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(Circulation. 2002;105:2130.)
© 2002 American Heart Association, Inc.

Editorial

Platelet–Monocyte Aggregates

Bridging Thrombosis and Inflammation

Jane E. Freedman, MD; Joseph Loscalzo, MD, PhD

From the Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass.

Correspondence to Jane E. Freedman, MD, Boston University School of Medicine, 715 Albany St, W507, Boston, MA 02118. E-mail freedmaj@bu.edu

Key Words: Editorials • atherosclerosis • thrombosis • leukocytes • myocardial infarction

Thrombus formation within a coronary vessel is the precipitating event in unstable coronary syndromes. The angiographic severity of coronary stenoses may not predict sites of subsequent acute coronary events, inasmuch as rupture of atheromatous plaque with thrombosis in relatively mildly stenosed vessels may underlie many acute coronary syndromes. The intact endothelium normally prevents platelet activation, but the intimal injury associated with endothelial denudation and plaque rupture exposes subendothelial collagen and von Willebrand factor, which support prompt platelet adhesion and activation. Circulating platelets can adhere either directly to collagen or indirectly, via the binding of von Willebrand factor, to the glycoprotein Ib/IX complex. Local platelet activation promotes thrombus formation and additional platelet recruitment by supporting cell surface thrombin formation and releasing potent platelet agonists, such as adenosine 5'-diphosphate, serotonin, and thromboxane A₂. The central role of platelet activation in acute coronary syndromes is supported by increased platelet-derived thromboxane and prostaglandin metabolites detected in patients with acute coronary syndromes¹ and the clear clinical benefit of treatment with aspirin for prevention of acute coronary events.²

See p 2166

The importance of platelet-dependent thrombosis has made the platelet aggregate a common therapeutic target in acute coronary syndromes. Recently, such therapies have included the use of aspirin, thienopyridines, and direct glycoprotein IIb/IIIa inhibitors. Although the mechanism of action of these various agents differs, they all inhibit fibrinogen-dependent platelet–platelet associations (ie, platelet aggregation). However, as highlighted by the recent disappointing clinical results of trials using oral glycoprotein IIb/IIIa inhibitors,³ merely preventing the process of platelet . . . [Full Text of this Article]

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