Molecular Imaging of Atheroma

Abstract

Despite significant therapeutic advances, atherosclerotic disease (ie, stroke and myocardial infarction) remains the largest cause of death in the United States. Molecular imaging provides insights into the biological processes within the atherosclerotic plaque, improves risk stratification, and enhances the assessment of novel therapies. Accordingly, molecular imaging has the potential to facilitate further gains in cardiovascular care. Today, 2 radiotracers are widely available to assess atherosclerotic plaque biology: 18F-sodium fluoride (NaF) and 18F-fluorodeoxyglucose (FDG). As there is overlap in their potential applications, important differences exist between them. It is critically important to understand the relative strengths and limitations of NaF and FDG to know how and when to optimally use them. See Article by Vesey et al FDG is a glucose analogue that enters living cells via glucose transporters. Soon after the radiotracer enters the glycolytic pathway, it is phosphorylated by hexokinase and is thereafter unable to be further metabolized via glycolysis. Accordingly, its accumulation in tissues, which can be measured noninvasively using positron emission tomography (PET) with computed tomography (CT) or magnetic resonance, provides a quantitative measure of glucose utilization.1,2 Clinically, FDG PET is frequently performed to assess for malignancies and myocardial viability. Another important use of FDG PET imaging is the identification of inflammatory foci. FDG PET imaging of inflammation leverages the fact that inflammatory cells, notably activated macrophages and neutrophils, have particularly high glycolytic rates.3 To that end, cardiac FDG PET imaging is clinically used to evaluate for the presence of cardiac sarcoidosis,4 prosthetic valve endocarditis,5 and suspected implanted device infections.6 …