Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology.

作者：Allard C. van der Wal, Anton E. Becker, Chris M. van der Loos, P. K. Das · 发表于：Circulation · 年份：1994 · DOI：10.1161/01.cir.89.1.36 · 被引用次数：1915 · 研究领域：Atherosclerosis and Cardiovascular Diseases、Coronary Interventions and Diagnostics、Acute Myocardial Infarction Research

BACKGROUND: The study was designed to verify the concept of plaques "at risk" and whether inflammation could play a role in plaque rupture and thrombosis. METHODS AND RESULTS: 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. CONCLUSIONS: The underlying atherosclerotic ...