Pathologic assessment of the vulnerable human coronary plaque
Pathologic assessment of the vulnerable human coronary plaque
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DOI：
10.1136/hrt.2004.041798
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发表时间：
2004-12-01
期刊：
影响因子：
5.7
通讯作者：
Gold, HK
中科院分区：
文献类型：
--
作者：
Kolodgie, FD;Virmani, R;Gold, HK
尽管对动脉粥样硬化的发生和发展以及危险因素的影响的理解取得了重大进展，但冠心病仍然是西方世界的主要杀手。1.如果要在21世纪继续该领域的进展，就必须关注易受血栓形成损害的高危患者以及导致斑块在精确位置和时间破裂的触发机制。虽然动物研究有助于确定动脉粥样硬化的分子机制，但仍然不存在令人信服的斑块破裂模型。因此，未来针对斑块不稳定性的治疗方法的发展取决于我们是否有能力自信地识别可能形成血栓的前驱病变;这将主要通过改进的成像方式来实现。深入了解冠状动脉血栓形成的机制，从潜在的斑块形态在猝死受害者尸检标本的详细分析。在这些病例中，50-75%的罪犯病变（致命斑块）显示冠状动脉血栓，而其余无血栓的患者则显示稳定的冠状动脉斑块。75%横截面积管腔狭窄。4.急性冠状动脉血栓形成的主要原因是斑块破裂，其前驱病变被称为易损斑块（图1），或我们实验室定义的薄帽纤维粥样硬化（TCFA）。在这篇综述中，我们将批判性地分析斑块破裂的病理学，重点是其与TCFA的关系和愈合的斑块破裂，以更好地了解最负责冠状动脉发病率和死亡率的病变。
Despite significant strides towards an understanding of the initiation and progression of atherosclerosis and the influence of risk factors, coronary heart disease remains the principal killer in the western world. 1 If progress in the field is to continue in the 21st century, one must focus on high risk patients with lesions that are vulnerable to thrombosis together with the triggering mechanisms that cause plaques to rupture at a precise location and time. Although animal studies have helped define the molecular mechanisms of atherosclerosis, a convincing model of plaque rupture still does not exist. Therefore, the development of future treatments targeted against plaque instability is contingent upon our ability to confidently recognise precursor lesions likely to thrombose; this will be primarily achieved via improved imaging modalities. Insights into the mechanisms of coronary thrombosis extend from detailed analyses of underlying plaque morphologies in necropsy specimens from sudden death victims. 2 3 In 50–75% of these cases, the culprit lesion (fatal plaque) shows a coronary thrombus whereas the remainder without thrombi exhibit stable coronary plaques with. 75% cross sectional area luminal narrowing. 4 The major cause of acute coronary thrombosis is plaque rupture, and the precursor lesion has been termed vulnerable plaque (fig 1) or, as defined by our laboratory, the thin cap fibroatheroma (TCFA). In this review, we will critically analyse the pathology of plaque rupture with emphasis on its relation to TCFAs and healed plaque ruptures to gain a better understanding of the lesion most responsible for coronary morbidity and mortality.