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Circulation. 1993;87:1781-1791

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Circulation, Vol 87, 1781-1791, Copyright © 1993 by American Heart Association


ARTICLES

Lipid lowering and plaque regression. New insights into prevention of plaque disruption and clinical events in coronary disease

BG Brown, XQ Zhao, DE Sacco and JJ Albers
Department of Medicine, University of Washington School of Medicine, Seattle.

The consensus of evidence from angiographic trials demonstrates both coronary artery and clinical benefits from lowering of lipids by a variety of regimens. The findings of reduced arterial disease progression and increased regression have been convincing but, at best, modest in their magnitude. For example, among those treated intensively in FATS, the mean improvement in proximal stenosis severity per patient was < 1% stenosis, and only 12% of all lesions showed convincing regression. In view of these modest arterial benefits, the associated reductions in cardiovascular events have been surprisingly great. For example, coronary events were reduced 75% in FATS; this was entirely a result of a 93% reduction in the likelihood that a mildly or moderately diseased arterial segment would experience substantial progression to a severe lesion at the time of a clinical event. We believe that the magnitude of the clinical benefit is best explained in terms of this observation, according to the following lines of reasoning. Clinical events most commonly spring from lesions that are initially of mild or moderate severity and then abruptly undergo a disruptive transformation to a severe culprit lesion. The process of plaque fissuring, leading to plaque disruption and thrombosis, triggers most clinical coronary events. Fissuring is predicted by a large accumulation of core lipid in the plaque and by a high density of lipid-laden macrophages in its thinned fibrous cap. Lesions with these characteristics constitute only 10-20% of the overall lesion population but account for 80-90% of the acute clinical events. In the experimental setting, normalization of an atherogenic lipid profile substantially decreases the number of lipid- laden intimal macrophages (foam cells) and depletes cholesterol from the core lipid pool. In the clinical setting, intensive lipid lowering virtually halts the progression of mild and moderate lesions to clinical events. Thus, the reduction in clinical events observed in these trials appears to be best explained by the relation of the lipid and foam cell content of the plaque to its likelihood of fissuring and by the effects of lipid-lowering therapy on these "high-risk" features of plaque morphology. The composite of data presented here supports the hypothesis that lipid-lowering therapy selectively depletes (regresses) that relatively small but dangerous subgroup of fatty lesions containing a large lipid core and dense clusters of intimal macrophages. By doing so, these lesions are effectively stabilized and clinical event rate is accordingly decreased.


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CirculationHome page
G. G. Zimmermann-Paul, H. H. Quick, P. Vogt, G. K. von Schulthess, D. Kling, and J. F. Debatin
High-Resolution Intravascular Magnetic Resonance Imaging : Monitoring of Plaque Formation in Heritable Hyperlipidemic Rabbits
Circulation, March 2, 1999; 99(8): 1054 - 1061.
[Abstract] [Full Text] [PDF]


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Cardiovasc ResHome page
R. Rabbani and E. J. Topol
Strategies to achieve coronary arterial plaque stabilization
Cardiovasc Res, February 1, 1999; 41(2): 402 - 417.
[Abstract] [Full Text] [PDF]


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HeartHome page
R A Archbold and A D Timmis
Cholesterol lowering and coronary artery disease: mechanisms of risk reduction
Heart, December 1, 1998; 80(6): 543 - 547.
[Full Text]


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J Am Coll CardiolHome page
G. Ruotolo, C.-G.o. Ericsson, C. Tettamanti, F. Karpe, L. Grip, B. Svane, J. Nilsson, U. de Faire, and A. Hamsten
Treatment effects on serum lipoprotein lipids, apolipoproteins and low density lipoprotein particle size and relationships of lipoprotein variables to progression of coronary artery disease in the Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT)
J. Am. Coll. Cardiol., November 15, 1998; 32(6): 1648 - 1656.
[Abstract] [Full Text] [PDF]


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CirculationHome page
R. J. Bache
Vasodilator Reserve : A Functional Assessment of Coronary Health
Circulation, September 29, 1998; 98(13): 1257 - 1260.
[Full Text] [PDF]


