Circulation. 1998;97:2382-2383
(Circulation. 1998;97:2382-2383.)
© 1998 American Heart Association, Inc.
Reactive Oxygen Species, Metalloproteinases, and Plaque Stability
M.J. Davies, MD, FRCP, FRCPath, FACC
From St George's Hospital Medical School, Histopathology
Department, London, UK.
Correspondence to M.J. Davies, MD, FRCP, FRCPath, FACC, St George's Hospital Medical School, BHF Cardiovascular Pathology Unit, Histopathology Department, Cranmer Terrace, London SW17 ORE, UK.
Key Words: Editorials metalloproteinases free radicals
Understanding
of the factors that lead to atherosclerotic plaque instability causing
thrombosis is increasing rapidly. The morphological characteristics of
plaques that are unstable, ie, complicated by recent thrombosis, lend
insight into the structural and cellular features of presently
stable plaques that are vulnerable, ie, at high risk of becoming
unstable in the future. The risk of any individual with
coronary atherosclerosis developing an acute
ischemic event depends on the number of such vulnerable plaques
present in that individual rather than the number of plaques
overall. One factor in the variation in risk for a further acute event
after, for example, an acute myocardial infarction is the variation
from individual to individual in the number of vulnerable plaques.
The features found in unstable plaques compared with stable
plaques have been shown by study of both necropsy and atherectomy
material to be a large core of extracellular lipid, a high density of
macrophages containing lipid, a reduced smooth muscle content,
and a thin cap.1 2 The majority of episodes of
major thrombi, particularly in white men with high plasma lipids, are
due to plaque rupture.3 4 In plaque rupture, the
fibrous cap of a plaque tears, exposing the highly thrombogenic lipid
core to blood in the lumen of the artery. The mechanical strength of
the plaque cap is therefore a vital component of plaque stability and
depends on the amount and organization of collagen and other connective
tissue proteins. Smooth muscle cells exist in lacunae in the plaque
cap, where they produce and maintain . . . [Full Text of this Article]
This article has been cited by other articles:

|
 |

|
 |
 
M. Rajappa, S.K. Sen, and A. Sharma
Role of Pro-/Anti-Inflammatory Cytokines and Their Correlation With Established Risk Factors in South Indians With Coronary Artery Disease
Angiology,
August 1, 2009;
60(4):
419 - 426.
[Abstract]
[PDF]
|
 |
|

|
 |

|
 |
 
D. Bose, K. Leineweber, T. Konorza, A. Zahn, M. Brocker-Preuss, K. Mann, M. Haude, R. Erbel, and G. Heusch
Release of TNF-{alpha} during stent implantation into saphenous vein aortocoronary bypass grafts and its relation to plaque extrusion and restenosis
Am J Physiol Heart Circ Physiol,
May 1, 2007;
292(5):
H2295 - H2299.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
C. M. Dollery and P. Libby
Atherosclerosis and proteinase activation
Cardiovasc Res,
February 15, 2006;
69(3):
625 - 635.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
E. Lubos, R. Schnabel, H. J. Rupprecht, C. Bickel, C. M. Messow, S. Prigge, F. Cambien, L. Tiret, T. Munzel, and S. Blankenberg
Prognostic value of tissue inhibitor of metalloproteinase-1 for cardiovascular death among patients with cardiovascular disease: results from the AtheroGene study
Eur. Heart J.,
January 2, 2006;
27(2):
150 - 156.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
D Tousoulis, G Davies, C Stefanadis, P Toutouzas, and J A Ambrose
Inflammatory and thrombotic mechanisms in coronary atherosclerosis
Heart,
September 1, 2003;
89(9):
993 - 997.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M O'Sullivan and M R Bennett
Gene therapy for coronary restenosis: is the enthusiasm justified?
Heart,
November 1, 2001;
86(5):
491 - 493.
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J S Sidhu and J C Kaski
Peroxisome proliferator activated receptor {gamma}: a potential therapeutic target in the management of ischaemic heart disease
Heart,
September 1, 2001;
86(3):
255 - 258.
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J.C. Kaski and E.G. Zouridakis
Inflammation, infection and acute coronary plaque events
Eur. Heart J. Suppl.,
August 1, 2001;
3(suppl_I):
I10 - I15.
[Abstract]
[PDF]
|
 |
|

|
 |

|
 |
 
P.a. Aukrust, R. K. Berge, T. Ueland, E. Aaser, J. K. Damas, L. Wikeby, A. Brunsvig, F. Muller, K. Forfang, S. S. Froland, et al.
Interaction between chemokines and oxidative stress: possible pathogenic role in acute coronary syndromes
J. Am. Coll. Cardiol.,
February 1, 2001;
37(2):
485 - 491.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
P. Aukrust, F. Muller, T. Ueland, T. Berget, E. Aaser, A. Brunsvig, N. O. Solum, K. Forfang, S. S. Froland, and L. Gullestad
Enhanced Levels of Soluble and Membrane-Bound CD40 Ligand in Patients With Unstable Angina : Possible Reflection of T Lymphocyte and Platelet Involvement in the Pathogenesis of Acute Coronary Syndromes
Circulation,
August 10, 1999;
100(6):
614 - 620.
[Abstract]
[Full Text]
[PDF]
|
 |
|