This dissertation, submitted by James H.F. Rudd to the University of Cambridge for the degree of Doctor of Philosophy, explores the use of氟代脱氧葡萄糖 (FDG) positron emission tomography (PET) to image atherosclerotic plaque inflammation. The study aims to quantify plaque inflammation to predict the risk of plaque rupture and monitor the effects of atheroma-modifying therapies. Key findings include: 1. **In Vitro Studies**: THP-1 monocytes and buffy-coat macrophages were stimulated with cellular activators, and their deoxyglucose uptake was observed, demonstrating that both cell types accumulate deoxyglucose in proportion to their metabolic activity. 2. **In Vivo Studies**: FDG uptake was assessed in endarterectomy specimens from patients with symptomatic carotid disease, confirming the accumulation of deoxyglucose in macrophage-rich areas. FDG-PET imaging in patients with transient ischemic attack showed significant accumulation within carotid plaques, with more FDG uptake in symptomatic plaques compared to asymptomatic lesions. 3. **Rabbit Model**: A rabbit model of atherosclerosis was established to investigate the potential of an animal PET scanner (MicroPet) to detect atheroma and the ability of FDG-PET to image and quantify atheroma progression and regression. Aortic atheroma was identified by FDG-PET, but full quantification was not possible due to the limitations of the microPet system. The study concludes that inflammation within atherosclerotic plaques can be successfully imaged by FDG-PET both in vitro and in vivo. Pilot data from an experimental study of atherosclerosis in rabbits suggest that serial imaging with this technique might be useful for monitoring the effects of anti-atheroma drugs.This dissertation, submitted by James H.F. Rudd to the University of Cambridge for the degree of Doctor of Philosophy, explores the use of氟代脱氧葡萄糖 (FDG) positron emission tomography (PET) to image atherosclerotic plaque inflammation. The study aims to quantify plaque inflammation to predict the risk of plaque rupture and monitor the effects of atheroma-modifying therapies. Key findings include: 1. **In Vitro Studies**: THP-1 monocytes and buffy-coat macrophages were stimulated with cellular activators, and their deoxyglucose uptake was observed, demonstrating that both cell types accumulate deoxyglucose in proportion to their metabolic activity. 2. **In Vivo Studies**: FDG uptake was assessed in endarterectomy specimens from patients with symptomatic carotid disease, confirming the accumulation of deoxyglucose in macrophage-rich areas. FDG-PET imaging in patients with transient ischemic attack showed significant accumulation within carotid plaques, with more FDG uptake in symptomatic plaques compared to asymptomatic lesions. 3. **Rabbit Model**: A rabbit model of atherosclerosis was established to investigate the potential of an animal PET scanner (MicroPet) to detect atheroma and the ability of FDG-PET to image and quantify atheroma progression and regression. Aortic atheroma was identified by FDG-PET, but full quantification was not possible due to the limitations of the microPet system. The study concludes that inflammation within atherosclerotic plaques can be successfully imaged by FDG-PET both in vitro and in vivo. Pilot data from an experimental study of atherosclerosis in rabbits suggest that serial imaging with this technique might be useful for monitoring the effects of anti-atheroma drugs.