The explosive growth of small voids in vulnerable cap rupture; cavitation and interfacial debonding.

While it is generally accepted that ruptures in fibrous cap atheromas cause most acute coronary deaths, and that plaque rupture occurs in the fibrous cap at the location where the tissue stress exceeds a certain critical peak circumferential stress, the exact mechanism of rupture initiation remains unclear. We recently reported the presence of multiple microcalcifications (μCalcs) <50 μm diameter embedded within the fibrous cap, μCalcs that could greatly increase cap instability by introducing up to a 5-fold increase in local tissue stress. Here, we explore the hypothesis that, aside from cap thickness, μCalc size and interparticle spacing are principal determinants of cap rupture risk. Also, we propose that cap rupture is initiated near the poles of the μCalcs due to the presence of tiny voids that explosively grow at a critical tissue stress and then propagate across the fibrous cap. We develop a theoretical model based on classic studies in polymeric materials by Gent (1980), which indicates that cavitation as opposed to interfacial debonding is the more likely mechanism for cap rupture produced by μCalcs <65 μm diameter. This analysis suggests that there is a critical μCalc size range, from 5 μm to 65 μm, in which cavitation should be prevalent. This hypothesis for cap rupture is strongly supported by our latest high resolution μCT studies in which we have observed trapped voids in the vicinity of μCalcs within fibrous caps in human coronaries.