Foo R S, De Bono D P
Division of Cardiology, Department of Medicine and Therapeutics, Leicester University, Glenfield Hospital, Clinical Sciences Wing, Leicester LE3 9QP, UK.
Singapore Med J. 2000 Dec;41(12):606-10.
Landmark pathological studies have deepened our understanding of the mechanisms behind acute coronary syndromes over the last decade. Thrombosis plays a key role and is a unifying feature in the pathogenesis. Platelet-rich thrombus superimposed over the disrupted atherosclerotic plaque or eroded plaque endothelium, with or without fibrin-thrombus extension, is evident in postmortem necropsy, angiographic and angioscopic studies. However features which contribute to the risk of acute events lie in the atherosclerotic plaque itself. Plaque content and not plaque size is the important factor. A vulnerable plaque may be invisible on clinical stress testing and even coronary angiography; but it is prone to rupture if it has only a thin cap and a proportionally larger lipid core. There is a cellular preponderance of activated macrophages and T-lymphocytes; and high activity of matrix metalloproteinases in vulnerable plaques. Smooth muscle cell proliferation and collagen synthesis are downregulated. These features may serve as possible targets for detecting plaques at risk or for reversing the risk of vulnerable plaques.
在过去十年中，具有里程碑意义的病理学研究加深了我们对急性冠状动脉综合征背后机制的理解。血栓形成起着关键作用，是发病机制中的一个统一特征。富含血小板的血栓叠加在破裂的动脉粥样硬化斑块或糜烂的斑块内皮上，无论有无纤维蛋白血栓延伸，在尸检、血管造影和血管内镜研究中都很明显。然而，导致急性事件风险的特征在于动脉粥样硬化斑块本身。斑块内容而非斑块大小才是重要因素。易损斑块在临床应激试验甚至冠状动脉造影中可能不可见；但如果它只有一个薄帽和相对较大的脂质核心，就容易破裂。易损斑块中存在活化巨噬细胞和T淋巴细胞的细胞优势；以及基质金属蛋白酶的高活性。平滑肌细胞增殖和胶原蛋白合成下调。这些特征可能成为检测有风险斑块或逆转易损斑块风险的潜在靶点。
