Imaging Atherosclerotic Plaque Inflammation With [ ¹⁸ F]-Fluorodeoxyglucose Positron Emission Tomography

TLDR

Atherosclerotic plaque rupture is driven by inflammatory cell activity, yet current imaging only provides anatomical data and 18F‑FDG PET offers a non‑invasive way to image this inflammation. The study aimed to determine whether 18F‑FDG PET could detect inflammation in carotid artery plaques. Eight symptomatic carotid atherosclerosis patients were scanned with 18F‑FDG PET and co‑registered CT. 18F‑FDG PET revealed that symptomatic carotid plaques had 27% higher uptake than asymptomatic lesions, normal arteries showed no uptake, and autoradiography confirmed macrophage‑rich accumulation, demonstrating that inflamed, unstable plaques can be visualized with this technique.

Abstract

Background — Atherosclerotic plaque rupture is usually a consequence of inflammatory cell activity within the plaque. Current imaging techniques provide anatomic data but no indication of plaque inflammation. The glucose analogue [ 18 F]-fluorodeoxyglucose ( 18 FDG) can be used to image inflammatory cell activity non-invasively by PET. In this study we tested whether 18 FDG-PET imaging can identify inflammation within carotid artery atherosclerotic plaques. Methods and Results — Eight patients with symptomatic carotid atherosclerosis were imaged using 18 FDG-PET and co-registered CT. Symptomatic carotid plaques were visible in 18 FDG-PET images acquired 3 hours post- 18 FDG injection. The estimated net 18 FDG accumulation rate (plaque/integral plasma) in symptomatic lesions was 27% higher than in contralateral asymptomatic lesions. There was no measurable 18 FDG uptake into normal carotid arteries. Autoradiography of excised plaques confirmed accumulation of deoxyglucose in macrophage-rich areas of the plaque. Conclusions — This study demonstrates that atherosclerotic plaque inflammation can be imaged with 18 FDG-PET, and that symptomatic, unstable plaques accumulate more 18 FDG than asymptomatic lesions.