myocardial infarction, stroke, or cardiovascular death in patients at high risk for cardiovascular events. Eikelboom JW, Hirsh J, Weitz J, Johnston M, Yi Q, Yusuf S. Circulation 2002; 105: 1650- 1655. , 2002 .

[30]  D. Fitzgerald,et al.  Occupancy of the internal and external pools of glycoprotein IIb/IIIa following abciximab bolus and infusion. , 2001, The Journal of pharmacology and experimental therapeutics.

[31]  J. Herbert,et al.  The Antiaggregating Activity of Clopidogrel Is due to a Metabolic Activation by the Hepatic Cytochrome P450-1A , 1994, Thrombosis and Haemostasis.

[32]  G R Wilkinson,et al.  The major genetic defect responsible for the polymorphism of S-mephenytoin metabolism in humans. , 1994, The Journal of biological chemistry.