Kullo I J, Edwards W D, Schwartz R S
Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA.
Ann Intern Med. 1998 Dec 15;129(12):1050-60. doi: 10.7326/0003-4819-129-12-199812150-00010.
To review the pathobiology and clinical implications of vulnerable coronary atherosclerotic plaques and to discuss the identification of vulnerable plaques and mechanisms of plaque stabilization.
English-language articles in the MEDLINE database that were published from 1966 to the present, identified by using the terms atherosclerotic plaque, myocardial revascularization, and plaque stabilization. Selected references cited in identified articles were reviewed.
Experimental, clinical, and basic research studies related to coronary atherosclerotic plaques.
Rupture at the site of a vulnerable atherosclerotic plaque is the most frequent cause of acute coronary syndromes. Typically, such plaque does not cause high-grade stenosis and has a large lipid core and a thin fibrous cap that is often infiltrated by inflammatory cells. Mechanical stresses contribute to plaque vulnerability, and certain triggers may cause plaque disruption directly. The most important consequence of plaque rupture is thrombosis. No method reliably identifies plaques prone to rupture. The reduction of coronary events by lipid-lowering agents despite only modest luminal changes suggests that these agents have a plaque-stabilizing effect. Surgical or percutaneous revascularization does not address the basic biology of coronary atherosclerosis and therefore may have little effect on plaque vulnerability.
Improved understanding of the biology of atheromatous plaques has led to the concept of plaque vulnerability. Identification and stabilization of vulnerable plaques are important new directions in the treatment of coronary atherosclerosis. The relative benefits of aggressive medical therapy aimed at plaque stabilization should be compared with those of revascularization in the management of chronic coronary artery disease.
综述易损冠状动脉粥样硬化斑块的病理生物学及临床意义,并探讨易损斑块的识别及斑块稳定机制。
通过使用“动脉粥样硬化斑块”“心肌血运重建”和“斑块稳定”等检索词,在MEDLINE数据库中检索1966年至今发表的英文文章。对检索到的文章中引用的参考文献进行了回顾。
与冠状动脉粥样硬化斑块相关的实验、临床及基础研究。
易损动脉粥样硬化斑块部位的破裂是急性冠状动脉综合征最常见的原因。通常,此类斑块不会导致高度狭窄,具有大的脂质核心和薄的纤维帽,且纤维帽常被炎症细胞浸润。机械应力会增加斑块的易损性,某些触发因素可能直接导致斑块破裂。斑块破裂最重要的后果是血栓形成。目前尚无可靠方法可识别易破裂的斑块。降脂药物尽管仅使管腔有适度改变,但能减少冠状动脉事件,这表明这些药物具有斑块稳定作用。外科手术或经皮血运重建未涉及冠状动脉粥样硬化的基本生物学机制,因此对斑块易损性可能影响不大。
对动脉粥样硬化斑块生物学特性的深入了解催生了斑块易损性这一概念。识别并稳定易损斑块是冠状动脉粥样硬化治疗的重要新方向。在慢性冠状动脉疾病的管理中,应将旨在稳定斑块的积极药物治疗的相对益处与血运重建的益处进行比较。