By Stephen D. Wiviott

ISBN-10: 1405176261

ISBN-13: 9781405176262

ISBN-10: 1444303341

ISBN-13: 9781444303346

* attracts from services of leaders in antiplatelet remedy* Easy-to-use format permits quick shopping* Edited via a member of the celebrated TIMI learn staff with long-standing adventure within the box

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Extra resources for Antiplatelet Therapy In Ischemic Heart Disease (American Heart Association Clinical Series)

Example text

40]. 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.

E. neutrophil– platelet aggregates) were identified by the binding of the PE-conjugated αIIb (CD41)specific monoclonal antibody 5B12 in the neutrophil region (lower right panel). SSC-H, side scatter height. Reproduced from Ref. [31] with permission. For analysis of leukocyte–platelet aggregates, citrated, fixed whole blood can be mailed on ice and the sample is stable for 72 h before analysis at the core laboratory. Summary Because of the variability between patients in the response of their platelets to antiplatelet therapy, there is increasing interest in the use of platelet function tests to monitor the effects of antiplatelet drugs, with the ultimate goal of guiding Chapter 2 Assessment of platelet function 27 antiplatelet therapy to the optimal dose for the prevention or treatment of thrombosis while minimizing hemorrhagic side effects.

Indomethacin causes a slow, time-dependent inhibition of COX-1 and COX-2 [34]. Inhibition of platelet TXA2 synthesis by traditional NSAIDs is intermittent and incomplete, which contrasts with the irreversible and permanent inhibition of platelet TXA2 synthesis by ASA. 3) [17], which is reflected in their side-effect profiles. NSAIDs with greater COX-2 inhibitory action have fewer GI and renal side effects than NSAIDs that primarily inhibit COX-1. Adverse effects of non-selective NSAIDs The most important adverse effects of NSAIDs result from inhibition of COX in the GI mucosa and kidneys.

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Antiplatelet Therapy In Ischemic Heart Disease (American Heart Association Clinical Series) by Stephen D. Wiviott


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