Coronary vascular events are most often caused by rupture of atherosclerotic plaques. Prior to their rupture, such plaques are likely to have at least one of several high-risk structural or biological processes known to associate with increased risk of atherothrombosis. Thus, efforts have long been directed to identify these high risk features non-invasively. While current imaging modalities are adept at measuring high-risk structural features, such as luminal stenosis and vessel wall morphology, they cannot directly report on the important high-risk biological features. On the other hand, molecular imaging techniques, such as positron emission tomography (PET) coupled with sensitive probes provide a unique opportunity to assess atherosclerotic plaque biology, and have the potential to complement structural information and thus, improve risk stratification and enable enhanced monitoring of therapeutic interventions.