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Focus on Molecular Imaging |
1 University of California, Irvine, California; 2 Kurume University School of Medicine, Kurume, Japan; and 3 Cardiovascular Pathology Institute, Gaithersburg, Maryland
Correspondence: For correspondence or reprints contact: Jagat Narula, University of California, UCI Medical Center, 101 The City Dr., Bldg. 53, Rt. 81, Orange, CA. E-mail: narula{at}uci.edu
ABSTRACT
Despite substantial advances in the diagnosis and management of coronary artery disease, acute coronary events continue to occur in many patients. It has been increasingly realized that the lesions responsible for acute events may not necessarily be critically obstructive and hence not be associated with inducible ischemia. Various morphologic features of plaque vulnerability have been described by CT angiography, intravascular ultrasound, and optical coherence tomography. The culprit plaques often demonstrate large plaque and necrotic core volumes, positive vascular remodeling, and attenuation of fibrous plaque caps. The remaining obligatory component of plaque vulnerability is fibrous cap inflammation; molecular imaging is best suited for identification of monocyte–macrophage infiltration. Whereas multiple candidate targets have been evaluated in preclinical molecular imaging studies, only 18F-FDG and 99mTc-annexin-A5 have been recently used in the settings of acute vascular events. These 2 imaging strategies have demonstrated the clinical feasibility of imaging for detection of inflammation.
Key Words: atherosclerosis vulnerable plaque molecular imaging inflammation 18F-labeled FDG PET apoptosis 99mTc-labeled annexin-A5
FOOTNOTES
COPYRIGHT © 2009 by the Society of Nuclear Medicine, Inc.
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