Atherosclerosis as a Recurrent Cycle of Inflammation and Repair

  • C. W. M. Adams


In the last century, Virchow first drew attention to the inflammatory aspect of atherosclerosis, and pointed to endarteritis as a factor in the multifactorial pathogenesis of the disease [37]. This observation has been largely ignored, mainly because most doctors regard inflammation as having only a microbiological connotation. Even though it has been suggested that herpes or other viruses may play a part in atherogenesis [18], there are many other types of inflammation apart from those caused by microbial agents. Trauma induced inflammatory changes that parallel those seen in atherosclerosis, such as fibrinous exudation in tenosynovitis and the reparative aspects of a peptic ulcer (namely epi- or endothelial, macrophage and fibroblastic activity). Immune reactions result in an inflammatory response marked mainly by lymphocytoid and plasmocytoid infiltration and by macrophage activation or arming. Some of these responses are seen in advanced atherosclerosis. Acute inflammation also causes foci of necrosis, either as a result of the cytotoxic nature of the inflammatory agent (e.g. the carbuncle caused by staphylococcal toxins) or compression of the local blood supply by inflammatory oedema. Necrosis is an important feature of atherosclerosis with clinical manifestations. Indeed, the arterial wall at various sites and at different ages shows all these manifestations of subacute or chronic inflammation, and inflammatory events often alternate with repair processes in a recurrent cycle producing “geological layers” in the lesion [27].


Arterial Wall Evans Blue Tunica Intima Arterial Intima Chronic Meningitis 
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© Springer-Verlag Berlin Heidelberg 1987

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  • C. W. M. Adams

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