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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:248.)
© 2007 American Heart Association, Inc.

Letters to the Editor

Neointimal Cracks (Plaque Rupture?) and Thrombosis in Wrapped Arteries Without Flow

Erling Falk; Stephen M. Schwartz; Zorina S. Galis; Michael E. Rosenfeld

From the University of Aarhus (E.F.), Denmark; the University of Washington (S.M.S., M.E.R.), Seattle; and the Indiana University and Lilly Research Laboratories (Z.S.G.), Indianapolis.

Correspondence to Erling Falk, Department of Cardiology, Aarhus University Hospital (Skejby), Brendstrupgaardsvej 100, DK-8200 Aarhus N, Denmark. E-mail erling.falk@ki.au.dk

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

The Editor’s pick for the June 2006 issue of Arteriosclerosis, Thrombosis, and Vascular Biology was the article by Sasaki et al¹ entitled "A Simple Method of Plaque Rupture Induction in Apolipoprotein E–Deficient Mice." The key term in this title is "plaque rupture." The article was accompanied by a supportive editorial by Jackson.² We would like to suggest that the enthusiasm for this experiment as a model for plaque rupture needs to be moderated by a better understanding of the model itself and of human plaque rupture.

In 1997, Lindner and coworkers described that flow cessation induced by ligation of the common carotid artery (CCA) near its bifurcation led to constrictive vascular remodeling and neointima formation in mice within 4 weeks.^3,4 Flow cessation was followed by loss of medial smooth muscle cells and early recruitment of leukocytes that infiltrated the developing neointima, media, and adventitia during the first week. Focal endothelial detachment with subendothelial accumulation of erythrocytes were also observed, but otherwise the endothelium appeared intact and thrombus was not seen except for the most distal part of the artery near the ligature. However, if the endothelium was removed before ligation, an occluding thrombus formed over the entire length of the carotid artery.³ Later, flow cessation was used to accelerate the formation of macrophage-rich lesions in apoE-deficient mice, and the role of macrophages in expansive arterial remodeling was described.⁵

Moroi et al introduced in 1998 another mouse model of neointima formation, induced by placing a nonconstrictive polyethylene cuff around the femoral . . . [Full Text of this Article]

This article has been cited by other articles:

				E. Falk, S. M. Schwartz, Z. S. Galis, and M. E. Rosenfeld Putative Murine Models of Plaque Rupture Arterioscler Thromb Vasc Biol, April 1, 2007; 27(4): 969 - 972. [Full Text] [PDF]

				C. L. Jackson Neointimal Cracks (Plaque Rupture?) and Thrombosis in Wrapped Arteries Without Flow Arterioscler Thromb Vasc Biol, January 1, 2007; 27(1): 250 - 251. [Full Text] [PDF]