(Circulation. 2001;103:934.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Healed Plaque Ruptures and Sudden Coronary Death
Evidence That Subclinical Rupture Has a Role in Plaque Progression
From the Department of Cardiovascular Pathology (A.P.B., F.D.K., A.F., D.K.W., R.V.), Armed Forces Institute of Pathology, Washington, DC; Louisiana State University (G.T.M.), New Orleans; and the University of Maryland (J.S.), Baltimore.
Background—Subclinical episodes of plaque disruption followed by healing are considered a mechanism of increased plaque burden. Detailed pathological studies of healed ruptures, however, are lacking.
Methods and Results—We identified acute and healed ruptures from 142 men who died of sudden coronary death and performed morphometric measurements of plaque burden, luminal stenosis, and smooth muscle cell phenotype. Healed ruptures were found in 61% of hearts and were associated with healed myocardial infarction, increased heart weight, dyslipidemia, and diabetes. Multiple healed rupture sites with layering were frequently found in segments with acute and healed rupture; the percent area luminal narrowing increased with increased numbers of healed sites of previous rupture. The underlying percent luminal narrowing for acute ruptures (mean 79±15%) exceeded that for healed ruptures (mean 66±14%, P=0.0001), and the area within the internal elastic lamina was significantly less in healed ruptures than in acute ruptures, when segments were grouped by distance from the ostium. Healed ruptures favored the accumulation of immature smooth muscle cells at repair sites, with a cellular proliferation index of 0.40±0.09%, significantly higher than the index at the sites of rupture (P=0.008).
Conclusions—These data provide evidence that silent plaque rupture is a form of wound healing that results in increased percent stenosis. Healed ruptures occur in arteries with less cross-sectional area luminal narrowing than acute ruptures and are a frequent finding in men who die suddenly with severe coronary atherosclerosis.
Key Words: plaque • death, sudden
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P. Schoenhagen, G. W. Stone, S. E. Nissen, C. L. Grines, J. Griffin, B. S. Clemson, D. G. Vince, K. Ziada, T. Crowe, C. Apperson-Hanson, et al. Coronary Plaque Morphology and Frequency of Ulceration Distant From Culprit Lesions in Patients With Unstable and Stable Presentation Arterioscler Thromb Vasc Biol, October 1, 2003; 23(10): 1895 - 1900. [Abstract] [Full Text] [PDF]
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P. Cullen, R. Baetta, S. Bellosta, F. Bernini, G. Chinetti, A. Cignarella, A. von Eckardstein, A. Exley, M. Goddard, M. Hofker, et al. Rupture of the Atherosclerotic Plaque: Does a Good Animal Model Exist? Arterioscler Thromb Vasc Biol, April 1, 2003; 23(4): 535 - 542. [Abstract] [Full Text] [PDF]
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M. Oberhoff and K. R Karsch Who wants his plaque sealed? Eur. Heart J., March 2, 2003; 24(6): 494 - 495. [Full Text] [PDF]
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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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S. Konstantinides, K. Schafer, and D. J. Loskutoff Do PAI-1 and Vitronectin Promote or Inhibit Neointima Formation?: The Exact Role of the Fibrinolytic System in Vascular Remodeling Remains Uncertain Arterioscler Thromb Vasc Biol, December 1, 2002; 22(12): 1943 - 1945. [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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P. Schoenhagen, E. M. Tuzcu, and S. G. Ellis Plaque Vulnerability, Plaque Rupture, and Acute Coronary Syndromes: (Multi)-Focal Manifestation of a Systemic Disease Process Circulation, August 13, 2002; 106(7): 760 - 762. [Full Text] [PDF]
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G. Rioufol, G. Finet, I. Ginon, X. Andre-Fouet, R. Rossi, E. Vialle, E. Desjoyaux, G. Convert, J.F. Huret, and A. Tabib Multiple Atherosclerotic Plaque Rupture in Acute Coronary Syndrome: A Three-Vessel Intravascular Ultrasound Study Circulation, August 13, 2002; 106(7): 804 - 808. [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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M. R. Bennett Breaking the Plaque: Evidence for Plaque Rupture in Animal Models of Atherosclerosis Arterioscler Thromb Vasc Biol, May 1, 2002; 22(5): 713 - 714. [Full Text] [PDF]
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H. Williams, J. L. Johnson, K. G. S. Carson, and C. L. Jackson Characteristics of Intact and Ruptured Atherosclerotic Plaques in Brachiocephalic Arteries of Apolipoprotein E Knockout Mice Arterioscler Thromb Vasc Biol, May 1, 2002; 22(5): 788 - 792. [Abstract] [Full Text] [PDF]
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A. P. Burke, F. D. Kolodgie, A. Farb, D. Weber, and R. Virmani Morphological Predictors of Arterial Remodeling in Coronary Atherosclerosis Circulation, January 22, 2002; 105(3): 297 - 303. [Abstract] [Full Text] [PDF]
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