Abstract
Proinflammatory macrophages participate importantly in the pathogenesis of cardiovascular diseases such as atherosclerosis, in- stent stenosis, myocardial infarction, and heart failure. Macrophages adapt to the local microenvironment and acquire various functions associated with physiological and pathological processes. In the context of atherosclerosis, activated macrophages participate critically in every stage of lesion progression, from fatty streak formation to the onset of acute thromobotic complications. Matrix-degrading enzymes and prothrombotic molecules elaborated from activated macrophages may promote plaque disruption and subsequent thrombosis. Clinical studies established that lipid-lowering therapy reduces the onset of acute coronary events. Preclinical evidence has further suggested that lipid lowering attenuates macrophage activity and inflammation. However, these features that are typical of plaques prone to the onset of acute thrombotic events are not often associated with plaque size or angiographical luminal stenoses. Molecular imaging, an emerging technology, can detect specific cell types or visualize biological processes responsible for the pathogenesis of atherothrombosis, unlike conventional anatomical imaging. Therefore, detection of plaque inflammation and macrophages in vivo using molecular imaging may identify subclinical atherosclerotic lesions, predict future risk, and help to establish more personalized therapeutic strategies for the prevention of fatal complications.
