ABSTRACT
Acute thrombus formation on the surface of a complex atherosclerotic lesion appears responsible for the majority of acute coronary events.1-4 Autopsy studies show that most of these thrombotic events are associated with disruption of an atherosclerotic plaque that contains specific structural and biologic features.5-7 Although extensive literature describes the morphology and biology of these lesions, little data exist regarding their long-term course in living humans.8,9 The search for an accurate animal model of plaque vulnerability should thus be a priority in vascular biology research.
