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Aspirin resistance

Asphalt chemicals, ethyleneamines application, 8 500t, 506 Asphalt emulsifier amine oxides, 2 473 fatty acid amides, 2 458 Asphalt emulsions, 10 131 Asphaltenes, in petroleum vacuum residua, 18 589-590 Asphyxiants, 21 836 Aspirating aerators, 26 165-169 compressed, 26 168-169 propeller driven, 26 168 submersible, 26 169, 170t subsurface, 26 168 Aspiratory, 11 236-237 Aspirin, 4 103-104, 104t, 701 22 17-21. See also Acetylsalicylic acid as trade name, 22 19 for cancer prevention, 2 826 Aspirin resistance, 4 104 ASP oil recovery process, 23 532-533 Assay format, competitive, 14 142 Assay limits, in Investigational New Drug Applications, 18 692 Assays, for silver, 22 650. See also... [Pg.75]

Szczeklik A, Musial J, Undas A, Sanak M. Aspirin resistance. J Thromb Haemost. 2005 3 1655-1662. [Pg.366]

Altman R, Luciardi HL, Muntaner J, Herrera RN, The antithrombotic profile of aspirin, Aspirin resistance, or simply failure Thromb J 2004 2 1. [Pg.40]

The laboratory evaluation of platelet response to aspirin therapy has demonstrated response variability and nonresponsiveness, Based on different ex vivo methods, studies have shown wide variability in the prevalence of aspirin resistance (< I-54,7%) (45,49-58) (Table I). Potential reasons for these discrepancies include (/) wide variability in the criteria to define aspirin resistance, (//) variability in the methods to measure responsiveness, (///) the timing of the laboratory test after aspirin treatment, (/V) the duration of aspirin treatment, and (v) the dose of aspirin administered,... [Pg.142]

There are many potential mechanisms responsible for the occurrence of aspirin resistance or nonresponsiveness. Many of these studies reporting aspirin resistance have employed methods that did not isolate COX-1 inhibition and/or used treatment failure as their definition for aspirin resistance. Cigarette smoking, noncompliance, transient expression of COX-2 in newly formed platelets, and extra-platelet sources of PGG2/PGH2 (endothelial cells, monocytes/macrophages) may contribute to an attenuated clinical response to aspirin (63-66). Erythrocytes may attenuate the effect of aspirin by... [Pg.142]

Abbreviations-. AA, arachidonic acid AMI, acute myocardial infarction AR, aspirin resistance ASA, aspirin CABG, coronary artery bypass graft surgery CAD, coronary artery disease CK-MB, creatinine kinase-MB CVA, cerebrovascular accident EPI, epinephrine HS, healthy subjects LTA, light transmittance aggregometry mm, millimolar PAR, platelet activity ratio PCI, percutaneous coronary intervention PR, platelet reactivity RPFA, rapid platelet function analyzer TXA2, thromboxane A2. [Pg.143]

Reports of high incidences of aspirin resistance may be due to laboratory measurements based on nonspecific methods that do not isolate the response of platelet COX-1 to aspirin or due to an inadequate dose required to fully inhibit the COX-1 in selected patients. Clopidogrel nonresponsiveness is a consistent phenomenon observed in research studies conducted at multiple medical centers around the world. Data from small studies support that patients with high ex vivo platelet reactivity to ADP during and after percutaneous intervention may be at greatest risk for subsequent ischemic events. [Pg.150]

Patrono C. Aspirin resistance definition, mechanisms and clinical read-outs. J Thromb Haemost 2003 1 1710-1713. [Pg.151]

Michelson AD, Catteneo M, Eikelboom JW, et al. Aspirin resistance position paper of the working group on aspirin resistance, platelet physiology subcommittee of the scientific and standardization committee, International society on thrombosis and haemostasis. J Thromb Haemost 2005 3 1309-131 I. [Pg.151]

Tantry U, Gurbel PA, Bliden KR DiChiaraJ. Inconsistency in the prevalence of platelet aspirin resistance as measured by COX-1 non-specific assays in patients treated with 81, 162, and 325 mg aspirin. J Am Coll Cardiol 2006 47 290A. [Pg.151]

Eikelboom JW Hirsh J, Weitz Jl, Johnston M, Yi Q, Yusuf S. Aspirin-resistant thromboxane biosynthesis and the risk of myocardial infarction, stroke, or cardiovascular death in patients at high risk for cardiovascular events. Circulation 2002 105 1650-1655. [Pg.151]

Gum PA, Kottke-Marchant K, Poggio ED, et al, Profile and prevalence of aspirin resistance in patients with cardiovascular disease, AmJ Cardiol 2001 88 230-235. [Pg.152]

Chen W-H, Lee P-Y Ng W, et al, Aspirin resistance is associated with a high incidence of myonecrosis after non-urgent percutaneous coronary intervention despite clopidogrel pretreatment. J Am Coll Cardiol 2004 43 1 122-1 126. [Pg.152]

Tantry US, Bliden KR Gurbel PA. Overestimation of platelet aspirin resistance detection by thrombelastograph platelet mapping and validation by conventional aggregometry using arachidonic acid stimulation. J Am Coll Cardiol 2005 46 1705-1709. [Pg.152]

Weber AA, Zimmermann KC, Meyer-Kirch rath J, Schror K, Cyclooxygenase-2 in human platelets as a possible factor in aspirin resistance. Lancet 1999 353 900,... [Pg.152]

Zimmermann N, WenkA, Kim U, etal. Functional and biochemical evaluation of platelet aspirin resistance after coronary artery bypass surgery. Circulation 2003 108 542-547. [Pg.152]

Payne DA, Jones Cl, Hayes PD, Webster SE, Ross Naylor A, Goodall AH. Platelet inhibition by aspirin is diminished in patients during carotid surgery a form oftransient aspirin resistance Thromb Haemost 2004 92 89-96. [Pg.152]

Bhatt DL. Aspirin resistance more than just a laboratory curiosity. J Am Coil Cardiol 2004 43 1 127-1 129. [Pg.521]

Csiszar A, Stef G, Pacher P, Ungvari Z. Oxidative stress-induced isoprostane formation may contribute to aspirin resistance in platelets. Prostaglandins Leukot. Essent. Fatty Acids 2002 66 557. [Pg.824]

FitzGerald GA. Parsing an enigma the pharmacodynamics of aspirin resistance. Lancet 2003 361(9357) 542-4. [Pg.1713]

Jefferson BK, Foster JH, McCarthy JJ et al (2005) Aspirin resistance and a single gene. Am J Cardiol 95 805-808... [Pg.187]

Goodman T, Ferro A, Sharma P. Pharmacogenetics of aspirin resistance a comprehensive systematic review. Br J Clin Pharmacol 2008 66(2) 222-32. [Pg.17]

Low doses (<100 mg) of aspirin quickly inhibit cyclooxygenase in all the platelets in the circulation. Therefore, the onset of the antiplatelet effect of aspirin is less than 60 minutes. It has been reported, however, that some patients either have or develop aspirin resistance and may require higher doses to achieve the desired antiplatelet effect. Despite this, routine testing for aspirin resistance is not recommended. It was observed recently that administration of ibuprofen prior to the administration of a daily aspirin dose prohibits the aspirin from binding irreversibly to the cyclooxygenase and may decrease its antiplatelet effect. Current recommendations are to administer aspirin at least 2 hours before ibuprofen or to wait at least 4 hours after an ibuprofen dose. [Pg.422]

Eikelboom JW, Hankey GJ. Aspirin resistance A new independent predictor of vascular events J Am Coll Cardiol 2003 41 966-968. [Pg.426]

Mason PJ, Jacobs AK, Freedman JE. Aspirin resistance and atherothrombotic disease. J Am Coll Cardiol 2005 46 986-993. [Pg.1266]

See other pages where Aspirin resistance is mentioned: [Pg.141]    [Pg.141]    [Pg.142]    [Pg.142]    [Pg.142]    [Pg.142]    [Pg.142]    [Pg.142]    [Pg.143]    [Pg.144]    [Pg.144]    [Pg.144]    [Pg.144]    [Pg.150]    [Pg.521]    [Pg.179]    [Pg.15]    [Pg.1235]    [Pg.1266]    [Pg.2299]   
See also in sourсe #XX -- [ Pg.141 , Pg.142 , Pg.143 ]

See also in sourсe #XX -- [ Pg.422 ]



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