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J Am Coll Cardiol, 2007; 50:319-326, doi:10.1016/j.jacc.2007.03.044
(Published online 6 July 2007). © 2007 by the American College of Cardiology Foundation |
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* Department of Cardiology, Fujita Health University, Toyoake, Japan
Department of Cardiology, Takase Clinic, Takasaki, Japan
Department of Radiology, Fujita Health University, Toyoake, Japan
International Registry of Pathology, Gaithersburg, Maryland
¶ Division of Cardiology, University of California Irvine, Irvine, California. Dr. James E. Muller acted as the Guest Editor for this article
Manuscript received July 25, 2006; revised manuscript received March 13, 2007, accepted March 15, 2007.
* Reprint requests and correspondence: Dr. Sadako Motoyama, 1-98 Dengakugakubo, Kutsukake-cho, Toyoake, Aichi, 470-1192, Japan. (Email: sadakom{at}fujita-hu.ac.jp).
Objectives: To evaluate the feasibility of noninvasive assessment of the characteristics of disrupted atherosclerotic plaques, the authors interrogated the culprit lesions in acute coronary syndromes (ACS) by multislice computed tomography (CT).
Background: Disrupted atherosclerotic plaques responsible for ACS histopathologically demonstrate large lipid cores and positive vascular remodeling. It is expected that plaques vulnerable to rupture should bear similar imaging signatures by CT.
Methods: Either 0.5-mm x 16-slice or 64-slice CT was performed in 38 patients with ACS and compared with 33 patients with stable angina pectoris (SAP) before percutaneous coronary intervention. The coronary plaques in ACS and SAP were evaluated for the CT plaque characteristics, including vessel remodeling, consistency of noncalcified plaque (NCP <30 HU or 30 HU <NCP <150 HU), and spotty or large calcification.
Results: In the CT profile of culprit ACS and SAP lesions, the frequency of 30 HU <NCP <150 HU (100% vs. 100%, p = NS) was not different, and large calcification (22% vs. 55%, p = 0.004) was significantly more frequent in the stable lesions. Positive remodeling (87% vs. 12%, p < 0.0001), NCP <30 HU (79% vs. 9%, p < 0.0001), and spotty calcification (63% vs. 21%, p = 0.0005) were significantly more frequent in the ACS lesions. Presence of all 3 (i.e., positive remodeling, NCP <30 HU, and spotty calcification) showed a high positive predictive value, and absence of all 3 showed a high negative predictive value for the culprit plaques associated with ACS.
Conclusions: The CT characteristics of plaques associated with ACS include positive vascular remodeling, low plaque density, and spotty calcification. It is logical to presume that plaques vulnerable to rupture harbor similar characteristics.
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