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(Circulation. 2003;108:641.)
© 2003 American Heart Association, Inc.

Editorial

Plaque Rupture, Lysophosphatidic Acid, and Thrombosis

Arthur A. Spector, MD

From the Departments of Biochemistry and Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City.

Correspondence to Arthur A. Spector, MD, Department of Biochemistry, 4-403 Bowen Science Bldg, University of Iowa, 51 Newton Rd, Iowa City, IA 52242. E-mail arthur-spector@uiowa.edu

Key Words: Editorials • atherosclerosis • plaque • lipids • thrombosis

An extract of the first 250 words of the full text is provided, because this article has no abstract.

How does rupture of an atherosclerotic plaque activate platelets, and what can be done to lessen the risk of an ensuing thrombotic episode? Several important new observations that may provide answers to these vital questions are described by Rother et al¹ in the present issue of Circulation. This group previously reported that lysophosphatidic acid (LPA), a phospholipid that activates platelets, is contained in the lipid-rich core of human atherosclerotic lesions.² They now identify the molecular species of LPA present in the core of carotid artery plaques obtained from surgical specimens, demonstrate that lipid extracted from soft plaques can activate human platelets, and show that LPA receptor antagonists inhibit this process. Rother et al¹ conclude that when a plaque ruptures, LPA contained in the exposed lipid sensitizes platelets to aggregating agents and thereby increases the thrombogenic potential. Furthermore, they suggest that LPA receptor antagonists will reduce the likelihood of thrombosis after plaque rupture. This is an interesting new approach that deserves careful consideration.

See p 741

Phospholipids and LPA

LPA is an intermediate in phospholipid metabolism that ordinarily is present in very small amounts in human plasma and tissues. It is a member of the lysophospholipid class of phospholipids. Lysophospholipids are formed by removal of 1 of the 2 fatty acid chains attached to the glycerol backbone of phosphoglycerides, the most abundant form of phospholipids. What makes LPA different from other lysophospholipids and gives it unique biochemical and functional properties is that it does not have a head group, such as choline or ethanolamine, . . . [Full Text of this Article]

Related Article:

Subtype-Selective Antagonists of Lysophosphatidic Acid Receptors Inhibit Platelet Activation Triggered by the Lipid Core of Atherosclerotic Plaques

Enno Rother, Richard Brandl, Daniel L. Baker, Pankaj Goyal, Harry Gebhard, Gabor Tigyi, and Wolfgang Siess
Circulation 2003 108: 741-747. [Abstract] [Full Text]

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