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Submitted on January 27, 2009
Accepted on May 11, 2009
From the Department of Cardiology (E.M.L., M.H.M.W., L.H.), Maastricht University Medical Center, The Netherlands; the Cardiovascular Research Institute Maastricht (E.M.L., M.H.M.W., L.H.), The Netherlands; and the Department of Cardiology (J.N.), University of California, Irvine.
* To whom correspondence should be addressed. E-mail: l.hofstra{at}cardio.unimaas.nl.
Abstract—The ability to identify atherosclerotic plaques that are prone to rupture, also called vulnerable plaques, may provide a major step forward in the recognition of patients that have a high risk of developing acute myocardial infarction. Current clinical risk profiling algorithms, such as the Framingham and Procam risk scores, have reasonable predictive value in the assessment of the 10 year risk. These clinical risk profiling scores typically classify patients into low risk (10-year risk, 5%), intermediate risk (5% to 20% risk), and high risk (greater than 20%). The challenge to imagers is to identify the risk that is beyond 2% yearly risk. Molecular imaging may help identify plaque inflammation and apoptosis of inflammatory cells, which are obligatory components of the plaque instability. These processes offer specific biological targets that can potentially be exploited to obtain biological information on atherosclerosis development in the individual patient.
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Z. A. Fayad Cardiovascular Molecular Imaging Arterioscler Thromb Vasc Biol, July 1, 2009; 29(7): 981 - 982. [Full Text] [PDF] |
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