Advertisement

Click here for more guidelines.

 
 




CME Topic Collections Past Issues Search Current Issue Home
     

J Am Coll Cardiol, 2004; 44:2099-2110, doi:10.1016/j.jacc.2004.06.077
© 2004 by the American College of Cardiology Foundation
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Moreno, P. R.
Right arrow Articles by Fuster, V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Moreno, P. R.
Right arrow Articles by Fuster, V.

The year in atherothrombosis

Pedro R. Moreno, MD, FACC*,{dagger} and Valentin Fuster, MD, PhD, FACC*,*

* Cardiovascular Institute, Mount Sinai School of Medicine, New York, New York
{dagger} Linda and Jack Gill Heart Institute, University of Kentucky, Lexington, Kentucky



View larger version (43K):

[in a new window]
 
Figure 1 (A) Low power view of a thin cap fibroatheroma with large necrotic core (Movat pentachrome, x20), heavily infiltrated by CD68-positive macrophages (B) (x200). (C) Shows intense staining for glycophorin A in erythrocyte membranes within the necrotic core, together with cholesterol clefts (x100). (D) Shows iron deposits (blue pigment) in a macrophage-rich region deep within the plaque (Mallory's stain, x200). (E) Shows diffuse, perivascular deposits of von Willebrand factor in microvessels, indicating that leaky vessels border the necrotic core (x400). Reproduced with permission from Kolodgie FD, Gold HK, Burke AP, et al. N Engl J Med 2003;349:2316–25.

 


View larger version (55K):

[in a new window]
 
Figure 2 Microvessels (mv) with intracellular von Willebrand factor (vWf) in flat endothelial cells (A). Microvessels with perivascular macrophages and increased endothelial vWf expression and perivascular vWf deposition (B). Reproduced with permission from Kockx MM, Cromheeke KM, Knaapen MW, et al. Arterioscler Thromb Vasc Biol 2003;23:440–6.

 


View larger version (78K):

[in a new window]
 
Figure 3 Active caspase-3 (A), tissue factor (B), and CD-68 immunostaining (C) show brown labeling of cells (arrows) along the border of the lipid-core (LIP) in serial sections of a human coronary atheroma. FIB = fibrotic. Reproduced with permission from Hutter R, Valdiviezo C, Sauter BV, et al. Circulation 2004;109:2001–8.

 


View larger version (17K):

[in a new window]
 
Figure 4 (A) Complete arterial occlusion at 28 days after femoral wire injury in complement reactive protein-transgenic (CRPtg) (n = 8) and wild-type mice (n = 12). (B to E) Photomicrographs of wild-type (left) and CRPtg (right) femoral arteries stained by Verhoeff elastin stain (B and C) and {alpha}-actin (D and E). Note the reduced smooth muscle cells content in the intraluminal lesion of the CRPtg mouse. Reproduced with permission from Danenberg HD, Szalai AJ, Swaminathan RV, et al. Circulation 2003;108:512–5.

 


View larger version (77K):

[in a new window]
 
Figure 5 Percent enhancement of adventitial signal (false-colored from blue to red) from aortic segments at renal artery (A), mid-aorta (B), and diaphragm (C) 2 h after {alpha}vß3-targeted nanoparticles in cholesterol-fed rabbits. Immunohistochemistry of {alpha}vß3-integrin showing thickened intima (I) and {alpha}vß3-integrin staining in adventitial neovessels (black arrowheads) (D). Immunostaining of neovascular {alpha}vß3-integrin (E) and platelet endothelial cell adhesion molecule (F) in aorta from cholesterol-fed animal in (A) at 600x. Solid arrows delineate {alpha}vß3-integrin expression, and open arrows mark PECAM expression at interface between media (M) and adventitia (Av). Reproduced with permission from Winter PM, Morawski AM, Caruthers SD, et al. Circulation 2003;108:2270–4.

 


View larger version (120K):

[in a new window]
 
Figure 6 Comparison between X-ray angiography (upper row, A) and postprocessed computed tomography (CT) coronary angiography (lower row, B) in the same patient. Three-dimensional volume-rendering postprocessed CT images can be adjusted to resemble conventional coronary angiography planes. DB = diagonal branch; Cx = circumflex; LAD = left anterior descending; LCx = left circumflex; OM = obtuse marginal; PDA = posterior descending artery; RCA = right coronary artery; RVD = right ventricular diagonal; V = vein. Reproduced with permission from Fayad ZA, Fuster V, Nikolaou K, Becker C. Circulation 2002;106:2026–34.

 


View larger version (11K):

[in a new window]
 
Figure 7 Relative risks of future cardiovascular events across a full clinical range of high sensitivity C-reactive protein (hsCRP) values. Blue bars = crude relative risks; red bars = risks adjusted for Framingham risk score. Adapted with permission from Ridker PM. Circulation 2004;109:1955–9.

 




 
  CME Topic Collections Past Issues Search Current Issue Home

Advertisement