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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 …

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