[1]
Kato M, Dote K, Sasaki S, et al. Presentations of acute coronary syndrome related to coronary lesion morphologies as assessed by intravascular ultrasound and optical coherence tomography. Int J Cardiol 2013; 165: 506-11.
[2]
Virmani R, Burke AP, Farb A, Kolodgie FD. Pathology of the vulnerable plaque. J Am Coll Cardiol 2006; 47(8)(Suppl.): 13-8.
[3]
Takada A, Saito K, Murai T, Ro A, Hamamatsu A. Pathological evaluation of coronary lesions in cases of cardiac rupture during acute myocardial infarction: An autopsy study of 148 out-of-hospital sudden death cases. Pathol Res Pract 2009; 205: 241-7.
[4]
Hombach V, Merkle N, Kestler HA, et al. Characterization of patients with acute chest pain using cardiac magnetic resonance imaging. Clin Res Cardiol 2008; 97: 760-7.
[5]
Sarafoff N, Schuster T, Vochem R, et al. Association of ST-elevation and non-ST-elevation presentation on ECG with transmurality and size of myocardial infarction as assessed by contrast-enhanced magnetic resonance imaging. J Electrocardiol 2013; 46: 100-6.
[6]
Widimsky P, Wijns W, Fajadet J, et al. Reperfusion therapy for ST elevation acute myocardial infarction in Europe: Description of the current situation in 30 countries. Eur Heart J 2010; 31: 943-57.
[7]
Roffi M, Patrono C, Collet J-P, et al. 2015 ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task force for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2016; 37: 267-315.
[8]
Dash D. Current status of antiplatelet therapy in acute coronary syndrome. Cardiovasc Hematol Agents Med Chem 2015; 13: 40-9.
[9]
Franchi F, Rollini F, Angiolillo DJ. Antithrombotic therapy for patients with STEMI undergoing primary PCI. Nat Rev Cardiol 2017; 14(6): 361-79.
[10]
Gryka RJ, Buckley LF, Anderson SM. Vorapaxar. The current role and future directions of a novel protease-activated receptor antagonist for risk reduction in atherosclerotic disease. Drugs R D 2017; 17: 65-72.
[11]
Steg PG, James SK, Atar D, et al. ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation the task force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC). Eur Heart J 2012; 33: 2569-619.
[12]
O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: A report of the American college of cardiology foundation/American heart association task force on practice guidelines. Circulation 2013; 127: 362-425.
[13]
Abbracchio MP, Burnstock G, Boeynaems J-M, et al. International union of pharmacology LVIII: An update on the P2Y G protein-coupled nucleotide receptors: From molecular mechanisms and pathophysiology to therapy. Pharmacol Rev 2006; 58: 281-341.
[14]
Jacobson KA, Deflorian F, Mishra S, Costanzi S. Pharmacochemistry of the platelet purinergic receptors. Purinergic Signal 2011; 7: 305-24.
[15]
Aursnes I, Gjesdal K, Abildgaard U. Platelet aggregation induced by ADP from unsheared erythrocytes at physiological Ca++-concentration. Br J Haematol 1981; 47(1): 149-52.
[16]
Valles J, Santos MT, Aznar J, et al. Erythrocytes metabolically enhance collagen-induced platelet responsiveness via increased thromboxane production, adenosine diphosphate release, and recruitment. Blood 1991; 78: 154-62.
[17]
Holmsen H. Collagen-induced release of adenosine diphosphate from blood platelets incubated with radioactive phosphate in vitro. Scand J Clin Lab Invest 1965; 17: 239-46.
[18]
Fuentes E, Palomo I. Extracellular ATP metabolism on vascular endothelial cells: A pathway with pro-thrombotic and anti-thrombotic molecules. Vascul Pharmacol 2015; 75: 1-6.
[19]
Jin J, Kunapuli SP. Coactivation of two different G protein-coupled receptors is essential for ADP-induced platelet aggregation. Proc Natl Acad Sci USA 1998; 95: 8070-4.
