Heart disease is a major leading cause of morbidity and mortality in the U.S. largely due to coronary artery atherosclerotic disease (CAD), which affects millions and costs billions annually. The concept of plaque vulnerability, based on likelihood of fibroatheroma rupture, has prompted many pursuits to identify high risk lesions, costing $150 million per year. However, identifying vulnerable plaques based on structure, via coronary angiograms or CT/MRI scans, has not translated to improved clinical outcome. Thus, the failure to identify and predict plaques at high risk of rupture, which may lead to myocardial infarction, heart failure and/or sudden cardiac death, is likely because structure may not optimally discern plaque vulnerability. Molecular imaging, in contrast, offers an innovative approach for discriminating the vulnerable plaque in that it not only visualizes structure, but also interrogates underlying molecular function. Based on the current methods to detect plaques, there is a need for a better method for measuring plaque rupture vulnerability.