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J Am Coll Cardiol, 2006; 47:13-18, doi:10.1016/j.jacc.2005.10.065
© 2006 by the American College of Cardiology Foundation
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Pathology of the Vulnerable Plaque

Renu Virmani, MD*,*, Allen P. Burke, MD*, Andrew Farb, MD{dagger} and Frank D. Kolodgie, PhD*

* CVPath, International Registry of Pathology, Gaithersburg, Maryland
{dagger} U.S. Food and Drug Administration, CDRH-ODE-DCD-ICDB, Rockville, Maryland


Figure 1
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  		Figure 1 Coronary plaque rupture. (A) Low-power view of a circumferential coronary plaque with fibrous cap rupture. Note the large necrotic core with numerous cholesterol clefts. There is a focal disruption of a thin fibrous cap (arrow) with an occlusive luminal thrombus (Movat Pentachrome, x20). (B) High-power view of the rupture site showing fibrous cap disruption (arrows); the thrombus shows communication with the underlying necrotic core (Movat Pentachrome, x400).

 

Figure 2
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  		Figure 2 Thin-cap fibroatheroma. (A) Low-power view of an eccentric coronary plaque showing a thin fibrous cap overlying a relatively large necrotic core; the vessel was injected with barium (Movat Pentachrome, x20). (B) Immunohistochemical staining reveals numerous CD68-positive macrophages within the fibrous cap (rose-red reaction product, x400). (C) Shows a cellular-rich thin fibrous cap with cholesterol clefts. (D) Staining for alpha-actin positive smooth muscle cells within the fibrous cap was virtually negative (x400). (Reproduced with permission from Kolodgie FD, Virmani R, Burke AP, Farb A, et al. Pathologic assessment of the vulnerable human coronary plaque. Heart 2004;90:1385–91.)

 

Figure 3
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  		Figure 3 Coronary plaque erosion. (A) Shows a low-power view of a coronary artery obstructed by a luminal thrombus (Th) with no established communication with the deep underlying plaque consistent with plaque erosion (Movat Pentachrome, x20). The plaque substrate shows a large lipid pool (Lp) with superficial smooth muscle cells and proteoglycans (bluish-green stain). (B) Eroded lesions with a necrotic core (Nc). There is a non-occlusive luminal thrombus with partial organization. (C) High-power view of the plaque/thrombus (Th) interface in the lesion shown in panel A, showing an absence of endothelium and a substrate rich in smooth muscle cells and proteoglycan matrix (x400). (Figure 3A is reproduced form Kolodgie FD, Burke AP, Farb A, et al. Arherioscler Throm Vasc Biol 2002;22:1642–8. Figures 3B and 3C are reproduced with permission from Kolodgie FD, Burke AP, Wight TN, et al. Curr Opin Lipidol 2004;15:575–82.)

 

Figure 4
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  		Figure 4 Calcified nodule. (A) Low-power view coronary artery showing a heavily calcified eccentric plaque with eruptive calcified nodules (Movat Pentachrome, x20). (B) Higher-power view of the plaque surface of the lesion in A, showing eruptive nodules with accumulated fibrin (x400).

 




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