van der Wal A C, Becker A E, van der Loos C M, Das P K
Department of Cardiovascular Pathology, University of Amsterdam, The Netherlands.
Circulation. 1994 Jan;89(1):36-44. doi: 10.1161/01.cir.89.1.36.
The study was designed to verify the concept of plaques "at risk" and whether inflammation could play a role in plaque rupture and thrombosis.
In 20 patients who had died of acute myocardial infarction, the thrombosed coronary artery was identified and the site of plaque rupture was traced in serial sections. The cellular characteristics of the fibrous cap at the immediate site of rupture were analyzed and compared with the adjacent cap tissue by use of monoclonal antibodies reactive with macrophages, T lymphocytes, and smooth muscle cells. A deep intimal rupture, extending into the lipid core, was encountered in 12 plaques, whereas 8 had superficial erosions only. Ten atherosclerotic plaques had a distinctly attenuated fibrous cap covering a large atheroma, 7 showed a thick fibrocellular cap overlying a lipid pool, and 3 showed a fibrocellular lesion without a clear lipid core. Macrophages, and to a lesser extent T lymphocytes, were the dominant cells at the immediate site of either rupture or superficial erosion in each instance. These sites, moreover, were always characterized by abundant expression of HLA-DR antigens on both inflammatory cells and adjacent smooth muscle cells, suggesting an active inflammatory reaction. In terms of overall cellular composition of the ruptured plaques, the dominant cell types were macrophages and T cells in 11, smooth muscle cells in 3, and mixtures of both in 6.
The underlying atherosclerotic plaque morphology in complicated coronary artery lesions causing acute myocardial infarction is heterogeneous with respect to both plaque architecture and cellular composition. However, the immediate site of plaque rupture or erosion is always marked by an inflammatory process. This suggests that inflammation plays a role in destabilizing the fibrous cap tissue and, thus, in enhancing the risk of coronary thrombosis.
本研究旨在验证“易损”斑块的概念，以及炎症是否在斑块破裂和血栓形成中起作用。
在20例死于急性心肌梗死的患者中，确定血栓形成的冠状动脉，并在连续切片中追踪斑块破裂的部位。使用与巨噬细胞、T淋巴细胞和平滑肌细胞反应的单克隆抗体，分析并比较破裂部位紧邻处纤维帽的细胞特征与相邻帽组织的细胞特征。12个斑块出现深入内膜的破裂，延伸至脂质核心，而8个斑块仅有表面糜烂。10个动脉粥样硬化斑块有明显变薄的纤维帽覆盖大的粥样瘤，7个斑块显示厚的纤维细胞帽覆盖脂质池，3个斑块显示纤维细胞病变但无明确的脂质核心。在每个破裂或表面糜烂的紧邻部位，巨噬细胞以及程度较轻的T淋巴细胞是主要细胞。此外，这些部位的炎症细胞和相邻平滑肌细胞上总是大量表达HLA-DR抗原，提示存在活跃的炎症反应。就破裂斑块的总体细胞组成而言，11个斑块中主要细胞类型为巨噬细胞和T细胞，3个为平滑肌细胞，6个为两者混合。
导致急性心肌梗死的复杂冠状动脉病变中，潜在的动脉粥样硬化斑块形态在斑块结构和细胞组成方面均具有异质性。然而，斑块破裂或糜烂的紧邻部位总是有炎症过程。这表明炎症在使纤维帽组织不稳定从而增加冠状动脉血栓形成风险方面起作用。
