Prevention of plaque rupture: A new paradigm of therapy

被引:38
作者
Forrester, JS [1 ]
机构
[1] Cedars Sinai Med Ctr, Div Cardiol, Los Angeles, CA 90048 USA
关键词
D O I
10.7326/0003-4819-137-10-200211190-00012
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Acute coronary syndromes-unstable angina, myocardial infarction, and sudden cardiac death-are caused by acute disruption of an unstable coronary atheroma. Unstable plaques have three histologic characteristics: a large lipid core, many inflammatory cells, and a thin fibrous cap. Because the unstable plaque is not necessarily obstructive, it may cause no symptoms before rupture. The cellular processes that lead to the characteristic histologic features of unstable plaque have recently been identified. This new understanding of the cell biology of plaque instability suggests new therapeutic strategies: passivation of the endothelium, reduction of low-density lipoprotein (LDL) in the vessel wall by decreasing serum LDL levels or accelerating reverse cholesterol transport, inhibition of LDL oxidation, inhibition of inflammatory cytokine expression, and inhibition of thrombus formation. Although the morbidity and mortality resulting from acute coronary disease have been reduced by more than :50% over the past 30 years, it is reasonable to anticipate further reductions of similar magnitude in the decade ahead.
引用
收藏
页码:823 / 833
页数:11
相关论文
共 103 条
[51]  
Lijnen HR, 1999, CIRC RES, V85, P1186
[52]   Improvement of coronary vasodilatation capacity through single LDL apheresis [J].
Mellwig, KP ;
Baller, D ;
Gleichmann, U ;
Moll, D ;
Betker, S ;
Weise, R ;
Notohamiprodjo, G .
ATHEROSCLEROSIS, 1998, 139 (01) :173-178
[53]   INTRAVENOUS-INJECTION OF RABBIT APOLIPOPROTEIN-A-I INHIBITS THE PROGRESSION OF ATHEROSCLEROSIS IN CHOLESTEROL-FED RABBITS [J].
MIYAZAKI, A ;
SAKUMA, S ;
MORIKAWA, W ;
TAKIUE, T ;
MIAKE, F ;
TERANO, T ;
SAKAI, M ;
HAKAMATA, H ;
SAKAMOTO, YI ;
NAITO, M ;
RUAN, YM ;
TAKAHASHI, K ;
OHTA, T ;
HORIUCHI, S .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1995, 15 (11) :1882-1888
[54]   Anti-atherosclerotic effects of an angiotensin converting enzyme inhibitor and an angiotensin II antagonist in Cynomolgus monkeys fed a high-cholesterol diet [J].
Miyazaki, M ;
Sakonjo, H ;
Takai, S .
BRITISH JOURNAL OF PHARMACOLOGY, 1999, 128 (03) :523-529
[55]  
Muhlestein JB, 2000, CIRCULATION, V102, P1755
[56]   Irbesartan, an angiotensin type 1 receptor inhibitor, regulates markers of inflammation in patients with premature atherosclerosis [J].
Navalkar, S ;
Parthasarathy, S ;
Santanam, N ;
Khan, BV .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2001, 37 (02) :440-444
[57]   The ACAT inhibitor, CI-1011 is effective in the prevention and regression of aortic fatty streak area in hamsters [J].
Nicolosi, RJ ;
Wilson, TA ;
Krause, BR .
ATHEROSCLEROSIS, 1998, 137 (01) :77-85
[58]   A tale of two diseases - Atherosclerosis and rheumatoid arthritis [J].
Pasceri, V ;
Yeh, ETH .
CIRCULATION, 1999, 100 (21) :2124-2126
[59]   HUMAN APOLIPOPROTEIN-A-I GENE-EXPRESSION INCREASES HIGH-DENSITY-LIPOPROTEIN AND SUPPRESSES ATHEROSCLEROSIS IN THE APOLIPOPROTEIN E-DEFICIENT MOUSE [J].
PLUMP, AS ;
SCOTT, CJ ;
BRESLOW, JL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (20) :9607-9611
[60]   Reactive oxygen species produced by macrophage-derived foam cells regulate the activity of vascular matrix metalloproteinases in vitro - Implications for atherosclerotic plaque stability [J].
Rajagopalan, S ;
Meng, XP ;
Ramasamy, S ;
Harrison, DG ;
Galis, ZS .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 98 (11) :2572-2579