Abstract 18028: [18F]-fluorodeoxyglucose is a Stronger Correlate of Intraplaque Inflammatory Burden in Human Carotid Plaque Than C-Reactive Protein: A Sub-Study of the Canadian Atherosclerosis Imaging Network (CAIN)

Abstract

Background and Purpose: Inflammation triggers and contributes to the progression of atherosclerosis. C-reactive protein (CRP), a circulating marker of inflammation, is a putative risk factor for cardiovascular disease, but this is not borne out in Mendelian randomization studies. Inflammation in carotid arteries can be imaged with hybrid [18F]-fluorodeoxyglucose (18FDG) positron emission tomography (PET) computed tomography (CT) imaging. In this investigation, circulating levels of CRP and 18FDG uptake in carotid vasculature were directly compared with intraplaque inflammatory burden, using macrophage-specific CD68 immunohistology. Methods: Nineteen prospectively recruited patients (66 ± 11 years, 15 male) scheduled for carotid endarterectomy underwent 18FDG-PET and CT angiography of carotids. CRP levels were assessed. Maximum 18FDG uptake in both internal carotids was quantified and normalized to blood (tissue:blood ratio, TBR). Following endarterectomy, excised plaque was fixed, sectioned and immunostained for CD68. CD68 expression was quantified. Results: Carotid endarterectomy was performed in 19 patients; one received a 2 nd carotid endarterectomy due to bilateral disease. The direct burden of inflammation, as quantified by CD68 immunohistology, correlated with maximum 18FDG uptake (r=0.716, p<0.001). There was no evidence of a correlation between CRP and CD68 (r=0.159, p=0.50), nor with maximum 18FDG uptake (r=0.238, p=0.31). Furthermore, 18FDG and CRP are different correlations where FDG is more strongly correlated with CD68 than CRP (p=0.02, Hoteling Williams test). Conclusion: 18FDG uptake is more strongly related to the extent of inflammatory burden within high-risk carotid plaque than CRP. CRP may not be an accurate criterion for assessing vulnerable carotid plaque (based on histopathology nor 18FDG uptake). Prospective outcomes-based trials are needed to establish 18FDG as a direct biomarker of vulnerable carotid plaque.