Development of a quantitative mechanical test of atherosclerotic plaque stability.

Atherosclerotic plaque rupture is the main cause of myocardial infarction and stroke. Both clinical and computational studies indicate that the shoulder region, where a plaque joins the vessel wall, is rupture-prone. Previous mechanistic studies focused on mechanical properties of the fibrous cap and tensile stresses, which could lead to tearing of the cap. Based on clinical observations of "mobile floating plaques," we postulate that de-adhesion between the fibrous cap and the underlying vessel wall may also play a role in plaque failure. Thus, measuring adhesive strength of the bond between plaque and vascular wall may provide useful new insights into plaque stability. Delamination experiments, widely used in examining inter-laminar adhesive strength of biological materials, were used to measure adhesive strength of advanced plaques in apolipoprotein E-knockout (apoE-KO) mice after 8 months on Western diet. We measured adhesive strength in terms of local energy release rate, G, during controlled plaque delamination. As a measure of the fracture energy required to delaminate a unit area of plaque from the underlying internal elastic lamina (IEL), G provides a quantitative measure of local adhesive strength of the plaque-IEL interface. The values for G acquired from 16 plaques from nine apoE-KO mouse aortas formed a positively skewed distribution with a mean of 24.5 J/m(2), median of 19.3 J/m(2), first quartile of 10.8 J/m(2), and third quartile of 34.1 J/m(2). These measurements are in the lower range of values reported for soft tissues. Histological studies confirmed delamination occurred at the interface between plaque and IEL.