Atherosclerosis imaging on the molecular level.

On the basis of clinical observations that acute coronary events often result from rupture of atherosclerotic plaques at sites with no or minor luminal narrowing, the search for techniques by which to identify vulnerable, rupture-prone lesions has developed into a quest for the holy grail of cardiovascular medicine. Vulnerable plaques may show characteristic morphologic features, but they may still differ in their biology and their activity, which ultimately leads to rupture. As a consequence, considerable efforts have been undertaken to identify biologic mechanisms of atherosclerotic lesions by use of molecular-targeted radiolabeled probes. A variety of approaches aiming at plaque inflammation, apoptosis, smooth muscle cell proliferation, extracellular matrix activation, or platelet binding have been introduced. Nevertheless, molecular imaging of atherosclerosis is still a work in progress. Challenges related to the best targeting approach, to translation of animal model results to the clinical setting, to adequate imaging methodology for visualization of coronary artery biology, and to a suitable target patient population will need to be overcome. But the field is steadily moving ahead and getting closer to the ultimate goal of an improved clinical risk assessment through in vivo assessment of vascular biology.