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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:986.)
© 2007 American Heart Association, Inc.

Editorials

Is Pathologic Intimal Thickening the Key to Understanding Early Plaque Progression in Human Atherosclerotic Disease?

Frank D. Kolodgie; Allen P. Burke; Gaku Nakazawa; Renu Virmani

From the CVPath Institute Inc, Gaithersburg, Md.

Correspondence to Renu Virmani, MD, Medical Director, CVPath Institute Inc, 19 Firstfield Road, Gaithersburg, Md 20878. E-mail rvirmani@cvpath.org

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
The term "Pathologic Intimal Thickening" (PIT) was recently introduced to define an early stage of atherosclerosis described in human coronary lesions found at autopsies of sudden death victims.¹ This descriptive identifier is based on the AHA type III (intermediate) lesion and, as originally presented by Stary and collegues, it’s believed to be the morphological and chemical bridge to more advanced plaques.² The precise histological features and clinical relevance of PIT remains unsettled, and use of the term is still far from widespread. In short, PIT identifies a lesion with an extracellular lipid pool with intimal smooth muscle cell loss typically adjacent to the medial wall in addition to varying degrees of macrophage infiltration near the lumen. These morphological features indicate a progressive lesion in the earlier stages of atherosclerosis, although there is yet the presence of a necrotic core. As recently studied by Nakashima and colleagues in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, it may provide a key in settling the chicken-versus-egg debate of atherosclerotic plaque progression: does lipid come first, or do macrophages?³ Is PIT the precursor lesion of fibroatheroma? The study in this issue uses 3-dimensional histology to attempt to address some of these issues, and, in doing so, may raise as many questions as it answers.

See page 1159

Although there are many detailed autopsy studies describing various lesion morphologies, little is known how human atherosclerosis progresses from early to more advanced plaques, marked by the formation of a necrotic . . . [Full Text of this Article]

Related Article:

Early Human Atherosclerosis: Accumulation of Lipid and Proteoglycans in Intimal Thickenings Followed by Macrophage Infiltration

Yutaka Nakashima, Hiroshi Fujii, Shinji Sumiyoshi, Thomas N. Wight, and Katsuo Sueishi
Arterioscler Thromb Vasc Biol 2007 27: 1159-1165. [Abstract] [Full Text] [PDF]

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				I. Tabas, K. J. Williams, and J. Boren Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis: Update and Therapeutic Implications Circulation, October 16, 2007; 116(16): 1832 - 1844. [Abstract] [Full Text] [PDF]