[20]
Turner NA, Moake JL, McIntire LV. Blockade of adenosine diphosphate receptors P2Y(12) and P2Y(1) is required to inhibit platelet aggregation in whole blood under flow. Blood 2001; 98: 3340-5.
[21]
Saraf S, Wellsted D, Sharma S, Gorog DA. Shear-induced global thrombosis test of native blood: Pivotal role of ADP allows monitoring of P2Y12 antagonist therapy. Thromb Res 2009; 124: 447-51.
[22]
Alkhamis TM, Beissinger RL, Chediak JR. Artificial surface effect on red blood cells and platelets in laminar shear flow. Blood 1990; 75: 1568-75.
[23]
Gremmel T, Yanachkov IB, Yanachkova MI, et al. Synergistic inhibition of both P2Y1 and P2Y12 adenosine diphosphate receptors as novel approach to rapidly attenuate platelet-mediated thrombosis. Arterioscler Thromb Vasc Biol 2016; 36: 501-9.
[24]
Adamski P, Koziński M, Ostrowska M, et al. Overview of pleiotropic effects of platelet P2Y12 receptor inhibitors. Thromb Haemost 2014; 112: 224-42.
[25]
Högberg C, Svensson H, Gustafsson R, Eyjolfsson A, Erlinge D. The reversible oral P2Y12 antagonist AZD6140 inhibits ADP-induced contractions in murine and human vasculature. Int J Cardiol 2010; 142: 187-92.
[26]
Froldi G, Bertin R, Dorigo P, Montopoli M, Caparrotta L. Endothelium-independent vasorelaxation by ticlopidine and clopidogrel in rat caudal artery. J Pharm Pharmacol 2011; 63: 1056-62.
[27]
Torngren K, Ohman J, Salmi H, Larsson J, Erlinge D. Ticagrelor improves peripheral arterial function in patients with a previous acute coronary syndrome. Cardiology 2013; 124: 252-8.
[28]
Antonino MJ, Mahla E, Bliden KP, Tantry US, Gurbel PA. Effect of long-term clopidogrel treatment on platelet function and inflammation in patients undergoing coronary arterial stenting. Am J Cardiol 2009; 103: 1546-50.
[29]
Totani L, Dell’Elba G, Martelli N, et al. Prasugrel inhibits platelet-leukocyte interaction and reduces inflammatory markers in a model of endotoxic shock in the mouse. Thromb Haemost 2012; 107: 1130-40.
[30]
Alexopoulos D. p2y12 receptor inhibitors in acute coronary syndromes: From the research laboratory to the clinic and vice versa. Cardiology 2014; 127: 211-9.
[31]
Bertrand ME, Rupprecht HJ, Urban P, Gershlick AH. Double-blind study of the safety of clopidogrel with and without a loading dose in combination with aspirin compared with ticlopidine in combination with aspirin after coronary stenting: The clopidogrel aspirin stent international cooperative study (CLASSICS). Circulation 2000; 102: 624-9.
[32]
Bhatt DL, Stone GW, Mahaffey KW, et al. Effect of platelet inhibition with cangrelor during PCI on ischemic events. N Engl J Med 2013; 368: 1303-13.
[33]
Laine M, Paganelli F, Bonello L. P2Y12-ADP receptor antagonists: Days of future and past. World J Cardiol 2016; 8: 327-32.
[34]
Siller-Matula JM, Trenk D, Krähenbühl S, Michelson AD, Delle-Karth G. Clinical implications of drug-drug interactions with P2Y12 receptor inhibitors. J Thromb Haemost 2014; 12: 2-13.
[35]
Sabouret P, Taiel-Sartral M. New antiplatelet agents in the treatment of acute coronary syndromes. Arch Cardiovasc Dis 2014; 107: 178-87.
