The diagram above seems a logical appraisal of the situation, published recently by Cocker and colleagues.
A proposed schematic staging inflammatory and calcification activity within atherosclerotic lesions with FDG and NaF as imaging biomarkers. During early stages of atherosclerosis, inflammation is the predominant mechanism active within plaque. During these stages, [18F]FDG may be taken up by the lesion. As inflammation peaks, the risk of plaque rupture may increase. Inflammation also contributes toward initiating calcium metabolism within lesions that results in the formation of early calcium deposits. This would be reflected by uptake of both FDG and hydroxyapatite-specific [18F]sodium fluoride (NaF). Once the density of calcium deposits exceeds a certain threshold, it becomes visible with CT. During active calcification, plaque may still be vulnerable. Eventually, the calcification and mineralization processes exceed the inflammatory activity present within plaque, which might be demarcated by only NaF uptake (in the absence of FDG), as well as calcium deposits on CT. Ongoing calcification eventually leads to forming an end- stage stable atheroma that is densely calcified with only evidence for calcium on CT. Model of plaque progression (top bar) is adapted from Koenig and Khuseyinova.