Evaluation of the F2R IVS-14A/T PAR1 polymorphism with subsequent cardiovascular events and bleeding in patients who have undergone percutaneous coronary intervention

[1]  Marc P. Bonaca,et al.  Vorapaxar in Patients With Diabetes Mellitus and Previous Myocardial Infarction , 2015, Circulation.

[2]  B. Gage,et al.  Genotype and risk of major bleeding during warfarin treatment. , 2014, Pharmacogenomics.

[3]  E. Braunwald,et al.  Coronary stent thrombosis with vorapaxar versus placebo: results from the TRA 2° P-TIMI 50 trial. , 2014, Journal of the American College of Cardiology.

[4]  F. Harrell,et al.  Racial Differences in Resistance to P2Y12 Receptor Antagonists in Type 2 Diabetic Subjects , 2014, The Journal of Pharmacology and Experimental Therapeutics.

[5]  K. Mahaffey,et al.  Effects of vorapaxar on platelet reactivity and biomarker expression in non-ST-elevation acute coronary syndromes , 2014, Thrombosis and Haemostasis.

[6]  Deepak L. Bhatt,et al.  Consensus and update on the definition of on-treatment platelet reactivity to adenosine diphosphate associated with ischemia and bleeding. , 2013, Journal of the American College of Cardiology.

[7]  Peter L Duffy,et al.  Platelet reactivity and clinical outcomes after coronary artery implantation of drug-eluting stents (ADAPT-DES): a prospective multicentre registry study , 2013, The Lancet.

[8]  David J Cohen,et al.  Association between bleeding events and in-hospital mortality after percutaneous coronary intervention. , 2013, JAMA.

[9]  Deepak L. Bhatt,et al.  Clopidogrel pharmacokinetics and pharmacodynamics vary widely despite exclusion or control of polymorphisms (CYP2C19, ABCB1, PON1), noncompliance, diet, smoking, co-medications (including proton pump inhibitors), and pre-existent variability in platelet function. , 2013, Journal of the American College of Cardiology.

[10]  E. Vicaut,et al.  Bedside monitoring to adjust antiplatelet therapy for coronary stenting. , 2012, The New England journal of medicine.

[11]  Marc P. Bonaca,et al.  Vorapaxar for secondary prevention of thrombotic events for patients with previous myocardial infarction: a prespecified subgroup analysis of the TRA 2°P-TIMI 50 trial , 2012, The Lancet.

[12]  Sunil V. Rao,et al.  Association between periprocedural bleeding and long-term outcomes following percutaneous coronary intervention in older patients. , 2012, JACC: Cardiovascular Interventions.

[13]  Marc P. Bonaca,et al.  Vorapaxar in the secondary prevention of atherothrombotic events. , 2012, The New England journal of medicine.

[14]  A. Carson,et al.  FIRST PHARMACOGENOMIC ANALYSIS USING WHOLE EXOME SEQUENCING TO IDENTIFY NOVEL GENETIC DETERMINANTS OF CLOPIDOGREL RESPONSE VARIABILITY: RESULTS OF THE GENOTYPE INFORMATION AND FUNCTIONAL TESTING (GIFT) EXOME STUDY , 2012 .

[15]  M. Hadamitzky,et al.  Validation of the Bleeding Academic Research Consortium Definition of Bleeding in Patients With Coronary Artery Disease Undergoing Percutaneous Coronary Intervention , 2012, Circulation.

[16]  D. Roden,et al.  Predicting Clopidogrel Response Using DNA Samples Linked to an Electronic Health Record , 2012, Clinical pharmacology and therapeutics.

[17]  G. Parodi,et al.  Residual platelet reactivity, bleedings, and adherence to treatment in patients having coronary stent implantation treated with prasugrel. , 2012, The American journal of cardiology.

[18]  Giuseppe Ambrosio,et al.  Thrombin-receptor antagonist vorapaxar in acute coronary syndromes. , 2012, The New England journal of medicine.

[19]  S. Werns.  Standard- vs High-Dose Clopidogrel Based on Platelet Function Testing After Percutaneous Coronary Intervention: The GRAVITAS Randomized Trial , 2012 .

[20]  J. Marchesini,et al.  Prospective evaluation of on-clopidogrel platelet reactivity over time in patients treated with percutaneous coronary intervention relationship with gene polymorphisms and clinical outcome. , 2011, Journal of the American College of Cardiology.

[21]  Marco Valgimigli,et al.  Standardized Bleeding Definitions for Cardiovascular Clinical Trials: A Consensus Report From the Bleeding Academic Research Consortium , 2011, Circulation.

[22]  W. Ray,et al.  An automated database case definition for serious bleeding related to oral anticoagulant use , 2011, Pharmacoepidemiology and drug safety.

[23]  I. Menown.  Aspirin, P2Y12 blockers, cilostazol, PAR-1 blockers and emerging antiplatelet therapies: can biomarkers guide clinical development and practice? , 2011, Biomarkers in medicine.

[24]  A. Kastrati,et al.  Antiplatelet effects of clopidogrel and bleeding in patients undergoing coronary stent placement , 2010, Journal of thrombosis and haemostasis : JTH.

[25]  A. de Boer,et al.  Besides CYP2C19*2, the variant allele CYP2C9*3 is associated with higher on-clopidogrel platelet reactivity in patients on dual antiplatelet therapy undergoing elective coronary stent implantation , 2010, Pharmacogenetics and genomics.

[26]  Deepak L. Bhatt.  Prasugrel in clinical practice. , 2009, The New England journal of medicine.

[27]  J. Ferrières,et al.  Genetic determinants of response to clopidogrel and cardiovascular events. , 2009, The New England journal of medicine.

[28]  J. O’Connell,et al.  Association of cytochrome P450 2C19 genotype with the antiplatelet effect and clinical efficacy of clopidogrel therapy. , 2009, JAMA.

[29]  P. Morange,et al.  Predictive value of post-treatment platelet reactivity for occurrence of post-discharge bleeding after non-ST elevation acute coronary syndrome. Shifting from antiplatelet resistance to bleeding risk assessment? , 2009, EuroIntervention : journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology.

[30]  E. Antman,et al.  Cytochrome p-450 polymorphisms and response to clopidogrel. , 2009, The New England journal of medicine.

[31]  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.

[32]  P. Bray.  Platelet hyperreactivity: predictive and intrinsic properties. , 2007, Hematology/oncology clinics of North America.

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

[34]  A. Leger,et al.  Protease-Activated Receptors in Cardiovascular Diseases , 2006, Circulation.

[35]  R. Storey,et al.  PAR-1 genotype influences platelet aggregation and procoagulant responses in patients with coronary artery disease prior to and during clopidogrel therapy , 2005, Platelets.

[36]  S. Coughlin,et al.  Protease‐activated receptors in hemostasis, thrombosis and vascular biology , 2005, Journal of thrombosis and haemostasis : JTH.

[37]  R. Storey,et al.  Inhibitory effects of P2Y12 receptor antagonists on TRAP-induced platelet aggregation, procoagulant activity, microparticle formation and intracellular calcium responses in patients with acute coronary syndromes , 2005, Platelets.

[38]  I. Bièche,et al.  An intronic polymorphism in the PAR-1 gene is associated with platelet receptor density and the response to SFLLRN. , 2003, Blood.

[39]  J. Fiessinger,et al.  Interdonor variability of platelet response to thrombin receptor activation: influence of PlA2 polymorphism , 1997, British journal of haematology.