[36]
Sugidachi A, Ogawa T, Kurihara A, et al. The greater in vivo antiplatelet effects of prasugrel as compared to clopidogrel reflect more efficient generation of its active metabolite with similar antiplatelet activity to that of clopidogrel’s active metabolite. J Thromb Haemost 2007; 5: 1545-51.
[37]
Gurbel PA, Bliden KP, Butler K, et al. Randomized double-blind assessment of the ONSET and OFFSET of the antiplatelet effects of ticagrelor versus clopidogrel in patients with stable coronary artery disease: The ONSET/OFFSET study. Circulation 2009; 120: 2577-85.
[38]
Anderson SD, Shah NK, Yim J, Epstein BJ. Efficacy and safety of ticagrelor: A reversible P2Y12 receptor antagonist. Ann Pharmacother 2010; 44: 524-37.
[39]
Choi K-N, Jin H-Y, Shin H-C, et al. Comparison of the antiplatelet effects of once and twice daily low-dose ticagrelor and clopidogrel after percutaneous coronary intervention. Am J Cardiol 2017; 120: 201-6.
[40]
Husted S, Emanuelsson H, Heptinstall S, Sandset PM, Wickens M, Peters G. Pharmacodynamics, pharmacokinetics, and safety of the oral reversible P2Y12 antagonist AZD6140 with aspirin in patients with atherosclerosis: A double-blind comparison to clopidogrel with aspirin. Eur Heart J 2006; 27: 1038-47.
[41]
Bonello L, Laine M, Kipson N, et al. Ticagrelor increases adenosine plasma concentration in patients with an acute coronary syndrome. J Am Coll Cardiol 2014; 63: 872-7.
[42]
Wittfeldt A, Emanuelsson H, Brandrup-Wognsen G, et al. Ticagrelor enhances adenosine-induced coronary vasodilatory responses in humans. J Am Coll Cardiol 2013; 61: 723-7.
[43]
van Giezen JJJ, Sidaway J, Glaves P, Kirk I, Björkman J-A. Ticagrelor inhibits adenosine uptake in vitro and enhances adenosine-mediated hyperemia responses in a canine model. J Cardiovasc Pharmacol Ther 2012; 17: 164-72.
[44]
van den Berg TNA, El Messaoudi S, Rongen GA, et al. Ticagrelor does not inhibit adenosine transport at relevant concentrations: A randomized cross-over study in healthy subjects in vivo. PLoS One 2015; 10: e0137560.
[45]
Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes. N Engl J Med 2009; 361: 1045-57.
[46]
Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med 2007; 357: 2001-15.
[47]
Jones WS, Baumgartner I, Hiatt WR, et al. Ticagrelor compared with clopidogrel in patients with prior lower extremity revascularization for peripheral artery disease. Circulation 2017; 135: 241-50.
[48]
Motovska Z, Hlinomaz O, Miklik R, et al. Prasugrel versus ticagrelor in patients with acute myocardial infarction treated with primary percutaneous coronary intervention: multicenter randomized prague-18 study. Circulation 2016; 134: 1603-12.
[49]
Laine M, Gaubert M, Frère C, et al. Comparison of Platelet reactivity following prasugrel and ticagrelor loading dose in ST-Segment elevation myocardial infarction patients: The COMPASSION study. Platelets 2015; 26: 570-2.
[50]
Bonello L, Laine M, Cluzel M, et al. Comparison of ticagrelor versus prasugrel to prevent periprocedural myonecrosis in acute coronary syndromes. Am J Cardiol 2015; 116: 339-43.
[51]
Taubert D, von Beckerath N, Grimberg G, et al. Impact of P-glycoprotein on clopidogrel absorption. Clin Pharmacol Ther 2006; 80: 486-501.
[52]
Tang M, Mukundan M, Yang J, et al. Antiplatelet agents aspirin and clopidogrel are hydrolyzed by distinct carboxylesterases, and clopidogrel is transesterificated in the presence of ethyl alcohol. J Pharmacol Exp Ther 2006; 319: 1467-76.
