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(Circulation. 1996;93:1354-1363.)
© 1996 American Heart Association, Inc.
Articles |
Coronary Plaque Erosion Without Rupture Into a Lipid Core
A Frequent Cause of Coronary Thrombosis in Sudden Coronary Death
From the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC, and Office of the Chief Medical Examiner (J.S.), Baltimore, Md.
Background Coronary thrombosis has been reported to occur most frequently in lipid-rich plaques with rupture of a thin fibrous cap and contact of the thrombus with a pool of extracellular lipid. However, the frequency of coronary artery thrombosis with or without fibrous cap rupture in sudden coronary death is unknown. In this study, we compared the incidence and morphological characteristics of coronary thrombosis associated with plaque rupture versus thrombosis in eroded plaques without rupture.
Methods and Results Fifty consecutive cases of sudden death due to coronary artery thrombosis were studied by histology and immunohistochemistry. Plaque rupture of a fibrous cap with communication of the thrombus with a lipid pool was identified in 28 cases. Thrombi without rupture were present in 22 cases, all of which had superficial erosion of a proteoglycan-rich plaque. The mean age at death was 53±10 years in plaque rupture cases versus 44±7 years in eroded plaques without rupture (P<.02). In the plaque-rupture group, 5 of 28 (18%) were women versus 11 of 22 (50%) with eroded plaques (P=.03). The mean percent luminal area stenosis was 78±12% in plaque rupture and 70±11% in superficial erosion (P<.03). Plaque calcification was present in 69% of ruptures versus 23% of erosions (P<.002). In plaque ruptures, the fibrous cap was infiltrated by macrophages in 100% and T cells in 75% of cases compared with 50% (P<.0001) and 32% (P<.004), respectively, in superficial erosions. Clusters of smooth muscle cells adjacent to the thrombi were present in 95% of erosions versus 33% of ruptures (P<.0001). HLA-DR expression was more often seen in macrophages and T cells in ruptures (25 of 28 cases) compared with expression in macrophages in superficial erosion arteries (8 of 22 cases, P=.0002).
Conclusions Erosion of proteoglycan-rich and smooth muscle cell–rich plaques lacking a superficial lipid core or plaque rupture is a frequent finding in sudden death due to coronary thrombosis, comprising 44% of cases in the present study. These lesions are more often seen in younger individuals and women, have less luminal narrowing and less calcification, and less often have foci of macrophages and T cells compared with plaque ruptures.
Key Words: plaque • thrombosis • death, sudden • coronary disease
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P. K. Shah Mechanisms of plaque vulnerability and rupture J. Am. Coll. Cardiol., February 19, 2003; 41(4_Suppl_S): 15S - 22S. [Abstract] [Full Text] [PDF]
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M. Valgimigli, L. Agnoletti, S. Curello, L. Comini, G. Francolini, F. Mastrorilli, E. Merli, R. Pirani, G. Guardigli, P. G. Grigolato, et al. Serum From Patients With Acute Coronary Syndromes Displays a Proapoptotic Effect on Human Endothelial Cells: A Possible Link to Pan-Coronary Syndromes Circulation, January 21, 2003; 107(2): 264 - 270. [Abstract] [Full Text] [PDF]
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D. Proudfoot, J.D. Davies, J.N. Skepper, P.L. Weissberg, and C.M. Shanahan Acetylated Low-Density Lipoprotein Stimulates Human Vascular Smooth Muscle Cell Calcification by Promoting Osteoblastic Differentiation and Inhibiting Phagocytosis Circulation, December 10, 2002; 106(24): 3044 - 3050. [Abstract] [Full Text] [PDF]
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M. E. Bertrand, M. L. Simoons, K. A.A. Fox, L. C. Wallentin, C. W. Hamm, E. McFadden, P. J. De Feyter, G. Specchia, and W. Ruzyllo Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation Eur. Heart J., December 1, 2002; 23(23): 1809 - 1840. [Full Text] [PDF]
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A. P. Burke, V. Fonseca, F. Kolodgie, A. Zieske, L. Fink, and R. Virmani Increased Serum Homocysteine and Sudden Death Resulting from Coronary Atherosclerosis With Fibrous Plaques Arterioscler. Thromb. Vasc. Biol., November 1, 2002; 22(11): 1936 - 1941. [Abstract] [Full Text] [PDF]
