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J Am Coll Cardiol, 2005; 46:1209-1218, doi:10.1016/j.jacc.2005.03.075 (Published online 15 September 2005).
© 2005 by the American College of Cardiology Foundation
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Atherothrombosis and High-Risk Plaque

Part II: Approaches by Noninvasive Computed Tomographic/Magnetic Resonance Imaging

Valentin Fuster, MD, PhD, FACC*, Zahi A. Fayad, PhD, FACC*,*, Pedro R. Moreno, MD, FACC*,*, Michael Poon, MD, FACC*,{dagger}, Roberto Corti, MD, FACC{ddagger} and Juan J. Badimon, PhD, FACC*

* Zena and Michael A. Wiener Cardiovascular Institute and the Marie-Josee and Henry R. Kravis Cardiovascular Health Center, The Mount Sinai School of Medicine
{dagger} Cabrini Hospital, New York, New York
{ddagger} Zurich University Hospital, Zurich, Switzerland



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Figure 1 Clinical overlap between peripheral arterial disease (PAD), coronary artery disease (coronary), and cerebrovascular disease (cerebral) in the Trans-Atlantic Inter-Society Consensus (TASC) working group with nearly 2,000 patients (left) and in the Clopidogrel versus Aspirin in Patients at Risk of Ischemia Events (CAPRIE) trial with nearly 20,000 patients (right). Compiled from data in the TASC Working Group (10) and the CAPRIE Steering Committee (12).

 


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Figure 2 Coronary calcium lesions in the left anterior coronary artery (arrow) using an electrocardiogram-gated non–contrast-enhanced multidetector-row computed tomography breath hold acquisition.

 


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Figure 3 Predicted seven-year event rates from Cox regression model for coronary heart disease death or non-fatal myocardial infarction (MI) for categories of Framingham Risk Score or coronary artery calcium score (CACS). Reprinted with permission from Greenland et al. (33).

 


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Figure 4 Contrast-enhanced, 16 detector-row computed tomography angiography of the coronary arteries in a 65-year-old patient. (A) Maximum-intensity projection along the course of the proximal left coronary artery shows a large non-calcified coronary artery plaque in the distal left main coronary artery (arrow). (B) A cross-sectional image reconstruction of the corresponding vessel region proves significant lumen obstruction due to the concentric plaque. (C) Using dedicated post-processing tools, the vessel can be stretched longitudinally and rotated in any direction for improved visualization of the plaque.

 


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Figure 5 A 38-year-old man presenting with atypical chest pain. The calcium screening examination revealed no calcifications within the coronary arterial tree (A). After administration of contrast agent, using a three-dimensional volume-rendering reconstruction technique, all epicardial vessels, including major side branches, could be depicted with sufficient image quality, allowing reliable exclusion of significant coronary artery lesions or the presence of extensive non-calcified atherosclerotic vessel wall changes (B, C, D). Ao = aorta; CV = cardiac vein; DBs = diagonal branches; LAD = left anterior descending coronary artery; LCX = left circumflex coronary artery; OM = obtuse marginal branch; PA = pulmonary artery; RCA = right coronary artery.

 


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Figure 6 In vivo black-blood magnetic resonance imaging cross-sectional T2-weighted image of a patient with a significant plaque in the right carotid artery (arrow). The magnified image (bottom left) shows a complex lipid-rich plaque.

 


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Figure 7 In vivo black-blood magnetic resonance images of a patient with a large plaque in the aortic arch (right panel) at the level of the descending aorta (left panel). The arrows indicate plaque. The asterisk indicates the areas of most prominent ulcerations.

 


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Figure 8 In vivo magnetic resonance black-blood cross-sectional images of human coronary arteries demonstrating (A) a plaque presumably with deposition of fat (arrow), (B) a concentric fibrotic lesion in the left anterior descending artery, and (C) an ectatic but atherosclerotic right coronary artery. LAD = left anterior descending; LV = left ventricle; RCA = right coronary artery; RV = right ventricle. Modified from Fayad et al. (88).

 


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Figure 9 T2-weighted magnetic resonance images at two different time points (baseline and 24 months after initiation of lipid-lowering therapy by statins) from the same patient. Details of the descending aorta are shown. At 24 months after lipid-lowering, the magnetic resonance imaging shows a thinner plaque and smaller lipid area (hypointense signal from 1 to 4 o’clock) compared with baseline (arrows). Bar scale indicates 10 mm.

 




 
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