Atherosclerotic plaque rupture - Local or systemic process?

被引:110
作者
Lutgens, E [1 ]
van Suylen, RJ [1 ]
Faber, BC [1 ]
Gijbels, MJ [1 ]
Eurlings, PM [1 ]
Bijnens, AP [1 ]
Cleutjens, KB [1 ]
Heeneman, S [1 ]
Daemen, MJAP [1 ]
机构
[1] Univ Maastricht, Cardiovasc Res Inst Maastricht, Dept Pathol, NL-6229 HX Maastricht, Netherlands
关键词
atherosclerosis; inflammation; pathology;
D O I
10.1161/01.ATV.0000097783.01596.E2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
It is generally established that the unstable plaque is the major cause of acute clinical sequelae of atherosclerosis. Unfortunately, terms indicating lesions prone to plaque instability, such as "vulnerable plaque," and the different phenotypes of unstable plaques, such as plaque rupture, plaque fissuring, intraplaque hemorrhage, and erosion, are often used interchangeably. Moreover, the different phenotypes of the unstable plaque are mostly referred to as plaque rupture. In the first part of this review, we will focus on the definition of true plaque rupture and the definitions of other phenotypes of plaque instability, especially on intraplaque hemorrhage, and discuss the phenotypes of available animal models of plaque instability. The second part of this review will address the pathogenesis of plaque rupture from a local and a systemic perspective. Plaque rupture is thought to occur because of changes in the plaque itself or systemic changes in the patient. Interestingly, contributing factors seem to overlap to a great extent and might even be interrelated. Finally, we will propose an integrative view on the pathogenesis of plaque rupture.
引用
收藏
页码:2123 / 2130
页数:8
相关论文
共 107 条
[11]   Distinct patterns of transforming growth factor-β isoform and receptor expression in human atherosclerotic lesions -: Colocalization implicates TGF-β in fibrofatty lesion development [J].
Bobik, A ;
Agrotis, A ;
Kanellakis, P ;
Dilley, R ;
Krushinsky, A ;
Smirnov, V ;
Tararak, E ;
Condron, M ;
Kostolias, G .
CIRCULATION, 1999, 99 (22) :2883-2891
[12]   Platelet glycoprotein IIb/IIIa inhibitors in acute coronary syndromes:: a meta-analysis of all major randomised clinical trials [J].
Boersma, E ;
Harrington, RA ;
Moliterno, DJ ;
White, H ;
Théroux, P ;
Van de Werf, F ;
de Torbal, A ;
Armstrong, PW ;
Wallentin, LC ;
Wilcox, RG ;
Simes, J ;
Califf, RM ;
Topol, EJ ;
Simoons, ML .
LANCET, 2002, 359 (9302) :189-198
[13]   A leukocyte homologue of the IL-8 receptor CXCR-2 mediates the accumulation of macrophages in atherosclerotic lesions of LDL receptor-deficient mice [J].
Boisvert, WA ;
Santiago, R ;
Curtiss, LK ;
Terkeltaub, RA .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (02) :353-363
[14]   Loss of SR-BI expression leads to the early onset of occlusive atherosclerotic coronary artery disease, spontaneous myocardial infarctions, severe cardiac dysfunction, and premature death in apolipoprotein E-deficient mice [J].
Braun, A ;
Trigatti, BL ;
Post, MJ ;
Sato, K ;
Simons, M ;
Edelberg, JM ;
Rosenberg, RD ;
Schrenzel, M ;
Krieger, M .
CIRCULATION RESEARCH, 2002, 90 (03) :270-276
[15]   ACC/AHA guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction-2002: Summary article - A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina) [J].
Braunwald, E ;
Antman, EM ;
Beasley, JW ;
Califf, RM ;
Cheitlin, MD ;
Hochman, JS ;
Jones, RH ;
Kereiakes, D ;
Kupersmith, J ;
Levin, TN ;
Pepine, CJ ;
Schaeffer, JW ;
Smith, EE ;
Steward, DE ;
Theroux, P ;
Gibbons, RJ ;
Alpert, JS ;
Faxon, DP ;
Fuster, V ;
Gregoratos, G ;
Hiratzka, LF ;
Jacobs, AK ;
Smith, SC .
CIRCULATION, 2002, 106 (14) :1893-1900
[16]   Influence of interferon-γ on the extent and phenotype of diet-induced atherosclerosis in the LDLR-deficient mouse [J].
Buono, C ;
Come, CE ;
Stavrakis, G ;
Maguire, GF ;
Connelly, PW ;
Lichtman, AH .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2003, 23 (03) :454-460
[17]   Platelet P-selectin facilitates atherosclerotic lesion development [J].
Burger, PC ;
Wagner, DD .
BLOOD, 2003, 101 (07) :2661-2666
[18]   Spontaneous plaque rupture and secondary thrombosis in apolipoprotein E-deficient and LDL receptor-deficient mice [J].
Calara, F ;
Silvestre, M ;
Casanada, F ;
Yuan, N ;
Napoli, C ;
Palinski, W .
JOURNAL OF PATHOLOGY, 2001, 195 (02) :257-263
[19]   Myocardial infarction mediated by endothelin receptor signaling in hypercholesterolemic mice [J].
Caligiuri, G ;
Levy, B ;
Pernow, J ;
Thorén, P ;
Hansson, GK .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (12) :6920-6924
[20]   Mouse models of angiogenesis, arterial stenosis, atherosclerosis and hemostasis [J].
Carmeliet, P ;
Moons, L ;
Collen, D .
CARDIOVASCULAR RESEARCH, 1998, 39 (01) :8-33