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CirculationHome page
G. S. Huggins, R. C. Pasternak, N. M. Alpert, A. J. Fischman, and H. Gewirtz
Effects of Short-Term Treatment of Hyperlipidemia on Coronary Vasodilator Function and Myocardial Perfusion in Regions Having Substantial Impairment of Baseline Dilator Reverse
Circulation, September 29, 1998; 98(13): 1291 - 1296.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
T. Neunteufl, K. Kostner, R. Katzenschlager, M. Zehetgruber, G. Maurer, and F. Weidinger
Additional benefit of vitamin E supplementation to simvastatin therapy on vasoreactivity of the brachial artery of hypercholesterolemic men
J. Am. Coll. Cardiol., September 1, 1998; 32(3): 711 - 716.
[Abstract] [Full Text] [PDF]


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Vasc MedHome page
P. K Shah
Role of inflammation and metalloproteinases in plaque disruption and thrombosis
Vascular Medicine, August 1, 1998; 3(3): 199 - 206.
[Abstract] [PDF]


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Vasc MedHome page
V. Fuster, J. J. Badimon, and J. H Chesebro
Atherothrombosis: mechanisms and clinical therapeutic approaches
Vascular Medicine, August 1, 1998; 3(3): 231 - 239.
[Abstract] [PDF]


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Clin. Chem.Home page
J. K. Liao
Endothelium and acute coronary syndromes
Clin. Chem., August 1, 1998; 44(8): 1799 - 1808.
[Abstract] [Full Text] [PDF]


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Clin. Chem.Home page
W. Stanford and B. H. Thompson
Coronary atherosclerosis and its effect on cardiac structure and function: evaluation by electron beam computed tomography
Clin. Chem., August 1, 1998; 44(8): 1871 - 1881.
[Abstract] [Full Text] [PDF]


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CirculationHome page
M. Aikawa, E. Rabkin, Y. Okada, S. J. Voglic, S. K. Clinton, C. E. Brinckerhoff, G. K. Sukhova, and P. Libby
Lipid Lowering by Diet Reduces Matrix Metalloproteinase Activity and Increases Collagen Content of Rabbit Atheroma : A Potential Mechanism of Lesion Stabilization
Circulation, June 23, 1998; 97(24): 2433 - 2444.
[Abstract] [Full Text] [PDF]


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BMJHome page
E. Delacrétaz, P. G Michalopoulos, J. Ruiz, H. Saner, and B. Meier
Management of hyperlipidaemia after coronary revascularisation: follow up study
BMJ, May 16, 1998; 316(7143): 1499 - 1500.
[Full Text]


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CirculationHome page
U. Laufs, V. La Fata, J. Plutzky, and J. K. Liao
Upregulation of Endothelial Nitric Oxide Synthase by HMG CoA Reductase Inhibitors
Circulation, March 31, 1998; 97(12): 1129 - 1135.
[Abstract] [Full Text] [PDF]


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CirculationHome page
G. Davi, M. Romano, A. Mezzetti, A. Procopio, S. Iacobelli, T. Antidormi, T. Bucciarelli, P. Alessandrini, F. Cuccurullo, and G. B. Bon
Increased Levels of Soluble P-Selectin in Hypercholesterolemic Patients
Circulation, March 17, 1998; 97(10): 953 - 957.
[Abstract] [Full Text] [PDF]


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CirculationHome page
A. M. Gotto Jr
Cholesterol Management in Theory and Practice
Circulation, December 16, 1997; 96(12): 4424 - 4430.
[Abstract] [Full Text]


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Arterioscler. Thromb. Vasc. Bio.Home page
C. Patrono and G. A. FitzGerald
Isoprostanes: Potential Markers of Oxidant Stress in Atherothrombotic Disease
Arterioscler Thromb Vasc Biol, November 1, 1997; 17(11): 2309 - 2315.
[Abstract] [Full Text]


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Arterioscler. Thromb. Vasc. Bio.Home page
G. Davi, P. Alessandrini, A. Mezzetti, G. Minotti, T. Bucciarelli, F. Costantini, F. Cipollone, G. B. Bon, G. Ciabattoni, and C. Patrono
In Vivo Formation of 8-Epi-Prostaglandin F2{alpha} Is Increased in Hypercholesterolemia
Arterioscler Thromb Vasc Biol, November 1, 1997; 17(11): 3230 - 3235.
[Abstract] [Full Text]


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CirculationHome page
J. Niebauer, R. Hambrecht, T. Velich, K. Hauer, C. Marburger, B. Kalberer, C. Weiss, E. von Hodenberg, G. Schlierf, G. Schuler, et al.
Attenuated Progression of Coronary Artery Disease After 6 Years of Multifactorial Risk Intervention : Role of Physical Exercise
Circulation, October 21, 1997; 96(8): 2534 - 2541.
[Abstract] [Full Text]