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F. D. Kolodgie, A. P. Burke, A. Farb, D. K. Weber, R. Kutys, T. N. Wight, and R. Virmani Differential Accumulation of Proteoglycans and Hyaluronan in Culprit Lesions: Insights Into Plaque Erosion Arterioscler. Thromb. Vasc. Biol., October 1, 2002; 22(10): 1642 - 1648. [Abstract] [Full Text] [PDF]
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A. Maehara, G. S. Mintz, A. B. Bui, O. R. Walter, M. T. Castagna, D. Canos, A. D. Pichard, L. F. Satler, R. Waksman, W. O. Suddath, et al. Morphologic and angiographic features of coronary plaque rupture detected by intravascular ultrasound J. Am. Coll. Cardiol., September 4, 2002; 40(5): 904 - 910. [Abstract] [Full Text] [PDF]
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P.J. Gallagher More histological information in acute coronary death Eur. Heart J., September 2, 2002; 23(18): 1406 - 1408. [Full Text] [PDF]
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R. Henriques de Gouveia, A.C. van der Wal, C.M. van der Loos, and A.E. Becker Sudden unexpected death in young adults. Discrepancies between initiation of acute plaque complications and the onset of acute coronary death Eur. Heart J., September 2, 2002; 23(18): 1433 - 1440. [Abstract] [Full Text] [PDF]
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G Pasterkamp and R Virmani The erythrocyte: a new player in atheromatous core formation Heart, August 1, 2002; 88(2): 115 - 116. [Full Text] [PDF]
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A. K. Majors, S. Sengupta, B. Willard, M. T. Kinter, R. E. Pyeritz, and D. W. Jacobsen Homocysteine Binds to Human Plasma Fibronectin and Inhibits Its Interaction With Fibrin Arterioscler. Thromb. Vasc. Biol., August 1, 2002; 22(8): 1354 - 1359. [Abstract] [Full Text] [PDF]
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R. P. Choudhury, V. Fuster, J. J. Badimon, E. A. Fisher, and Z. A. Fayad MRI and Characterization of Atherosclerotic Plaque: Emerging Applications and Molecular Imaging Arterioscler. Thromb. Vasc. Biol., July 1, 2002; 22(7): 1065 - 1074. [Abstract] [Full Text] [PDF]
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J. A. Ambrose and E. E. Martinez A New Paradigm for Plaque Stabilization Circulation, April 23, 2002; 105(16): 2000 - 2004. [Abstract] [Full Text] [PDF]
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A. B. Newman, B. L. Naydeck, J. Whittle, K. Sutton-Tyrrell, D. Edmundowicz, and L. H. Kuller Racial Differences in Coronary Artery Calcification in Older Adults Arterioscler. Thromb. Vasc. Biol., March 1, 2002; 22(3): 424 - 430. [Abstract] [Full Text] [PDF]
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M. de Lorgeril, P. Salen, P. Defaye, P. Mabo, and F. Paillard Dietary prevention of sudden cardiac death Eur. Heart J., February 2, 2002; 23(4): 277 - 285. [Full Text] [PDF]
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A. P. Burke, A. Farb, J. Pestaner, G. T. Malcom, A. Zieske, R. Kutys, J. Smialek, and R. Virmani Traditional Risk Factors and the Incidence of Sudden Coronary Death With and Without Coronary Thrombosis in Blacks Circulation, January 29, 2002; 105(4): 419 - 424. [Abstract] [Full Text] [PDF]
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P. N. Seshiah, D. J. Kereiakes, S. S. Vasudevan, N. Lopes, B. Y. Su, N. A. Flavahan, and P. J. Goldschmidt-Clermont Activated Monocytes Induce Smooth Muscle Cell Death: Role of Macrophage Colony-Stimulating Factor and Cell Contact Circulation, January 15, 2002; 105(2): 174 - 180. [Abstract] [Full Text] [PDF]
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A. Schmermund and R. Erbel Unstable Coronary Plaque and Its Relation to Coronary Calcium Circulation, October 2, 2001; 104(14): 1682 - 1687. [Abstract] [Full Text] [PDF]
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B. Lindahl, E. Diderholm, B. Lagerqvist, P. Venge, L. Wallentin, and the FRISC II Investigators Mechanisms behind the prognostic value of troponin T in unstable coronary artery disease: a FRISC II substudy J. Am. Coll. Cardiol., October 1, 2001; 38(4): 979 - 986. [Abstract] [Full Text] [PDF]
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S. M. Schwartz, T. S. Hatsukami, and C. Yuan Molecular Markers, Fibrous Cap Rupture, and the Vulnerable Plaque: New Experimental Opportunities Circ. Res., September 14, 2001; 89(6): 471 - 473. [Full Text] [PDF]
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