Cardiovascular

Read e-book online Antiplatelet Therapy In Ischemic Heart Disease (American PDF

By Stephen D. Wiviott

ISBN-10: 1405176261

ISBN-13: 9781405176262

ISBN-10: 1444303341

ISBN-13: 9781444303346

* attracts from services of leaders in antiplatelet treatment* Easy-to-use structure allows speedy shopping* Edited by means of a member of the celebrated TIMI learn workforce with long-standing event within the box

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

Example text

The antithrombotic effect of aspirin is resultant from the decreased production of TXA2, a potent vasoconstrictor and platelet agonist. The Antithrombotic Trialists’ Collaboration reported that aspirin therapy was associated with 15% reduction in vascular mortality, 34% reduction in myocardial infarction, and 25% reduction in stroke among high-risk patients with atherothrombotic disease [2]. Aspirin has also been shown to reduce the acute ischemic complications of coronary angioplasty [3–5]. While the benefits of aspirin are widely accepted, cardiovascular events may still occur in patients treated with aspirin.

6). Comparison of the VASP assay with ADP-induced turbidometric platelet aggregation demonstrated that the level of thienopyridine-induced inhibition is higher in the VASP assay, presumably because platelet aggregation can still occur via ADP stimulation of P2Y1 in the presence of a thienopyridine [28]. Patients with a poorer platelet response to clopidogrel, as determined by the VASP assay, have been reported to have a higher incidence of subacute stent thrombosis [30]. Platelet surface P-selectin and/or the activated conformation of platelet surface GP IIb/IIIa (reported by monoclonal antibody PAC1) can also be measured by whole blood flow cytometry [31].

Pharmacodynamics ASA irreversibly inhibits the initial committed step of prostanoid biosynthesis by preventing the conversion of AA to PGG2 by COX-1 and COX-2. ASA initially binds an arginine 120 residue, a common docking site for all NSAIDs, after which it acetylates a COX serine residue [21]. In the human COX-1 enzyme, serine is acetylated at position 529 whereas in COX-2 this occurs at position 516 [21]. Acetylation of the serine residue by ASA stops AA from accessing the catalytic site of the COX [11] and prevents formation of the downstream prostanoids.

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


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