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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:1694.)
© 2000 American Heart Association, Inc.

Letters to the Editor

When Is Atherosclerosis Not Atherosclerosis?

Godfrey S. Getz

Department of Pathology, University of Chicago

To the Editor:

When is atherosclerosis not atherosclerosis? In the last decade, there have been 2 revolutions in the study of atherosclerosis. On the one hand, a more sophisticated appreciation of the relationship between the morphology and fate of human atherosclerotic plaques and clinical outcomes has been developed. On the other hand, the blossoming of mouse genetics has allowed us the possibility of exploring prospectively the mechanisms that lead to various types of atherosclerotic lesions. These advances, in the view of the author, should compel us as experimentalists, mainly using murine models, to fashion a more nuanced view and description of experimental atherosclerosis.

The last issue of Arteriosclerosis, Thrombosis, and Vascular Biology contained a review on a comprehensive morphologic classification scheme for atherosclerotic lesions, which was derived by studies of lesions from autopsy examinations of sudden coronary deaths.¹ There was also a commentary by Dr H. Stary² updating the natural history and histological classification of human atherosclerotic lesions. This follows several prior publications by the lesions committee of the Arteriosclerosis Council of the American Heart Association. The update of the histological classification by Stary² refers to the early stages I, II, and III of lesions, which are made up mostly of macrophage foam cells, with perhaps some extracellular lipid as well. He points out that these stages can regress to normal and thus are not necessarily evolving to mature atherosclerotic lesions. The morphological classification discussed by Dr Virmani and colleagues,¹ refers to these early foam cell lesions as "nonatherosclerotic . . . [Full Text of this Article]

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