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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:250.)
© 2007 American Heart Association, Inc.

Letters to the Editor

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

Christopher L. Jackson

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

Correspondence to Bristol Heart Institute, University of Bristol, 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.

In Response:

Falk and colleagues raise a number of important issues regarding lesion formation and the modeling of plaque rupture in mice.¹ The first of these concerns the question of whether the processes that lead to neointima breakdown in the model of Sasaki et al² are congruent with those occurring during the breakdown of a fibrous cap overlying a lipid-rich necrotic core. Falk et al consider that there is no obvious reason to suppose that there is any such congruence. The second deals with the genesis of thrombi in the model of Sasaki et al compared with over a ruptured atherosclerotic plaque. Falk et al argue that the processes of thrombogenesis in conditions of rapid blood flow are likely to be different to those in stagnant blood in a ligated artery, a point well supported by a plethora of experimental evidence that has accrued over many years.³ Falk et al conclude on these bases that the relevance of the model of Sasaki et al to human plaque rupture is not clear, with the implication that it is of limited utility.

To be of utility, animal models of human disease should enable us to learn about the pathophysiology of the disease and, relatedly, provide a faithful test-bed for potential new therapies. These are essentially pragmatic issues: the quality of the data are of overriding importance and the procedures used during disease induction, and even the appearance of the signs of the disease, need not closely parallel what happens in humans. This . . . [Full Text of this Article]