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Antiplatelet Agents in the Prevention and Therapy of Thrombosis

Antiplatelet Agents in the Prevention and Therapy of Thrombosis Platelets contribute significantly to vaso-occlusive thrombosis, one of the major causes of death and disease throughout the world. Consequently, inhibiting platelet function is a potentially important therapeutic goal. Increasing evidence indicates the value of aspirin, a relatively weak anti­ platelet agent in the prophylaxis and treatment of vascular disease, and of ticlopidine, a somewhat more potent antiplatelet agent that may be somewhat more effective clinically. Recent advances in our understanding of platelet physiology provide crucial information for the rational design of newer agents that can neutralize thrombin and block the platelet recep­ tor most important in platelet aggregation (GPIIb/IIIa). Several such agents, which are much more potent than aspirin in vitro and in animal models of thrombosis, are now in human clinical trials. INTRODUCTION There is abundant evidence that platelets contribute significantly to the vaso-occlusive thrombotic process that produces ischemic damage in car­ diovascular, cerebrovascular, and peripheral vascular diseases (1-3). This pathologic role derives from the inability of platelets to differentiate between a damaged normal blood vessel that requires platelet interactions to arrest hemorrhage,and a fractured atherosclerotic plaque, where plate171 0066-4219/92/0401-0171$02.00 COLLER let deposition and aggregation may be lethal. Moreover, from an evol­ utionary standpoint, individuals with enhanced http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Medicine Annual Reviews

Antiplatelet Agents in the Prevention and Therapy of Thrombosis

Annual Review of Medicine , Volume 43 (1) – Feb 1, 1992

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Publisher
Annual Reviews
Copyright
Copyright 1992 Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0066-4219
eISSN
1545-326X
DOI
10.1146/annurev.me.43.020192.001131
pmid
1580582
Publisher site
See Article on Publisher Site

Abstract

Platelets contribute significantly to vaso-occlusive thrombosis, one of the major causes of death and disease throughout the world. Consequently, inhibiting platelet function is a potentially important therapeutic goal. Increasing evidence indicates the value of aspirin, a relatively weak anti­ platelet agent in the prophylaxis and treatment of vascular disease, and of ticlopidine, a somewhat more potent antiplatelet agent that may be somewhat more effective clinically. Recent advances in our understanding of platelet physiology provide crucial information for the rational design of newer agents that can neutralize thrombin and block the platelet recep­ tor most important in platelet aggregation (GPIIb/IIIa). Several such agents, which are much more potent than aspirin in vitro and in animal models of thrombosis, are now in human clinical trials. INTRODUCTION There is abundant evidence that platelets contribute significantly to the vaso-occlusive thrombotic process that produces ischemic damage in car­ diovascular, cerebrovascular, and peripheral vascular diseases (1-3). This pathologic role derives from the inability of platelets to differentiate between a damaged normal blood vessel that requires platelet interactions to arrest hemorrhage,and a fractured atherosclerotic plaque, where plate171 0066-4219/92/0401-0171$02.00 COLLER let deposition and aggregation may be lethal. Moreover, from an evol­ utionary standpoint, individuals with enhanced

Journal

Annual Review of MedicineAnnual Reviews

Published: Feb 1, 1992

There are no references for this article.