Platelet Function Testing in Patients with Coronary Artery Disease: Is the Who and the When any Clearer than the What and the What Then?
Antiplatelet therapy is one of the central pillars of treatment for patients with coronary artery disease. Aspirin and clopidogrel, the most widely used ADP-receptor antagonist, have each been shown to incrementally reduced the risk of recurrent adverse cardiovascular events by approximately 20%.1,2 These agents inhibit distinct but interrelated signaling pathways that mediate and potentiate platelet aggregation at sites of vascular injury. Exposure to subintimal collagen, von Willebrand factor and strong agonists such as thrombin stimulate platelets to generate thromboxane A2 (TXA2) through cyclooxygenase-1 (COX-1)-mediated metabolism of arachidonic acid and to release of ADP stored in dense granules. TXA2 and ADP not only promote sustained activation of the platelet in which they are formed, but both are also released and amplify the thrombotic stimulus by activating adjacent quiescent platelets via binding to specific membrane receptors. Aspirin and clopidogrel synergistically suppress platelet activation and thrombosis by irreversibly binding to and inhibiting the COX-1 enzyme and the P2Y12 ADP receptor, respectively. (SELECT FULL TEXT TO CONTINUE)
- Received May 15, 2012.
- Accepted May 16, 2012.
- Copyright © 2012, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited