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斑块破裂的预防:一种新的治疗模式。

Prevention of plaque rupture: a new paradigm of therapy.

作者信息

Forrester James S

机构信息

Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA.

出版信息

Ann Intern Med. 2002 Nov 19;137(10):823-33. doi: 10.7326/0003-4819-137-10-200211190-00012.

DOI:10.7326/0003-4819-137-10-200211190-00012
PMID:12435220
Abstract

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.

摘要

急性冠状动脉综合征——不稳定型心绞痛、心肌梗死和心源性猝死——是由不稳定冠状动脉粥样硬化斑块的急性破裂引起的。不稳定斑块具有三个组织学特征:大的脂质核心、许多炎症细胞和薄的纤维帽。由于不稳定斑块不一定阻塞血管,因此在破裂前可能不会引起症状。导致不稳定斑块特征性组织学特征的细胞过程最近已被确定。对斑块不稳定细胞生物学的这一新认识提示了新的治疗策略:使内皮细胞失活、通过降低血清低密度脂蛋白(LDL)水平或加速逆向胆固醇转运来降低血管壁中的低密度脂蛋白、抑制LDL氧化、抑制炎症细胞因子表达以及抑制血栓形成。尽管在过去30年中,急性冠状动脉疾病导致的发病率和死亡率已降低了50%以上,但预计在未来十年中仍有可能进一步降低类似幅度。

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