Published online before print November 2, 2006, doi: 10.1161/01.ATV.0000251503.35795.4f
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© 2007 American Heart Association, Inc.
Brief Reviews |
Biomarkers of Atherosclerotic Plaque Instability and Rupture
From the Department of Internal Medicine II–Cardiology, University of Ulm Medical Center, Germany.
Correspondence to Wolfgang Koenig, MD, FRCP, FESC, FACC, Department of Internal Medicine II–Cardiology, University of Ulm Medical Center, Robert-Koch Str. 8, D-89081 Ulm, Germany. E-mail wolfgang.koenig{at}uniklinik-ulm.de
Editor: Willliam Haynes
Noninvasive Assessment of Atherosclerosis: From Structure to Function
ATVB In Focus
Previous Brief Reviews in this Series:
•Choudhury RP, Fuster V, Badimon JJ. Fisher EA, Fayad ZA. MRI and characterization of atherosclerotic plaque: emerging applications and molecular imaging. 2002;22:1065–1074.
•Bonetti PO, Lerman LO, Lerman A. Endothelial dysfunction: a marker of atherosclerotic risk. 2003;23:168–175.
•Oliver JJ, Webb DJ. Noninvasive assessment of arterial stiffness and risk of atherosclerotic events. 2003;23:554–566.
•Madjid M, Zarrabi A, Litovsky S, Willerson JT, Casscells W. Finding vulnerable atherosclerotic plaques: is it worth the effort? 2004;24:1775–1782.
•Morrow JD. Quantification of isoprostanes as indices of oxidant stress and the risk of atherosclerosis in humans. 2005;25:279–286.
•Feinbloom D, Bauer KA. Assessment of hemostatis risk factors in predicting arterial thrombotic events. 2005;25:2043–2053.
•Oliver JJ, Webb DJ, Newby, DE. Stimulated tissue plasminogen activator release as a marker of endothelial function in humans. 2005:25:2470–2479.
Basic research over the last two decades has identified a large number of molecules pertinent to the atherosclerotic process, which have clearly improved our understanding of the underlying pathology. It is now well established that inflammation represents a major feature which is present in the vessel wall throughout all stages of the disease until the final pathophysiologic steps, representing plaque destabilization and eventually plaque rupture. Several cells typical for the atherosclerotic plaque, like monocyte-derived macrophages and T-lymphocytes are able to produce and secrete such mediator molecules, like cytokines, chemokines, growth-factors, enzymes, and disintegrins, which lead to activation of endothelial cells, proliferation of smooth muscle cells, lesion progression, and finally to the weakening of a vulnerable plaque by matrix degradation of its fibrous cap. Today, many of these molecules involved can be measured systemically by sensitive assays, and elevated concentrations in the circulation have been shown to be associated with future cardiovascular events. Determination of several of these molecules carries important prognostic information, independent of traditional risk factors, and may turn out to be useful in improving risk stratification. However, for most of these biomarkers the clinical utility has not yet been established.
Basic research over the last two decades has identified a large number of biomarkers of atherosclerotic plaque destabilization and rupture, which carry important prognostic information and might be useful in improving risk stratification in the future. To date, however, none of them can be recommended for routine clinical use.
Key Words: biomarkers • atherosclerosis • pathophysiology • risk prediction
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