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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.

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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				E. M. Laufer, M. H.M. Winkens, J. Narula, and L. Hofstra Molecular Imaging of Macrophage Cell Death for the Assessment of Plaque Vulnerability Arterioscler Thromb Vasc Biol, July 1, 2009; 29(7): 1031 - 1038. [Abstract] [Full Text] [PDF]

				S. Motoyama, M. Sarai, H. Harigaya, H. Anno, K. Inoue, T. Hara, H. Naruse, J. Ishii, H. Hishida, N. D. Wong, et al. Computed Tomographic Angiography Characteristics of Atherosclerotic Plaques Subsequently Resulting in Acute Coronary Syndrome J. Am. Coll. Cardiol., June 30, 2009; 54(1): 49 - 57. [Abstract] [Full Text] [PDF]

				E. Braunwald Noninvasive Detection of Vulnerable Coronary Plaques: Locking the Barn Door Before the Horse Is Stolen J. Am. Coll. Cardiol., June 30, 2009; 54(1): 58 - 59. [Full Text] [PDF]

				C. Cheng, A. M. Noordeloos, V. Jeney, M. P. Soares, F. Moll, G. Pasterkamp, P. W. Serruys, and H. J. Duckers Heme Oxygenase 1 Determines Atherosclerotic Lesion Progression Into a Vulnerable Plaque Circulation, June 16, 2009; 119(23): 3017 - 3027. [Abstract] [Full Text] [PDF]

				F. Hyafil, J.-C. Cornily, J. H.F. Rudd, J. Machac, L. J. Feldman, and Z. A. Fayad Quantification of Inflammation Within Rabbit Atherosclerotic Plaques Using the Macrophage-Specific CT Contrast Agent N1177: A Comparison with 18F-FDG PET/CT and Histology J. Nucl. Med., June 1, 2009; 50(6): 959 - 965. [Abstract] [Full Text] [PDF]

				T. Ibrahim, M. R. Makowski, A. Jankauskas, D. Maintz, M. Karch, S. Schachoff, W. J. Manning, A. Schomig, M. Schwaiger, and R. M. Botnar Serial contrast-enhanced cardiac magnetic resonance imaging demonstrates regression of hyperenhancement within the coronary artery wall in patients after acute myocardial infarction. J. Am. Coll. Cardiol. Img., May 1, 2009; 2(5): 580 - 588. [Abstract] [Full Text] [PDF]

				A. Phinikaridou, K. J. Hallock, Y. Qiao, and J. A. Hamilton A robust rabbit model of human atherosclerosis and atherothrombosis J. Lipid Res., May 1, 2009; 50(5): 787 - 797. [Abstract] [Full Text] [PDF]

				U. Hoffmann and F. Bamberg Is Computed Tomography Coronary Angiography the Most Accurate and Effective Noninvasive Imaging Tool to Evaluate Patients With Acute Chest Pain in the Emergency Department?: CT Coronary Angiography Is the Most Accurate and Effective Noninvasive Imaging Tool for Evaluating Patients Presenting With Chest Pain to the Emergency Department Circ Cardiovasc Imaging, May 1, 2009; 2(3): 251 - 263. [Full Text] [PDF]

				N. Gonzalo, P. Barlis, P. W. Serruys, H. M. Garcia-Garcia, Y. Onuma, J. Ligthart, and E. Regar Incomplete Stent Apposition and Delayed Tissue Coverage Are More Frequent in Drug-Eluting Stents Implanted During Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction Than in Drug-Eluting Stents Implanted for Stable/Unstable Angina: Insights From Optical Coherence Tomography J. Am. Coll. Cardiol. Intv., May 1, 2009; 2(5): 445 - 452. [Abstract] [Full Text] [PDF]

				E. Aikawa, M. Aikawa, P. Libby, J.-L. Figueiredo, G. Rusanescu, Y. Iwamoto, D. Fukuda, R. H. Kohler, G.-P. Shi, F. A. Jaffer, et al. Arterial and Aortic Valve Calcification Abolished by Elastolytic Cathepsin S Deficiency in Chronic Renal Disease Circulation, April 7, 2009; 119(13): 1785 - 1794. [Abstract] [Full Text] [PDF]

				N. Gonzalo, H. M. Garcia-Garcia, E. Regar, P. Barlis, J. Wentzel, Y. Onuma, J. Ligthart, and P. W. Serruys In Vivo Assessment of High-Risk Coronary Plaques at Bifurcations With Combined Intravascular Ultrasound and Optical Coherence Tomography J. Am. Coll. Cardiol. Img., April 1, 2009; 2(4): 473 - 482. [Abstract] [Full Text] [PDF]

				S. E. Nissen The Vulnerable Plaque "Hypothesis": Promise, but Little Progress J. Am. Coll. Cardiol. Img., April 1, 2009; 2(4): 483 - 485. [Full Text] [PDF]

				J. J. Fox and H. W. Strauss One Step Closer to Imaging Vulnerable Plaque in the Coronary Arteries J. Nucl. Med., April 1, 2009; 50(4): 497 - 500. [Full Text] [PDF]

				S. Ohshima, A. Petrov, S. Fujimoto, J. Zhou, M. Azure, D. S. Edwards, T. Murohara, N. Narula, S. Tsimikas, and J. Narula Molecular Imaging of Matrix Metalloproteinase Expression in Atherosclerotic Plaques of Mice Deficient in Apolipoprotein E or Low-Density-Lipoprotein Receptor J. Nucl. Med., April 1, 2009; 50(4): 612 - 617. [Abstract] [Full Text] [PDF]

				P. Libby Molecular and cellular mechanisms of the thrombotic complications of atherosclerosis J. Lipid Res., April 1, 2009; 50(Supplement): S352 - S357. [Abstract] [Full Text] [PDF]

				Y. Sun, M. Ishibashi, T. Seimon, M. Lee, S. M. Sharma, K. A. Fitzgerald, A. O. Samokhin, Y. Wang, S. Sayers, M. Aikawa, et al. Free Cholesterol Accumulation in Macrophage Membranes Activates Toll-Like Receptors and p38 Mitogen-Activated Protein Kinase and Induces Cathepsin K Circ. Res., February 27, 2009; 104(4): 455 - 465. [Abstract] [Full Text] [PDF]