Table 1. Molecular imaging targets for atherosclerosis.
| Molecular probe | Target process | Results from clinical studies | Pitfalls |
|---|---|---|---|
| [18F]FDG | Inflammation: glucose metabolism of inflammatory cells | - Symptomatic culprit carotid plaques showed higher [18F]FDG uptake than non-culprit contralateral plaques.22,23 | - Physiologic [18F]FDG signal in the myocardium hampering the epicardial coronary evaluation. |
| - Association between [18F]FDG uptake in carotid plaques and macrophage-specific antibody staining (CD68) of carotid endarterectomy specimens.24,25 | |||
| - Association with the presence of recent or remote cardiovascular events.26,27,28,29 | |||
| - Vascular [18F]FDG uptake in systemic inflammatory disease patients was higher than in healthy volunteers.30,31 | |||
| 68Ga or 64Cu labeled DOTA-agents | Inflammation: SSTR of activated macrophage | - Binding showed significant correlation with cardiovascular risk factors.32,33,34,35 | - Relatively inaccessible radiotracer |
| - Non-colocalization of [18F]FDG and [68Ga]Ga-DOTATATE uptake in large arteries of atherosclerotic plaques was found.32 | |||
| - Uptake was higher in culprit coronary and carotid lesions versus non-culprit arteries and exhibited superiority to differentiate high-risk from low-risk coronary atherosclerotic plaques over [18F]FDG PET uptake.36 | |||
| [18F]FCH | Inflammation: membrane metabolism of inflammatory cells | - Uptake was not colocalized with CT visible calcification, and furthermore, none of the calcified lesions showed any [18F]FCH uptake.37 | - Insufficient validation as an atherosclerosis imaging |
| - A prospective clinical trial (NCT02640313) is currently underway, to see the efficiency of [18F]FCH PET/MRI in detecting intraplaque inflammation and identify vulnerable plaques that are prone to rupture in comparison to the stable ones. | |||
| 11C-PK11195 | Inflammation: TSPO of macrophages | - Binding was correlated with immunostaining for CD68.38 | - Necessity of on-site cyclotron due to short half-life (20 min) |
| - Uptake was observed in the arterial wall of symptomatic patients, but in none of the asymptomatic controls.39 | - Non-specific binding | ||
| - Uptake in culprit plaques from carotid endarterectomy tissue was higher compared with plaques from asymptomatic patients.40 | - Low signal intensity | ||
| [18F]FMISO | Hypoxia | - Symptomatic plaques showed higher [18F]FMISO uptake than contralateral asymptomatic plaques, and [18F]FMISO uptake correlated with higher [18F]FDG uptake.41 | - Higher cost |
| - Insufficient validation as an atherosclerosis imaging |
FDG, fluorodeoxyglucose; DOTA, 1,4,7,10-tetraazacyclododecane-N,N′,N″,N‴-tetraacetic acid-D-Phe1; SSTR, somatostatin receptor; FCH, fluorocholine; DOTATATE, DOTA-Tyr3-octreotate; TSPO, 18-kDa translocator protein; FMISO, fluoromisonidazole.