Background: The current wisdom is that destabilization of human atheromatous
fibroinflammatory plaques may result in thrombosis and is responsible for most acute
ischemic syndromes. This paradigm has led to vigorous research to understand the
pathogenesis of plaque vulnerability and subsequent rupture, to find reliable systemic
serological markers and to identify imaging techniques in order to determine vulnerability of
individual plaques. Methods: Research examining the pathobiology of the vulnerable …