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Arterioscler. Thromb. Vasc. Bio.Home page
W. V. Rodrigueza, K. D. Mazany, A. D. Essenburg, M. E. Pape, T. J. Rea, C. L. Bisgaier, and K. J. Williams
Large Versus Small Unilamellar Vesicles Mediate Reverse Cholesterol Transport In Vivo Into Two Distinct Hepatic Metabolic Pools : Implications for the Treatment of Atherosclerosis
Arterioscler Thromb Vasc Biol, October 1, 1997; 17(10): 2132 - 2139.
[Abstract] [Full Text]


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CirculationHome page
M. D. Guazzi, M. Bussotti, L. Grancini, N. De Cesare, M. Guazzi, I. L. Pera, and A. Loaldi
Evidence of Multifocal Activity of Coronary Disease in Patients With Acute Myocardial Infarction
Circulation, August 19, 1997; 96(4): 1145 - 1151.
[Abstract] [Full Text]


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Arterioscler. Thromb. Vasc. Bio.Home page
C. Yuan, C. Petty, K. D. O'Brien, T. S. Hatsukami, J. F. Eary, and B. G. Brown
In Vitro and In Situ Magnetic Resonance Imaging Signal Features of Atherosclerotic Plaque-Associated Lipids
Arterioscler Thromb Vasc Biol, August 1, 1997; 17(8): 1496 - 1503.
[Abstract] [Full Text]


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CirculationHome page
W. R. M. Aengevaeren, G. J. H. Uijen, J. W. Jukema, A. V. G. Bruschke, and T. van der Werf
Functional Evaluation of Lipid-Lowering Therapy by Pravastatin in the Regression Growth Evaluation Statin Study (REGRESS)
Circulation, July 15, 1997; 96(2): 429 - 435.
[Abstract] [Full Text]


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Arch Intern MedHome page
J. R. Crouse III, R. P. Byington, H. M. Hoen, and C. D. Furberg
Reductase Inhibitor Monotherapy and Stroke Prevention
Arch Intern Med, June 23, 1997; 157(12): 1305 - 1310.
[Abstract] [PDF]


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Arch Intern MedHome page
S. M. Grundy
Cholesterol and Coronary Heart Disease: The 21st Century
Arch Intern Med, June 9, 1997; 157(11): 1177 - 1184.
[Abstract] [PDF]


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NEJMHome page
A. P. Burke, A. Farb, G. T. Malcom, Y.-h. Liang, J. Smialek, and R. Virmani
Coronary Risk Factors and Plaque Morphology in Men with Coronary Disease Who Died Suddenly
N. Engl. J. Med., May 1, 1997; 336(18): 1276 - 1282.
[Abstract] [Full Text] [PDF]


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Arterioscler. Thromb. Vasc. Bio.Home page
P. Alaupovic, W. J. Mack, C. Knight-Gibson, and H. N. Hodis
The Role of Triglyceride-Rich Lipoprotein Families in the Progression of Atherosclerotic Lesions as Determined by Sequential Coronary Angiography From a Controlled Clinical Trial
Arterioscler Thromb Vasc Biol, April 1, 1997; 17(4): 715 - 722.
[Abstract] [Full Text]


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CirculationHome page
S. M. Grundy, G. J. Balady, M. H. Criqui, G. Fletcher, P. Greenland, L. F. Hiratzka, N. Houston-Miller, P. Kris-Etherton, H. M. Krumholz, J. LaRosa, et al.
When to Start Cholesterol-Lowering Therapy in Patients With Coronary Heart Disease : A Statement for Healthcare Professionals From the American Heart Association Task Force on Risk Reduction
Circulation, March 18, 1997; 95(6): 1683 - 1685.
[Full Text]


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Arch Intern MedHome page
L. K. Andersen, H. K. Jensen, S. Juul, and O. Faergeman
Patients' Attitudes Toward Detection of Heterozygous Familial Hypercholesterolemia
Arch Intern Med, March 10, 1997; 157(5): 553 - 560.
[Abstract] [PDF]


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CirculationHome page
G. O'Driscoll, D. Green, and R. R. Taylor
Simvastatin, an HMG–Coenzyme A Reductase Inhibitor, Improves Endothelial Function Within 1 Month
Circulation, March 4, 1997; 95(5): 1126 - 1131.
[Abstract] [Full Text]