FIBROUS AND LIPID-RICH ATHEROSCLEROTIC PLAQUES ARE PART OF INTERCHANGEABLE MORPHOLOGIES RELATED TO INFLAMMATION - A CONCEPT

Background: The morphology of advanced atherosclerotic plaques varies from solid fibrous lesions, considered essentially stable, to lipid-ri ch lesions with large atheromas prone to rupture. The latter situation is often associated with large amounts of foam cells. An in-situ infl ammatory process influenced by activated T cells and macrophages can b e demonstrated in atherosclerotic plaques; however, the relationship b etween the inflammation and clinically relevant morphological types ha s not yet been investigated. A study of plaque morphology, focusing on the relationship between inflammatory cells, smooth muscle cells, and the collagen matrix, on the one hand, and the 'classic' plaque morpho logies (fibrous versus lipid-rich), on the other, may shed light on th is concept. Materials and methods: Immunocytochemical techniques were used in combination with connective tissue stains to study the topogra phic distribution of smooth muscle cells, collagen, and inflammatory c ells in different morphologic types of advanced atherosclerotic plaque s in aortic and carotid arteries obtained at autopsy. Results: Lesions with an inconspicuous lipid core were defined as fibrous (n = 7). The y contained a dense collagen matrix and the dominant cell type was the smooth muscle cell; lymphocytes and macrophages were sparse. Lesions with a large lipid core were defined as lipid-rich (n = 13). They cont ained a thin fibrous cap with a loosely arranged matrix dominated by m acrophages and T cells. Most lesions (n = 21), however, had a morpholo gy that ranged between fibrous and lipid-rich. The cellular components consisted either of mixed smooth muscle and inflammatory cells or of local distinct zones of inflammatory cells within a fibrous cap otherw ise dominated by smooth muscle cells and collagen. Thus, zones of seve re inflammation were invariably associated with dissolution of the con nective tissue matrix and abundant human leukocyte antigen-DR expressi on on inflammatory cells and the remaining smooth muscle cells. Conclu sion: Our observations support the concept that inflammatory mechanism s modulate plaque morphology, by promoting either synthesis or lysis o f the fibrous cap. Our hypothesis is that fibrous and atheromatous les ions are essentially interchangeable.