Fibrous and lipid-rich atherosclerotic plaques are part of interchangeable morphologies related to inflammation: a concept

The morphology of advanced atherosclerotic plaques varies from solid fibrous lesions, considered essentially stable, to lipid-rich lesions with large atheromas prone to rupture. The latter situation is often associated with large amounts of foam cells. An in-situ inflammatory process influenced by activated T cells and macrophages can be demonstrated in atherosclerotic plaques; however, the relationship between the inflammation and clinically relevant morphological types has 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 morphologies (fibrous versus lipid-rich), on the other, may shed light on this concept. Immunocytochemical techniques were used in combination with connective tissue stains to study the topographic distribution of smooth muscle cells, collagen, and inflammatory cells in different morphologic types of advanced atherosclerotic plaques in aortic and carotid arteries obtained at autopsy. Lesions with an inconspicuous lipid core were defined as fibrous (n = 7). They 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 contained a thin fibrous cap with a loosely arranged matrix dominated by macrophages and T cells. Most lesions (n = 21), however, had a morphology 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 otherwise dominated by smooth muscle cells and collagen. Thus, zones of severe inflammation were invariably associated with dissolution of the connective tissue matrix and abundant human leukocyte antigen-DR expression on inflammatory cells and the remaining smooth muscle cells. Our observations support the concept that inflammatory mechanisms modulate plaque morphology, by promoting either synthesis or lysis of the fibrous cap. Our hypothesis is that fibrous and atheromatous lesions are essentially interchangeable