[53]
Plosker GL, Lyseng-Williamson KA. Clopidogrel: A review of its use in the prevention of thrombosis. Drugs 2007; 67: 613-46.
[54]
Zahno A, Brecht K, Bodmer M, Bur D, Tsakiris DA, Krähenbühl S. Effects of drug interactions on biotransformation and antiplatelet effect of clopidogrel in vitro. Br J Pharmacol 2010; 161: 393-404.
[55]
Peer CJ, Spencer SD, VanDenBerg DAH, Pacanowski MA, Horenstein RB, Figg WD. A sensitive and rapid ultra HPLC-MS/MS method for the simultaneous detection of clopidogrel and its derivatized active thiol metabolite in human plasma. J Chromatogr B Analyt Technol Biomed Life Sci 2012; 880: 132-9.
[56]
Rehmel JLF, Eckstein JA, Farid NA, et al. Interactions of two major metabolites of prasugrel, a thienopyridine antiplatelet agent, with the cytochromes P450. Drug Metab Dispos Biol Fate Chem 2006; 34: 600-7.
[57]
Farid NA, Smith RL, Gillespie TA, et al. The disposition of prasugrel, a novel thienopyridine, in humans. Drug Metab Dispos 2007; 35: 1096-104.
[58]
Teng R, Oliver S, Hayes MA, Butler K. Absorption, distribution, metabolism, and excretion of ticagrelor in healthy subjects. Drug Metab Dispos 2010; 38: 1514-21.
[59]
Zhou D, Andersson TB, Grimm SW. In vitro evaluation of potential drug-drug interactions with ticagrelor: Cytochrome P450 reaction phenotyping, inhibition, induction, and differential kinetics. Drug Metab Dispos 2011; 39: 703-10.
[60]
Mega JL, Close SL, Wiviott SD, et al. Genetic variants in ABCB1 and CYP2C19 and cardiovascular outcomes after treatment with clopidogrel and prasugrel in the TRITON-TIMI 38 trial: A pharmacogenetic analysis. Lancet Lond Engl 2010; 376: 1312-9.
[61]
Luo M, Li J, Xu X, Sun X, Sheng W. ABCB1 C3435T polymorphism and risk of adverse clinical events in clopidogrel treated patients: a meta-analysis. Thromb Res 2012; 129: 754-9.
[62]
Breitenstein B, Brückl TM, Ising M, Müller-Myhsok B, Holsboer F, Czamara D. ABCB1 gene variants and antidepressant treatment outcome: A meta-analysis. Am J Med Genet Part B Neuropsychiatr Genet Off Publ Int Soc Psychiatr Genet 2015; 168: 274-83.
[63]
Werk AN, Cascorbi I. Functional gene variants of CYP3A4. Clin Pharmacol Ther 2014; 96: 340-8.
[64]
Kreutz RP, Owens J, Jin Y, et al. Cytochrome P450 3A4*22, PPAR-α, and ARNT polymorphisms and clopidogrel response. Clin Pharmacol Adv Appl 2013; 5: 185-92.
[65]
Gurbel PA, Shuldiner AR, Bliden KP, Ryan K, Pakyz RE, Tantry US. The relation between CYP2C19 genotype and phenotype in stented patients on maintenance dual antiplatelet therapy. Am Heart J 2011; 161: 598-604.
[66]
Fricke-Galindo I, Céspedes-Garro C, Rodrigues-Soares F, et al. Interethnic variation of CYP2C19 alleles, ‘predicted’ phenotypes and ‘measured’ metabolic phenotypes across world populations. Pharmacogenomics J 2016; 16: 113-23.
[68]
Strom CM, Goos D, Crossley B, et al. Testing for variants in CYP2C19: Population frequencies and testing experience in a clinical laboratory. Genet Med Off J Am Coll Med Genet 2012; 14: 95-100.
