Abstract
Inflammation and microcalcification are interrelated processes contributing to atherosclerotic plaque vulnerability. Positron-emission tomography can quantify these processes in vivo. This study investigates (1) 18F-fluorodeoxyglucose (FDG) and 18F-sodium fluoride (NaF) uptake in culprit versus nonculprit carotid atheroma, (2) spatial distributions of uptake, and (3) how macrocalcification affects this relationship. Individuals with acute ischemic stroke with ipsilateral carotid stenosis of ≥50% underwent FDG-positron-emission tomography and NaF-positron-emission tomography. Tracer uptake was quantified using maximum tissue-to-background ratios (TBRmax) and macrocalcification quantified using Agatston scoring. In 26 individuals, median most diseased segment TBRmax (interquartile range) was higher in culprit than in nonculprit atheroma for both FDG (2.08 [0.52] versus 1.89 [0.40]; P<0.001) and NaF (2.68 [0.63] versus 2.39 [1.02]; P<0.001). However, whole vessel TBRmax was higher in culprit arteries for FDG (1.92 [0.41] versus 1.71 [0.31]; P<0.001) but not NaF (1.85 [0.28] versus 1.79 [0.60]; P=0.10). NaF uptake was concentrated at carotid bifurcations, while FDG was distributed evenly throughout arteries. Correlations between FDG and NaF TBRmax differed between bifurcations with low macrocalcification (rs=0.38; P<0.001) versus high macrocalcification (rs=0.59; P<0.001). This is the first study to demonstrate increased uptake of both FDG and NaF in culprit carotid plaques, with discrete distributions of pathophysiology influencing vulnerability in vivo. These findings have implications for our understanding of the natural history of the disease and for the clinical assessment and management of carotid atherosclerosis.
Highlights
Inflammation and microcalcification are interrelated processes contributing to atherosclerotic plaque vulnerability
NaF uptake was higher in culprit versus asymptomatic atheroma, though FDG did not differ significantly,[18] findings at odds with most published vascular FDG-positron-emission tomography (PET) studies. This study addressed this uncertainty by investigating the ability of FDG- and NaF-PET/computed tomography (CT) to identify culprit plaque in a cohort of magnetic resonance imaging–confirmed ischemic strokes
Of 31 participants recruited to the ICARUSS study, 27 underwent dual FDG- and NaF-PET/CT
Summary
Individuals with acute ischemic stroke with ipsilateral carotid stenosis of ≥50% underwent FDG-positron-emission tomography and NaF-positron-emission tomography. The data that support the findings of this study are available from the corresponding author upon reasonable request. The ICARUSS (Imaging Carotid Atherosclerosis in the Recovery and Understanding of Stroke Severity) Study prospectively recruited individuals presenting with first-ever ischemic stroke within the previous 7 days with ipsilateral common or internal carotid artery stenosis of ≥50% on CT angiography or ultrasound Doppler at Addenbrooke’s Hospital, Cambridge, United Kingdom. All individuals had magnetic resonance imaging– confirmed ischemic strokes using diffusion-weighted imaging. Individuals presenting with a transient ischemic attack were not recruited. Carotid artery stenosis was measured using the North American Symptomatic Carotid Endarterectomy Trial criteria,[20] and plaque characteristics (echogenicity and regularity) were recorded. The study was approved by a national research ethics committee (Nottingham One Research Ethics Committee, 14/EM/0128)
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