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Circulation, Vol 89, 36-44, Copyright © 1994 by American Heart Association
AC van der Wal, AE Becker, CM van der Loos and PK Das
BACKGROUND: The study was designed to verify the concept of plaques "at
risk" and whether inflammation could play a role in plaque rupture and
thrombosis. METHODS AND RESULTS: In 20 patients who had died of acute
myocardial infarction, the thrombosed coronary artery was identified and
the site of plaque rupture was traced in serial sections. The cellular
characteristics of the fibrous cap at the immediate site of rupture were
analyzed and compared with the adjacent cap tissue by use of monoclonal
antibodies reactive with macrophages, T lymphocytes, and smooth muscle
cells. A deep intimal rupture, extending into the lipid core, was
encountered in 12 plaques, whereas 8 had superficial erosions only. Ten
atherosclerotic plaques had a distinctly attenuated fibrous cap covering a
large atheroma, 7 showed a thick fibrocellular cap overlying a lipid pool,
and 3 showed a fibrocellular lesion without a clear lipid core.
Macrophages, and to a lesser extent T lymphocytes, were the dominant cells
at the immediate site of either rupture or superficial erosion in each
instance. These sites, moreover, were always characterized by abundant
expression of HLA-DR antigens on both inflammatory cells and adjacent
smooth muscle cells, suggesting an active inflammatory reaction. In terms
of overall cellular composition of the ruptured plaques, the dominant cell
types were macrophages and T cells in 11, smooth muscle cells in 3, and
mixtures of both in 6. CONCLUSIONS: The underlying atherosclerotic plaque
morphology in complicated coronary artery lesions causing acute myocardial
infarction is heterogeneous with respect to both plaque architecture and
cellular composition. However, the immediate site of plaque rupture or
erosion is always marked by an inflammatory process. This suggests that
inflammation plays a role in destabilizing the fibrous cap tissue and,
thus, in enhancing the risk of coronary thrombosis.
ARTICLES
Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology
Department of Cardiovascular Pathology, University of Amsterdam, The Netherlands.
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 E. J. Harvey and D. P. Ramji Interferon-{gamma} and atherosclerosis: Pro- or anti-atherogenic? Cardiovasc Res, July 1, 2005; 67(1): 11 - 20. [Abstract] [Full Text] [PDF]
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R. Wessely Interference by interferons: Janus faces in vascular proliferative diseases Cardiovasc Res, June 1, 2005; 66(3): 433 - 443. [Abstract] [Full Text] [PDF]
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A. Mauriello, G. Sangiorgi, S. Fratoni, G. Palmieri, E. Bonanno, L. Anemona, R. S. Schwartz, and L. G. Spagnoli Diffuse and Active Inflammation Occurs in Both Vulnerable and Stable Plaques of the Entire Coronary Tree: A Histopathologic Study of Patients Dying of Acute Myocardial Infarction J. Am. Coll. Cardiol., May 17, 2005; 45(10): 1585 - 1593. [Abstract] [Full Text] [PDF]
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J. Johnson, K. Carson, H. Williams, S. Karanam, A. Newby, G. Angelini, S. George, and C. Jackson Plaque Rupture After Short Periods of Fat Feeding in the Apolipoprotein E-Knockout Mouse: Model Characterization and Effects of Pravastatin Treatment Circulation, March 22, 2005; 111(11): 1422 - 1430. [Abstract] [Full Text] [PDF]
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H.-K. Yip, C.-L. Hang, C.-Y. Fang, Y.-K. Hsieh, C.-H. Yang, W.-C. Hung, and C.-J. Wu Level of High-Sensitivity C-Reactive Protein Is Predictive of 30-Day Outcomes in Patients With Acute Myocardial Infarction Undergoing Primary Coronary Intervention Chest, March 1, 2005; 127(3): 803 - 808. [Abstract] [Full Text] [PDF]
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P. Avanzas, R. Arroyo-Espliguero, J. Quiles, D. Roy, and J. C. Kaski Elevated serum neopterin predicts future adverse cardiac events in patients with chronic stable angina pectoris Eur. Heart J., March 1, 2005; 26(5): 457 - 463. [Abstract] [Full Text] [PDF]
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 S. E. Kimmel, J. A. Berlin, M. Reilly, J. Jaskowiak, L. Kishel, J. Chittams, and B. L. Strom Patients Exposed to Rofecoxib and Celecoxib Have Different Odds of Nonfatal Myocardial Infarction Ann Intern Med, February 1, 2005; 142(3): 157 - 164. [Abstract] [Full Text] [PDF]
