Cattaneo M. Aspirin and clopidogrel: efficacy, safety, and the issue of drug resistance. Please enable it to take advantage of the complete set of features! Search for other works by this author on: Although various studies have investigated individual responsiveness to clopidogrel in patients undergoing coronary interventions, there are no studies regarding patients undergoing stent placement of supra-aortic arteries supplying the brain. The effects of clopidogrel on platelets vary among patients, with approximately 4% to 30% of patients being low responders or nonresponders 2 and having an increased risk of ischemic events after stent implantation. Oxford University Press is a department of the University of Oxford.

2018 Apr 26;13:757-772. doi: 10.2147/CIA.S158513. (For EIA, we used the physiologic VASP binding partner zyxin as a capture molecule. Geiger J, Brich J, Honig-Liedl P, Eigenthaler M, Schanzenbacher P, Herbert JM, et al. Specific impairment of human platelet P2Y(AC) ADP receptor-mediated signaling by the antiplatelet drug clopidogrel. Despite this, we consider the P-VASP assay more specific, quantitative, and reliable than previous assays (e.g., aggregometry or P-selectin expression) available for analyzing platelet responses to thienopyridines (Clopidogrel inhibition of ADP-induced (5 μmol/L) platelet aggregation.Platelet activation was measured in the clopidogrel-treated (⋄; 300 mg/day loading dose and 75 mg/day maintenance dose; n = 15) and control (▪; n = 5) groups by standard aggregometry as described in the Clopidogrel inhibition of ADP-induced (5 μmol/L) platelet aggregation.Platelet activation was measured in the clopidogrel-treated (⋄; 300 mg/day loading dose and 75 mg/day maintenance dose; n = 15) and control (▪; n = 5) groups by standard aggregometry as described in the Comparison of individual standard aggregation values before (Comparison of individual standard aggregation values before (⋄, clopidogrel-treated group (n = 9); ▪, placebo group (n = 3). Wenaweser P, Hess O, Meier B. Thienopyridines, a safety net with holes in it. Address correspondence to this author at: Institut für Klinische Biochemie und Pathobiochemie und Zentrallabor, Universität Würzburg, Josef-Schneider Strasse 2, 97080 Würzburg, Germany. This study suggests that ticagrelor may be much better than doubling dose clopidogrel in patients with CYP2C19*2 in according to platelet reactivity monitoring. Citrate-anticoagulated blood was aspirated into an ADP/collagen- or epinephrine/collagen-coated cartridge of a PFA-100 instrument. (⋄, clopidogrel-treated group (n = 9); ▪, placebo group (n = 3). Barragan P, Bouvier JL, Roquebert PO, Macaluso G, Commeau P, Comet B, et al. Institut für Klinische Biochemie und Pathobiochemie und Zentrallabor and Rudolf-Virchow Zentrum für Experimentelle Biomedizin Geiger J, Honig-Liedl P, Schanzenbacher P, Walter U. Ligand specificity and ticlopidine effects distinguish three human platelet ADP receptors. eCollection 2018.Front Pharmacol. 2012 May-Jun;13(3):159-66. doi: 10.1016/j.carrev.2012.02.009.

eCollection 2017.Clin Appl Thromb Hemost. For FACS, we determined the PRI \[\mathrm{PRI}_{\mathrm{(FACS)}}\ {=}\ \frac{\mathrm{MFI}_{(\mathrm{PGE}_{1})}\ {-}\ \mathrm{MFI}_{(\mathrm{PGE}_{1}\ {+}\ \mathrm{ADP})}}{\mathrm{MFI}_{(\mathrm{PGE}_{1})}}\] \[R_{(\mathrm{PGE}_{1})}{=}\frac{A_{405(\mathrm{P-VASP},\ \mathrm{PGE}_{1})}}{A_{405(\mathrm{VASP,\ PGE}_{1})}}\] \[R_{(\mathrm{PGE}_{1}\ {+}\ \mathrm{ADP})}{=}\frac{A_{405(\mathrm{P-VASP,\ PGE}_{1}\ {+}\ \mathrm{ADP})}}{A_{405(\mathrm{VASP,\ PGE}_{1}\ {+}\ \mathrm{ADP})}}\] \[PRI_{(\mathrm{EIA})}{=}\frac{R_{(\mathrm{PGE}_{1})}{-}R_{(\mathrm{PGE}_{1}\ {+}\ \mathrm{ADP})}}{R_{(\mathrm{PGE}_{1})}}\] © 2005 The American Association for Clinical ChemistryThis article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model ( Obergfell A, Strotmann J, Bonz A, Bauersachs J, Ertl G, Walter U, et al. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwideFor full access to this pdf, sign in to an existing account, or purchase an annual subscription.Institut für Klinische Biochemie und Pathobiochemie und Zentrallabor and Rudolf-Virchow Zentrum für Experimentelle Biomedizin Search for other works by this author on: Resistance to thienopyridines: clinical detection of coronary stent thrombosis by monitoring of vasodilator-stimulated phosphoprotein phosphorylation. Silverchair Information Systems Fontana P, Dupont A, Gandrille S, Bachelot-Loza C, Reny JL, Aiach M, et al. Contribution of hepatic cytochrome P450 3A4 metabolic activity to the phenomenon of clopidogrel resistance. Search for other works by this author on: Raman S, Jilma B. Most clinical studies on clopidogrel rely on standard platelet aggregometry to measure inhibition of ADP-induced aggregation . We observed no inhibition in the placebo group (Fig. We observed a clear effect with both the FACS assay [PRIAlthough aggregation was substantially reduced, we found no obvious ex vivo influence of ASA on VASP phosphorylation (Fig. We then transferred 100 μL of each sample to a glutathione The intraassay imprecision (CV) for the EIA was 5.6% for sodium nitroprusside-treated, lysed whole human blood, used as the calibrator, measured with both antibodies (16C2 and IE273) on one microtiter plate [We examined the possible interference of ASA treatment with the VASP phosphorylation assay by measuring platelet aggregation and VASP phosphorylation at baseline and 12 h and 7 days after ASA intake in 6 healthy volunteers taking no medication other than 100 mg of ASA. 8Variable responses to clopidogrel can be explained by increased reactivity of resting platelets, differences in cytochrome P450 metabolism, genetic polymorphisms of the ADP receptor, or a combination of these factors (Clopidogrel resistance has been assessed by use of various indicators that reflect platelet function.