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Elias Atallah, Hassan Saad, Kimon Bekelis, Nohra Chalouhi, Stavropoula Tjoumakaris, David Hasan, Jorge Eller, David Stidd, Robert H. Rosenwasser and Pascal Jabbour

. Approximately 30% of patients exhibit antiplatelet resistance. 1 This variability in the response to clopidogrel is implied by the degree of insufficient platelet inhibition in CYP2C19 heterozygous patients. A small number of centers have substituted clopidogrel with different antiaggregation drugs, such as prasugrel or ticagrelor, in the management of these resistant cases. 6 , 15 Prasugrel and ticagrelor achieve more potent and rapid inhibition of platelet aggregation and decreased intersubject response variability. 7 , 9 In our study, we identified all patients who were

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Osman Ocal, Mustafa Yilmaz, Bora Peynircioglu, Burcak Bilginer, Ahmet Peker and Anil Arat

units [PRU] 320, percent inhibition 0, adenosine diphosphate [ADP] 101, and thrombin receptor activating peptide [TRAP] 139). She was switched to prasugrel by loading her with 2 tablets of prasugrel (2 10-mg tablets, the only formulation currently available to the authors). The next day, VerifyNow and Multiplate tests showed a high level of platelet inhibition (PRU 2, percent inhibition 99, ADP 18, and TRAP 90), and a decision was made to proceed with the second stage of intervention. With the patient under general anesthesia, the right common femoral artery was

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Keri S. Kim, Justin F. Fraser, Stephen Grupke and Aaron M. Cook

, with most practitioners prescribing DAT for at least 3 months. Numerous other agents have been investigated to a limited degree in this clinical context, including prasugrel, ticagrelor, cilostazol, and glycoprotein IIb/IIIa inhibitors, such as abciximab and eptifibatide. These agents are primarily used in the case of clopidogrel resistance or, in the case of glycoprotein IIb/IIIa inhibitors, acute procedural thrombosis. The use of more than 1 antiplatelet agent in neuroendovascular procedures permits the prescriber to take advantage of the additive effects of these

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L. Ian Taylor, James C. Dickerson, Robert J. Dambrino, M. Yashar S. Kalani, Philipp Taussky, Chad W. Washington and Min S. Park

, requires extensive metabolism by CYP enzymes, particularly CYP2C19. 44 For this reason, the levels of active metabolite can be affected by drug-drug interactions as well as genetic variability. In instances in which clopidogrel is not used in dual APT or is believed to be ineffective, it is often replaced by another P2Y12 receptor antagonist, such as prasugrel or ticagrelor. Prasugrel, an irreversible P2Y12 inhibitor, also requires hepatic metabolism; however, prasugrel is more potent and appears to be less affected by genetic variations in P450 enzymes than clopidogrel

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Rahul A. Sastry, Matthew J. Koch, Benjamin L. Grannan, Christopher J. Stapleton, William E. Butler and Aman B. Patel

demonstrated aneurysm regrowth to a size of 2.7 ⋅ 5.4 mm, with evidence of coil compaction at the superior left dome ( Fig. 4 ). Given these findings, a flow diversion treatment strategy was chosen as definitive therapy. While in the endovascular suite, the patient received a loading dose of 325 mg aspirin and 30 mg prasugrel. The pseudoaneurysm was re-coiled with 2 Penumbra SMART coils and 1 Axium Prime coil. Afterward, a 3 mm ⋅ 12–mm Pipeline Flex embolization device was introduced and placed from the left P 1 posterior cerebral artery (PCA) to the BA ( Fig. 5 ). The

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Julius Griauzde, Vijay M. Ravindra, Neeraj Chaudhary, Joseph J. Gemmete, Marcus D. Mazur, Christopher D. Roark, William T. Couldwell, Min S. Park, Philipp Taussky and Aditya S. Pandey

prasugrel and aspirin. They were maintained on prasugrel for 6 months and aspirin indefinitely; prasugrel was used in these cases because of the interference of the administered abciximab with P2Y12 testing. In cases in which PED treatment was used for a recurrent lesion, patients being treated with clopidogrel and aspirin were confirmed to have achieved a therapeutic response to the medications prior to the procedure. Clopidogrel was continued for 6 months and aspirin was continued indefinitely. Follow-up angiographic imaging (MR angiography, CT angiography, or digital

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James D. Rossen, Nohra Chalouhi, Shafik N. Wassef, Jacob Thomas, Taylor J. Abel, Pascal M. Jabbour, David K. Kung and David M. Hasan

effects. 6 Coronary stent thrombosis was reduced with the administration of thienopyridine prasugrel compared with clopidogrel in patients undergoing stent placement for high-risk acute coronary syndromes. 13 The risk of thrombosis related to a coronary drug-eluting stent after discontinuation of clopidogrel has led to the recommendation to prolong therapy from 6 to 12 months in these circumstances. 7 Clustering of adverse clinical cardiac events following clopidogrel withdrawal has led to concern over a prothrombotic “rebound” effect in this setting. 10 The

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Albert H. Chiu, Joost De Vries, Cian J. O'Kelly, Howard Riina, Ian McDougall, Jonathan Tippett, Martina Wan, Airton Leonardo de Oliveira Manoel and Thomas R. Marotta

, depending on the neurointerventionist's preference, and was not continued after the operation. Antiplatelet regimens varied among operators. For elective cases, patients received 325 mg aspirin between 2 and 5 days prior to the procedure, including the day of surgery, and either 75 mg clopidogrel daily or 10 mg prasugrel daily 5 days prior to surgery (including the day of surgery), and continued receiving a dual antiplatelet blockade for a minimum of 3 months. If there were no complications or other concerns, the clopidogrel or prasugrel was stopped at 3 months and the

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Robert F. James, Viktoras Palys, Jason R. Lomboy, J. Richard Lamm Jr. and Scott D. Simon

the antiplatelet activity of clopidogrel prasugrel (Effient) 7 thienopyridines (prodrugs ‡ ): selective irreversible platelet P2Y12 receptor inhibition → decreased ADP binding to P2Y12 → increased cAMP levels † 60 mg (loading) followed by 10 mg/day (5 mg/day if weight <60 kg or age >75 yrs) intestinal esterase plays important role; therefore drug requires fewer hepatic metabolic steps for activation; metabolism independent of CYP genotype; excretion: urine (68%), feces (27%); elimination T1/2: 2–15 hrs (active metabolite) P2Y12 platelet receptor cascade

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Christoph J. Griessenauer, Christopher S. Ogilvy, Paul M. Foreman, Michelle H. Chua, Mark R. Harrigan, Christopher J. Stapleton, Aman B. Patel, Lucy He, Matthew R. Fusco, J Mocco, Peter A. Winkler, Apar S. Patel and Ajith J. Thomas

.5) Morphology, no. of aneurysms   Saccular 65 (94.2)   Fusiform/dissecting 4 (5.8) Intramural thrombus, no. of aneurysms 3 (4.3) Adjunctive coils, no. of aneurysms 2 (2.9) No. of PEDs   1 66 (95.7)   2 3 (4.3) Antiplatelet therapy, no. of aneurysms   325 mg aspirin daily + 75 mg clopidogrel daily 52 (75.4)   325 mg aspirin daily + 150 mg clopidogrel daily 2 (2.9)   325 mg aspirin daily + 10 mg prasugrel daily 5 (7.2)   325 mg aspirin daily + 90 mg ticagrelor twice daily 10 (14.5) Platelet function