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M. Fisher, A. Paganini-Hill, A. Martin, M. Cosgrove, J. F. Toole, H. J.M. Barnett, and J. Norris Carotid Plaque Pathology: Thrombosis, Ulceration, and Stroke Pathogenesis Stroke, February 1, 2005; 36(2): 253 - 257. [Abstract] [Full Text] [PDF]
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R. Glaser, F. Selzer, D. P. Faxon, W. K. Laskey, H. A. Cohen, J. Slater, K. M. Detre, and R. L. Wilensky Clinical Progression of Incidental, Asymptomatic Lesions Discovered During Culprit Vessel Coronary Intervention Circulation, January 18, 2005; 111(2): 143 - 149. [Abstract] [Full Text] [PDF]
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M. Madjid, I. Awan, J. T. Willerson, and S. W. Casscells Leukocyte count and coronary heart disease: Implications for risk assessment J. Am. Coll. Cardiol., November 16, 2004; 44(10): 1945 - 1956. [Abstract] [Full Text] [PDF]
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H.-K. Yip, C.-J. Wu, H.-W. Chang, C.-H. Yang, K.-H. Yeh, S. Chua, and M. Fu Levels and Values of Serum High-Sensitivity C-Reactive Protein Within 6 Hours After the Onset of Acute Myocardial Infarction Chest, November 1, 2004; 126(5): 1417 - 1422. [Abstract] [Full Text] [PDF]
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A M A Shehab, R J MacFadyen, M McLaren, R Tavendale, J J F Belch, and A D Struthers Sudden unexpected death in heart failure may be preceded by short term, intraindividual increases in inflammation and in autonomic dysfunction: a pilot study Heart, November 1, 2004; 90(11): 1263 - 1268. [Abstract] [Full Text] [PDF]
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T. J. DeGraba Immunogenetic Susceptibility of Atherosclerotic Stroke: Implications on Current and Future Treatment of Vascular Inflammation Stroke, November 1, 2004; 35(11_suppl_1): 2712 - 2719. [Abstract] [Full Text] [PDF]
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R. Stocker and J. F. Keaney Jr. Role of Oxidative Modifications in Atherosclerosis Physiol Rev, October 1, 2004; 84(4): 1381 - 1478. [Abstract] [Full Text] [PDF]
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M. Madjid, A. Zarrabi, S. Litovsky, J. T. Willerson, and W. Casscells Finding Vulnerable Atherosclerotic Plaques: Is It Worth the Effort? Arterioscler Thromb Vasc Biol, October 1, 2004; 24(10): 1775 - 1782. [Abstract] [Full Text] [PDF]
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J. Quilici, N. Banzet, P. Paule, J.-B. Meynard, M. Mutin, J.-L. Bonnet, P. Ambrosi, J. Sampol, and F. Dignat-George Circulating Endothelial Cell Count as a Diagnostic Marker for Non-ST-Elevation Acute Coronary Syndromes Circulation, September 21, 2004; 110(12): 1586 - 1591. [Abstract] [Full Text] [PDF]
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Y. Agmon, B. K. Khandheria, I. Meissner, T. M. Petterson, W. M. O'Fallon, D. O. Wiebers, T. J. H. Christianson, J. P. McConnell, J. P. Whisnant, J. B. Seward, et al. C-Reactive Protein and Atherosclerosis of the Thoracic Aorta: A Population-Based Transesophageal Echocardiographic Study Arch Intern Med, September 13, 2004; 164(16): 1781 - 1787. [Abstract] [Full Text] [PDF]
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B. D. MacNeill, I.-K. Jang, B. E. Bouma, N. Iftimia, M. Takano, H. Yabushita, M. Shishkov, C. R. Kauffman, S. L. Houser, H.T. Aretz, et al. Focal and multi-focal plaque macrophage distributions in patients with acute and stable presentations of coronary artery disease J. Am. Coll. Cardiol., September 1, 2004; 44(5): 972 - 979. [Abstract] [Full Text] [PDF]
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 L. Mazzolai, M. A. Duchosal, M. Korber, K. Bouzourene, J. F. Aubert, H. Hao, V. Vallet, H. R. Brunner, J. Nussberger, G. Gabbiani, et al. Endogenous Angiotensin II Induces Atherosclerotic Plaque Vulnerability and Elicits a Th1 Response in ApoE-/- Mice Hypertension, September 1, 2004; 44(3): 277 - 282. [Abstract] [Full Text] [PDF]
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P Avanzas, R Arroyo-Espliguero, J Cosin-Sales, G Aldama, C Pizzi, J Quiles, and J C Kaski Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes Heart, August 1, 2004; 90(8): 847 - 852. [Abstract] [Full Text] [PDF]
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K. A. Lindstedt, M. J. Leskinen, and P. T. Kovanen Proteolysis of the Pericellular Matrix: A Novel Element Determining Cell Survival and Death in the Pathogenesis of Plaque Erosion and Rupture Arterioscler Thromb Vasc Biol, August 1, 2004; 24(8): 1350 - 1358. [Abstract] [Full Text] [PDF]
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