Effect of cytochrome p450 polymorphisms on platelet reactivity after treatment with clopidogrel in acute coronary syndrome.

[1]  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.

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

[3]  P. Morange,et al.  High post-treatment platelet reactivity is associated with a high incidence of myonecrosis after stenting for non-ST elevation acute coronary syndromes , 2007, Thrombosis and Haemostasis.

[4]  F. Neumann,et al.  Impact of the degree of peri-interventional platelet inhibition after loading with clopidogrel on early clinical outcome of elective coronary stent placement. , 2006, Journal of the American College of Cardiology.

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

[6]  A. Bura,et al.  Cytochrome P450 2C19 loss-of-function polymorphism is a major determinant of clopidogrel responsiveness in healthy subjects. , 2006, Blood.

[7]  E. Trabetti,et al.  Contribution of Gene Sequence Variations of the Hepatic Cytochrome P450 3A4 Enzyme to Variability in Individual Responsiveness to Clopidogrel , 2006, Arteriosclerosis, thrombosis, and vascular biology.

[8]  P. Morange,et al.  High post‐treatment platelet reactivity identified low‐responders to dual antiplatelet therapy at increased risk of recurrent cardiovascular events after stenting for acute coronary syndrome , 2006, Journal of thrombosis and haemostasis : JTH.

[9]  R. Storey,et al.  Common sequence variations in the P2Y12 and CYP3A5 genes do not explain the variability in the inhibitory effects of clopidogrel therapy , 2006, Platelets.

[10]  D. Goldstein,et al.  Drug‐metabolizing enzymes: Evidence for clinical utility of pharmacogenomic tests , 2005, Clinical pharmacology and therapeutics.

[11]  P. Gurbel,et al.  Platelet reactivity in patients and recurrent events post-stenting: results of the PREPARE POST-STENTING Study. , 2005, Journal of the American College of Cardiology.

[12]  G. Wilkinson,et al.  Drug metabolism and variability among patients in drug response. , 2005, The New England journal of medicine.

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

[14]  H. Hod,et al.  Clopidogrel Resistance Is Associated With Increased Risk of Recurrent Atherothrombotic Events in Patients With Acute Myocardial Infarction , 2004, Circulation.

[15]  C. Macaya,et al.  Platelet aggregation according to body mass index in patients undergoing coronary stenting: should clopidogrel loading-dose be weight adjusted? , 2004, The Journal of invasive cardiology.

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

[17]  Kevin P. Bliden,et al.  Clopidogrel for Coronary Stenting Response Variability, Drug Resistance, and the Effect of Pretreatment Platelet Reactivity , 2003, Circulation.

[18]  M. Gawaz,et al.  Prevalence of clopidogrel non-responders among patients with stable angina pectoris scheduled for elective coronary stent placement , 2003, Thrombosis and Haemostasis.

[19]  P. Järemo,et al.  Individual variations of platelet inhibition after loading doses of clopidogrel , 2002, Journal of internal medicine.

[20]  K. K. Kohli,et al.  Correlation between omeprazole hydroxylase and CYP2C19 genotype in North Indians , 2001, European Journal of Clinical Pharmacology.

[21]  Salim Yusuf,et al.  Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: the PCI-CURE study , 2001, The Lancet.

[22]  S. Yusuf,et al.  Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. , 2001, The New England journal of medicine.

[23]  David Julius,et al.  Identification of the platelet ADP receptor targeted by antithrombotic drugs , 2001, Nature.

[24]  Hong-Guang Xie,et al.  Effect of the gene dosage of CYP2C19 on diazepam metabolism in Chinese subjects , 1999 .

[25]  U. Walter,et al.  Flow Cytometry Analysis of Intracellular VASP Phosphorylation for the Assessment of Activating and Inhibitory Signal Transduction Pathways in Human Platelets , 1999, Thrombosis and Haemostasis.

[26]  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.

[27]  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.

[28]  J. Herbert,et al.  Importance of hepatic metabolism in the antiaggregating activity of the thienopyridine clopidogrel. , 1992, Biochemical pharmacology.

[29]  C. Macaya,et al.  Identification of low responders to a 300-mg clopidogrel loading dose in patients undergoing coronary stenting. , 2005, Thrombosis research.

[30]  L. Waskell,et al.  The metabolism of clopidogrel is catalyzed by human cytochrome P450 3A and is inhibited by atorvastatin. , 2003, Drug metabolism and disposition: the biological fate of chemicals.