1. A. Mechanism of action of aspirin
A. Mechanism of action of aspirin. Arachidonic acid, a 20-carbon fatty acid containing four double bonds, is released from membrane phospholipids by several forms of phospholipase A2, which are activated by diverse stimuli. Arachidonic acid is converted by cytosolic prostaglandin H synthases, which have both cyclooxygenase and hydroperoxidase (HOX) activity, to the unstable intermediates prostaglandin G2 and prostaglandin H2, respectively. The synthases are also termed cyclooxygenases and exist in two forms, cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). Low-dose aspirin selectively inhibits COX-1, whereas high-dose aspirin inhibits both COX-1 and COX-2. Prostaglandin H2 is converted by tissue-specific isomerases to multiple prostanoids. These bioactive lipids activate specific cell-membrane receptors of the superfamily of G-protein–coupled receptors, such as the thromboxane receptor, the prostaglandin D2 receptors, the prostaglandin E2 receptors, the prostaglandin F2a receptors, and the prostacyclin receptor. B. Absolute effects of antiplatelet therapy with aspirin on the risk of vascular events. The benefit of aspirin therapy in reducing vascular events, including nonfatal myocardial infarction, nonfatal stroke, or death from vascular causes, in five groups of high-risk patients is shown. The figure is based on an analysis of data from the Antithrombotic Trialists' Collaboration. Reproduced with permission from Patrono et al.19
Source: Chapter 61. Pharmacologic Therapy for Acute Coronary Syndromes, Hurst's The Heart, 13e
Citation: Fuster V, Walsh RA, Harrington RA. Hurst's The Heart, 13e; 2011 Available at: Accessed: October 11, 2017
Copyright © 2017 McGraw-Hill Education. All rights reserved