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J Am Coll Cardiol, 2006; 47:57-68, doi:10.1016/j.jacc.2005.11.049 © 2006 by the American College of Cardiology Foundation |


* Addenbrookes Hospital, University of Cambridge, Cambridge, United Kingdom
Imaging Science Laboratory, Mount Sinai Hospital, New York, New York
University of California-Irvine School of Medicine, Irvine, California
Manuscript received June 16, 2005; revised manuscript received October 10, 2005, accepted November 16, 2005.
* Reprint requests and correspondence: Dr. Peter L. Weissberg, Division of Cardiovascular Medicine, Box 110, Level 6 ACCI, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QQ, United Kingdom (Email: weissbergp{at}bhf.org.uk).
Imaging of atheromatous plaques has traditionally centered on assessing the degree of luminal stenosis. More recently it has become clear that the vulnerable atherosclerotic plaques responsible for the majority of life-threatening syndromes are characterized by high numbers of inflammatory cells and proteins. This has highlighted the urgent need for suitable imaging techniques that can identify and quantify levels of inflammation within atheromatous lesions. Positron emission tomography and single-photon emission computed tomography imaging hold promise in this regard. Tracer compounds capable of assessing macrophage recruitment, foam cell generation, matrix metalloproteinase production, macrophage apoptosis, and macrophage metabolism have been developed and tested in the carotid and peripheral circulation. The identification of inflamed lesions within the coronary circulation, however, remains elusive owing to small plaque size, cardiac and respiratory motion, and lack of a suitable specific nuclear tracer.
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