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Fig. 1
The structure and composition of thrombi associated with STEMI and UA/NSTEMI. Reproduced with permission from Otterstad and Brosstad, Scandinavian Cardiovascular Journal 2003;37:316-323, Taylor & Francis Ltd. http://www.informaworld.com.
Fig. 2
Principal targets in a pharmacologic antiplatelet strategy for STEMI. Adapted with permission from Otterstad and Brosstad, Scandinavian Cardiovascular Journal 2003;37:316-323, Taylor & Francis Ltd. http://www.informaworld.com. Acetylsalicylic acid (aspirin) permanently acetylates and inhibits the enzyme COX-1 and “switches off” platelet thromboxane A2 production. Clopidogrel irreversibly inhibits platelet ADP receptors, which regulate adenylate cyclase via inhibitory G proteins. Glycoprotein IIb/IIIa inhibitors (abciximab, eptifibatide, tirofiban) block fibrinogen binding to ADP receptors and inhibit platelet aggregation in a dose-dependent manner. TxA2 indicates thromboxane A2.
Fig. 3
Efficacy of clopidogrel at 30 days in the CLARITY-TIMI 28 study. Reproduced with permission from Sabatine et al, New England Journal of Medicine 2005;352:1179-1189. Copyright 2005, Massachusetts Medical Society. All rights reserved. The odds ratio for the end point of death from cardiovascular causes, recurrent myocardial infarction, or recurrent ischemia leading to the need for urgent revascularization was significantly lower in the clopidogrel than in the placebo group at 30 days (11.6% vs 14.1%; odds ratio 0.80; P = .03).
Fig. 4
Efficacy of clopidogrel in the COMMIT/CCS2–The Clopidogrel Arm. Reproduced with permission from the COMMIT Collaborative Group, The Lancet 2005;336:1607-1621. The time-to-event (death, reinfarction, or stroke before first discharge from hospital) analysis was based on a first relevant event during the treatment period. The mean treatment duration in survivors was 14.9 days. Events after discharge were not included. A risk reduction of 9% (P = .002) was achieved for the primary composite end point of death, reinfarction, and stroke in 22958 patients in the clopidogrel arm.
Abstract
Antiplatelet therapy to reduce the risks of recurrent myocardial infarction and restenosis after primary percutaneous coronary intervention is critically important to optimize the early treatment of ST-segment elevation myocardial infarction (STEMI). Traditionally, acetylsalicylic acid (ASA; aspirin) has been recommended for patients with suspected STEMI, but this agent targets only one of several pathways of platelet aggregation. Antiplatelet agents with different inhibitory mechanisms may act synergistically with ASA. Glycoprotein IIb/IIIa inhibitors are generally not used with fibrinolytic agents in acute STEMI management; indeed, glycoprotein IIb/IIIa inhibitors plus bolus fibrinolytics increase the risk of intracranial hemorrhage. Aggressive antiplatelet therapy with clopidogrel reduces mortality in STEMI patients and offers significant clinical benefits, without an associated increase in major bleeding events. Recent trials support the development of an early and aggressive approach to more complete platelet inhibition using clopidogrel, in combination with ASA, for patients with STEMI.
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☆Editorial assistance for the development of this was provided by Jackie Campbell, with the financial support of the BMS/sanofi-aventis Pharmaceuticals Partnership.
