By Stephen D. Wiviott
* attracts from services of leaders in antiplatelet treatment* Easy-to-use structure allows quick looking* Edited by means of a member of the distinguished TIMI examine crew with long-standing adventure within the box
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Additional info for Antiplatelet Therapy In Ischemic Heart Disease (American Heart Association Clinical Series)
Aspirin resistance, defined by its pharmacological action, is persistent production of TXA2 despite therapy, measured by the presence of TXA2 metabolites in serum or urine. In contrast, persistent platelet aggregation despite aspirin treatment defines failure of aspirin-mediated platelet inhibition, and this may occur via non-TX mediated pathways of platelet activation. It has been suggested that aspirin resistance is a misleading term since, in some situations, aspirin successfully inhibits TX synthesis but platelet aggregation persists.
Whole blood flow cytometry has a number of advantages as a test of platelet function [31,39]. Platelets are analyzed in their physiological milieu of whole blood and only tiny volumes of blood are required. Whole blood flow cytometry has particular advantages in clinical trials. Samples can be simply prepared at a local site with no required expertise, and then mailed to a core laboratory. The local site does not need access to an aggregometer or other platelet function analyzer or local expertise.
11 Loll PJ, Picot D, Garavito RM. The structural basis of ASA activity inferred from the crystal structure of inactivated prostaglandin H2 synthase. Nat Struct Biol 1995; 2: 637–643. 12 Loll PJ, Picot D, Ekabo O, Garavito RM. Synthesis and use of iodinated nonsteroidal anti-inflammatory drug analogues as crystallographic probes of the prostaglandin H2 synthase cyclooxygenase active site. Biochemistry 1996; 35: 7330–7340. 13 Botting RM. Inhibitors of cyclooxygenases:mechanisms, selectivity and uses.