This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Badimon, J. J. Articles by Fuster, V. Search for Related Content PubMed PubMed Citation Articles by Badimon, J. J. Articles by Fuster, V.

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1753.)
© 2002 American Heart Association, Inc.

Editorials

Can We Image the "Active" Thrombus?

Juan Jose Badimon; Valentin Fuster

From the Cardiovascular Institute and Health Center, Mount Sinai School of Medicine, New York, NY.

Correspondence to Valentin Fuster MD, PhD, Director, Cardiovascular Institute, Richard Gorlin MD/Heart Research Foundation, Professor of Cardiology, Mount Sinai School of Medicine, New York, NY 10029. E-mail Valentin.Fuster@mssm.edu

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

Thrombus formation after the disruption of an atherosclerotic plaque is fundamental to the onset of acute coronary syndromes and progression of atherosclerotic disease. The importance of thrombosis in the pathophysiology of coronary artery disease has been supported by the significant clinical benefits associated with the use of antithrombotic agents.¹ Thrombin is a major agonist for platelet activation and, thus, thrombus formation. Thrombin is generated through the interaction of the tissue factor contained in the lipid-rich core of the disrupted atherosclerotic lesions and the flowing blood. The generated thrombin activates and recruits circulating platelets to the injured area. Thrombin, by converting fibrinogen into fibrin, anchors the forming thrombus onto the disrupted surface. In addition, several other processes including thrombus stabilization, embriogenesis, angiogenesis, and cell migration and proliferation are also modulated by thrombin.

See page 1929

Because of the central role played by thrombin in thrombogenesis, the inhibition of thrombin activity and/or generation is the objective of several antithrombotic regimens. Despite their demonstrated clinical benefits, unfractionated and low molecular weight heparins are not capable of inhibiting thrombus-bound thrombin. Several direct and specific thrombin inhibitors have been shown to inactivate both free and clot-bound thrombin. These agents are in various phases of development, with some being approved for therapeutic use. Hirudin, bivalirudin, and argatroban are the parenteral direct thrombin inhibitors approved by US Food and Drug Administration. Despite promising results obtained in preclinical and initial human studies, the initial benefits observed were not maintained at long-term follow-up in larger, randomized clinical trials involving . . . [Full Text of this Article]

This article has been cited by other articles:

				F. A. Jaffer, P. Libby, and R. Weissleder Molecular Imaging of Cardiovascular Disease Circulation, August 28, 2007; 116(9): 1052 - 1061. [Full Text] [PDF]

				J C Spratt and E Camenzind Plaque stabilisation by systemic and local drug administration Heart, December 1, 2004; 90(12): 1392 - 1394. [Full Text] [PDF]

				B Meier Plaque sealing by coronary angioplasty Heart, December 1, 2004; 90(12): 1395 - 1398. [Full Text] [PDF]

				F. A. Jaffer, C.-H. Tung, J. J. Wykrzykowska, N.-H. Ho, A. K. Houng, G. L. Reed, and R. Weissleder Molecular Imaging of Factor XIIIa Activity in Thrombosis Using a Novel, Near-Infrared Fluorescent Contrast Agent That Covalently Links to Thrombi Circulation, July 13, 2004; 110(2): 170 - 176. [Abstract] [Full Text] [PDF]