Objective:

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.

Methods:

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).

Results:

Sixty-one patients were included. Plaque inflammatory FDG SUV_max was associated with increasing tertiles of low-density lipoprotein (LDL) (trend p = 0.004), total cholesterol (p = 0.009), and triglycerides (p = 0.01), and with lower high-density lipoprotein (HDL) (p = 0.005). When analyzed as a continuous variable, LDL was associated with symptomatic ICA SUV_mean (Spearman rho 0.44, p = 0.009), SUV_ROImax (rho 0.33, p = 0.01), and SUV_max (rho 0.35, p = 0.06). Total cholesterol was associated with SUV_mean (rho 0.33, p = 0.009), with trends for SUV_max (rho 0.24, p = 0.059) and SUV_ROImax (rho 0.23, p = 0.08). Triglycerides were associated with SUV_max (rho 0.32, p = 0.01) and SUV_ROImax (rho 0.35, p = 0.005). HDL was associated with lower SUV_max (rho −0.37, p = 0.004) and SUV_ROImax (rho −0.44, p = 0.0004). On multivariable linear regression analysis adjusting for age, sex, degree of carotid stenosis, statins, and smoking, LDL (p = 0.008) and total cholesterol (p = 0.04) were independently associated with SUV_max.

Conclusion:

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.

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