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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:1191.)
© 2006 American Heart Association, Inc.

Editorials

Ruptures of Delight?

A New Mouse Model of Plaque Rupture

Christopher L. Jackson

From the Bristol Heart Institute, University of Bristol, UK.

Correspondence to Christopher L. Jackson, Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, United Kingdom. E-mail chris.jackson@bristol.ac.uk

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

There is a strange discrepancy in the world of vascular biology. It is clear from many investigations that the rupture of an atherosclerotic plaque is the most common triggering event for occlusive thrombus formation in a coronary artery, leading to myocardial infarction. However, many large vascular biology meetings do not include specific sessions on this topic. Indeed, even flagship journals such as Arteriosclerosis, Thrombosis, and Vascular Biology do not list "plaque rupture" among the standard keywords to be used during manuscript submission. Why does an issue of such clinical importance have such a low profile?

See page 1304

The probable cause is the difficulty inherent in studying the phenomenon of plaque rupture, so that there are actually relatively few manuscripts and communications that address it directly (a quick interrogation of the PubMed database suggests that only about 1.5% of research articles published during the last 5 years in the atherosclerosis/coronary heart disease field deal specifically with plaque rupture). Although ruptured plaques can be identified and excised at post mortem, determining how recently the rupture has occurred is an imprecise matter. Intact plaques to be used as comparators may be in danger of impending rupture—but their proximity to the clinical horizon may again be difficult to assess accurately.

The usual recourse in such circumstances is to an animal model, but experimental models of plaque rupture have come into our hands only recently. Following the pioneering work of Dr Rosenfeld’s group in Seattle, first published in 2000,¹ his group, ours, and others . . . [Full Text of this Article]

Related Article:

A Simple Method of Plaque Rupture Induction in Apolipoprotein E–Deficient Mice

Takeshi Sasaki, Masafumi Kuzuya, Kae Nakamura, Xian Wu Cheng, Tami Shibata, Kohji Sato, and Akihisa Iguchi
Arterioscler Thromb Vasc Biol 2006 26: 1304-1309. [Abstract] [Full Text] [PDF]

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				C. L. Jackson Defining and Defending Murine Models of Plaque Rupture Arterioscler Thromb Vasc Biol, April 1, 2007; 27(4): 973 - 977. [Full Text] [PDF]

				E. Falk, S. M. Schwartz, Z. S. Galis, and M. E. Rosenfeld Neointimal Cracks (Plaque Rupture?) and Thrombosis in Wrapped Arteries Without Flow Arterioscler Thromb Vasc Biol, January 1, 2007; 27(1): 248 - 249. [Full Text] [PDF]

				M. Kuzuya and T. Sasaki Neointimal Cracks (Plaque Rupture?) and Thrombosis in Wrapped Arteries Without Flow Arterioscler Thromb Vasc Biol, January 1, 2007; 27(1): 252 - 252. [Full Text] [PDF]