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J Am Coll Cardiol, 2000; 36:13-21
© 2000 by the American College of Cardiology Foundation
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Techniques characterizing the coronary atherosclerotic plaque: influence on clinical decision making?

Gerard Pasterkamp, MD, PhDa,b, Erling Falk, MD, PhD, FACCc, Hein Woutmana,b and Cornelius Borst, MD, PhD, FACCa,b

a Experimental Cardiology Laboratory, University Medical Center Utrecht, Utrecht, The Netherlands
b Interuniversity Cardiology Institute of the Netherlands, Utrecht, The Netherlands
c Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark. Dr. Gerard Pasterkamp is a fellow of the Catharijne Foundation, Utrecht



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Figure 1 Picro Sirius staining for collagen of atherosclerotic cross-sections. (A) Atherosclerotic plaque with a fibrous cap overlying lipid-rich areas. Thickness of the cap near the arrows is approximately 400 µm. (B) Atherosclerotic plaque with the atheroma adjacent to the lumen due to rupture of the thin fibrous cap. Thickness of the fibrous cap near the rupture (black arrows) is approximately 300 µm. (C) Rupture of the fibrous cap (black arrow).

 


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Figure 2 Echogram (upper panel, left), elastogram (upper panel, right) and histologic sections with alfa actin stain (left bottom panel), and picro Sirius red stain without (bottom middle panel) and with polarized light (bottom right panel) of a human femoral artery. The echogram reveals an eccentric plaque between the 2 and 11 o’clock position. The elastogram shows that the plaque can be divided into two parts: a low strain part (0.2%) between the 4 and 11 o’clock position and a high strain part (1.0%) between the 2 and 4 o’clock position, both compared to the moderate strain (0.5%) in the normal vessel wall. Histologic study reveals that the region between the 4 and 11 o’clock position is fibrous material and the region between the 2 and 4 o’clock position lacks smooth muscle cells (white arrow, left bottom panel) and collagen (white arrow right bottom panel) (with courtesy of C de Korte and T van der Steen, Erasmus University, Rotterdam).

 


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Figure 3 Magnetic resonance imaging of abdominal aorta (arrow) in normal mouse and apoE-KO mouse showing differences between normal and atherosclerotic arteries. On all MRIs, lumen is dark. Normal abdominal aorta wall thickness is approximately 50 µm and was not clearly visible at spatial in plane resolution of 97 µm. Wild-type mice were free of atherosclerotic lesions as shown on MRIs in A and B and histopathology (C). Large atherosclerotic lesion (arrow) that encircles the abdominal aorta of an apoE-KO mouse is shown on the MRI in D and E and was confirmed by histopathologic study (F). All MRIs have pixel size of 97 x 97 x 500 µm3 (adapted from Fayad et al [50]).

 


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Figure 4 Optical coherence tomography image of a longitudinal cross-section of a nonatherosclerotic coronary artery. Top panel: elastin von Gieson staining of the artery of which the lumen is collapsed. M = media, A = adventitia. Bottom panel: the corresponding OCT image (scale is in centimeters) (with courtesy of T van Leeuwen and J Perree, Academic Medical Center, Amsterdam).

 


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Figure 5 Intravascular ultrasound image of a calcified coronary artery (left), and the relative weights of calcium salts (top) and total cholesterol (bottom) in the same artery plane determined by Raman spectroscopy. The IVUS images were obtained from an intact artery segment, which were marked by a needle (12 o’clock). Raman spectra were obtained from the artery after the artery was opened. The IVUS image shows a calcification, in agreement with the calcium salts detected with Raman spectroscopy. Cholesterol was detected with Raman spectroscopy but could not be discriminated within the IVUS image (with courtesy of R Buschman and TJ Römer, Leiden University Medical Center).

 





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