Pathology of the Vulnerable Plaque
Renu Virmani, MD*,*,
Allen P. Burke, MD*,
Andrew Farb, MD and
Frank D. Kolodgie, PhD*
* CVPath, International Registry of Pathology, Gaithersburg, Maryland
U.S. Food and Drug Administration, CDRH-ODE-DCD-ICDB, Rockville, Maryland
Manuscript received June 16, 2005;
revised manuscript received October 10, 2005,
accepted October 24, 2005.
* Reprint requests and correspondence: Dr. Renu Virmani, CVPath, International Registry of Pathology, 19 Firstfield Road, Gaithersburg, Maryland 20878. (Email: rvirmani{at}cvpath.org).
The majority of patients with acute coronary syndromes (ACS) present with unstable angina, acute myocardial infarction, and sudden coronary death. The most common cause of coronary thrombosis is plaque rupture followed by plaque erosion, whereas calcified nodule is infrequent. If advances in coronary disease are to occur, it is important to recognize the precursor lesion of ACS. Of the three types of coronary thrombosis, a precursor lesion for acute rupture has been postulated. The non-thrombosed lesion that most resembles the acute plaque rupture is the thin cap fibroatheroma (TCFA), which is characterized by a necrotic core with an overlying fibrous cap measuring <65 µm, containing rare smooth muscle cells but numerous macrophages. Thin cap fibroatheromas are most frequently observed in patients dying with acute myocardial infarction and least common in plaque erosion. They are most frequently observed in proximal coronary arteries, followed by mid and distal major coronary arteries. Vessels demonstrating TCFA do not usually show severe narrowing but show positive remodeling. In TCFAs the necrotic core length is approximately 2 to 17 mm (mean 8 mm) and the underlying cross-sectional area narrowing in over 75% of cases is <75% (diameter stenosis <50%). The area of the necrotic core in at least 75% of cases is  3 mm2. These lesions have lesser degree of calcification than plaque ruptures. Thin cap fibroatheromas are common in patients with high total cholesterol (TC) and high TC/high-density lipoprotein cholesterol ratio, in women >50 years, and in those patients with elevated high levels of high sensitivity C-reactive protein. It has only recently been recognized that their identification in living patients might help reduce the incidence of sudden coronary death.
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Abbreviations and Acronyms
| | ACS = acute coronary syndromes | | CRP = C-reactive protein | | HDL = high-density lipoprotein | | MPO = myeloperoxidase | | TC = total cholesterol | | TCFA = thin cap fibroatheroma |
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March 6, 2007;
49(9):
933 - 938.
[Abstract]
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A. C. Thomas, G. B. Sala-Newby, Y. Ismail, J. L. Johnson, G. Pasterkamp, and A. C. Newby
Genomics of Foam Cells and Nonfoamy Macrophages From Rabbits Identifies Arginase-I as a Differential Regulator of Nitric Oxide Production
Arterioscler. Thromb. Vasc. Biol.,
March 1, 2007;
27(3):
571 - 577.
[Abstract]
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S. Tsimikas, M. Aikawa, F. J. Miller Jr, E. R. Miller, M. Torzewski, S. R. Lentz, C. Bergmark, D. D. Heistad, P. Libby, and J. L. Witztum
Increased Plasma Oxidized Phospholipid:Apolipoprotein B-100 Ratio With Concomitant Depletion of Oxidized Phospholipids From Atherosclerotic Lesions After Dietary Lipid-Lowering: A Potential Biomarker of Early Atherosclerosis Regression
Arterioscler. Thromb. Vasc. Biol.,
January 1, 2007;
27(1):
175 - 181.
[Abstract]
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J.-F. Surmely, K. Nasu, H. Fujita, M. Terashima, T. Matsubara, E. Tsuchikane, M. Ehara, Y. Kinoshita, Q. X. Zheng, N. Tanaka, et al.
Coronary plaque composition of culprit/target lesions according to the clinical presentation: a virtual histology intravascular ultrasound analysis
Eur. Heart J.,
December 2, 2006;
27(24):
2939 - 2944.
[Abstract]
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F. D. Kolodgie, A. P. Burke, K. S. Skorija, E. Ladich, R. Kutys, A. T. Makuria, and R. Virmani
Lipoprotein-Associated Phospholipase A2 Protein Expression in the Natural Progression of Human Coronary Atherosclerosis
Arterioscler. Thromb. Vasc. Biol.,
November 1, 2006;
26(11):
2523 - 2529.
[Abstract]
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P. Libby and P. M. Ridker
Inflammation and Atherothrombosis: From Population Biology and Bench Research to Clinical Practice
J. Am. Coll. Cardiol.,
October 27, 2006;
48(9_Suppl_A):
A33 - A46.
[Abstract]
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J. Ryan and D. J. Cohen
Are Drug-Eluting Stents Cost-Effective?: It Depends on Whom You Ask
Circulation,
October 17, 2006;
114(16):
1736 - 1744.
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R. P. Giugliano and E. Braunwald
The Year in Non-ST-Segment Elevation Acute Coronary Syndromes
J. Am. Coll. Cardiol.,
July 18, 2006;
48(2):
386 - 395.
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J. E. Muller, A. Tawakol, S. Kathiresan, and J. Narula
New opportunities for identification and reduction of coronary risk treatment of vulnerable patients, arteries, and plaques.
J. Am. Coll. Cardiol.,
April 18, 2006;
47(8 Suppl):
C2 - C6.
[Abstract]
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