[69]
Grosdidier C, Quilici J, Loosveld M, et al. Effect of CYP2C19*2 and *17 genetic variants on platelet response to clopidogrel and prasugrel maintenance dose and relation to bleeding complications. Am J Cardiol 2013; 111: 985-90.
[70]
Park JJ, Park KW, Kang J, et al. Genetic determinants of clopidogrel responsiveness in Koreans treated with drug-eluting stents. Int J Cardiol 2013; 163: 79-86.
[71]
Scott SA, Sangkuhl K, Stein CM, et al. Clinical pharmacogenetics implementation consortium guidelines for CYP2C19 genotype and clopidogrel therapy: 2013 update. Clin Pharmacol Ther 2013; 94: 317-23.
[72]
Zhu H-J, Patrick KS, Yuan H-J, et al. Two CES1 gene mutations lead to dysfunctional carboxylesterase 1 activity in man: Clinical significance and molecular basis. Am J Hum Genet 2008; 82: 1241-8.
[73]
Lewis JP, Horenstein RB, Ryan K, et al. The functional G143E variant of carboxylesterase 1 is associated with increased clopidogrel active metabolite levels and greater clopidogrel response. Pharmacogenet Genomics 2013; 23: 1-8.
[74]
Tantry US, Jeong Y-H, Navarese EP, Kubica J, Gurbel PA. Influence of genetic polymorphisms on platelet function, response to antiplatelet drugs and clinical outcomes in patients with coronary artery disease. Expert Rev Cardiovasc Ther 2013; 11: 447-62.
[75]
Mega JL, Close SL, Wiviott SD, et al. Cytochrome P450 genetic polymorphisms and the response to prasugrel relationship to pharmacokinetic, pharmacodynamic, and clinical outcomes. Circulation 2009; 119: 2553-60.
[76]
Varenhorst C, James S, Erlinge D, et al. Genetic variation of CYP2C19 affects both pharmacokinetic and pharmacodynamic responses to clopidogrel but not prasugrel in aspirin-treated patients with coronary artery disease. Eur Heart J 2009; 30: 1744-52.
[77]
Cuisset T, Loosveld M, Morange PE, et al. CYP2C19*2 and *17 alleles have a significant impact on platelet response and bleeding risk in patients treated with prasugrel after acute coronary syndrome. JACC Cardiovasc Interv 2012; 5: 1280-7.
[78]
Marsh S, Xiao M, Yu J, et al. Pharmacogenomic assessment of carboxylesterases 1 and 2. Genomics 2004; 84: 661-8.
[79]
Kurokawa T, Fukami T, Yoshida T, Nakajima M. Arylacetamide deacetylase is responsible for activation of prasugrel in human and dog. Drug Metab Dispos Biol Fate Chem 2016; 44: 409-16.
[80]
Merali Z, Ross S, Paré G. The pharmacogenetics of carboxylesterases: CES1 and CES2 genetic variants and their clinical effect. Drug Metabol Drug Interact 2014; 29: 143-51.
[81]
Teng R, Butler K. A pharmacokinetic interaction study of ticagrelor and digoxin in healthy volunteers. Eur J Clin Pharmacol 2013; 69: 1801-8.
[82]
Cascorbi I, Gerloff T, Johne A, et al. Frequency of single nucleotide polymorphisms in the P-glycoprotein drug transporter MDR1 gene in white subjects. Clin Pharmacol Ther 2001; 69: 169-74.
[83]
Wallentin L, James S, Storey RF, et al. Effect of CYP2C19 and ABCB1 single nucleotide polymorphisms on outcomes of treatment with ticagrelor versus clopidogrel for acute coronary syndromes: A genetic substudy of the PLATO trial. Lancet 2010; 376: 1320-8.
[84]
Holmberg MT, Tornio A, Joutsi-Korhonen L, et al. Grapefruit juice markedly increases the plasma concentrations and antiplatelet effects of ticagrelor in healthy subjects. Br J Clin Pharmacol 2013; 75: 1488-96.
