Serum lipids associated with inflammation-related PET-FDG uptake in symptomatic carotid plaque

Abstract

<h3>Objective:</h3> We hypothesized that serum lipids, which experimental data suggest may be key initiators of carotid plaque inflammation, would be associated with plaque inflammation on ¹⁸fluorodeoxyglucose (FDG)-PET in patients with acutely symptomatic carotid stenosis. <h3>Methods:</h3> In this cohort study, consecutive patients with acute symptomatic internal carotid artery (ICA) stenosis (≥50%) underwent carotid PET-CT. We quantified plaque FDG uptake as follows: (1) average maximum standardized uptake values (SUV_max) across 10 regions of interest (ROI); (2) highest single ROI SUV measure (SUV_ROImax); (3) averaged mean SUV across 10 ROIs (SUV_mean). <h3>Results:</h3> Sixty-one patients were included. Plaque inflammatory FDG SUV_max was associated with increasing tertiles of low-density lipoprotein (LDL) (trend <i>p</i> = 0.004), total cholesterol (<i>p</i> = 0.009), and triglycerides (<i>p</i> = 0.01), and with lower high-density lipoprotein (HDL) (<i>p</i> = 0.005). When analyzed as a continuous variable, LDL was associated with symptomatic ICA SUV_mean (Spearman rho 0.44, <i>p</i> = 0.009), SUV_ROImax (rho 0.33, <i>p</i> = 0.01), and SUV_max (rho 0.35, <i>p</i> = 0.06). Total cholesterol was associated with SUV_mean (rho 0.33, <i>p</i> = 0.009), with trends for SUV_max (rho 0.24, <i>p</i> = 0.059) and SUV_ROImax (rho 0.23, <i>p</i> = 0.08). Triglycerides were associated with SUV_max (rho 0.32, <i>p</i> = 0.01) and SUV_ROImax (rho 0.35, <i>p</i> = 0.005). HDL was associated with lower SUV_max (rho −0.37, <i>p</i> = 0.004) and SUV_ROImax (rho −0.44, <i>p</i> = 0.0004). On multivariable linear regression analysis adjusting for age, sex, degree of carotid stenosis, statins, and smoking, LDL (<i>p</i> = 0.008) and total cholesterol (<i>p</i> = 0.04) were independently associated with SUV_max. <h3>Conclusion:</h3> Serum LDL and total cholesterol were associated with acutely symptomatic carotid plaque FDG uptake, supporting experimental data suggesting lipids may promote plaque inflammation, mediating rupture and clinical events.