Higher cholesterol efflux capacity inversely correlates with plaque number (B=-0.33/SD), plaque extension (OR=0.84), and arterial inflammation in early subclinical atherosclerosis.
Does cholesterol efflux capacity associate with subclinical atherosclerosis and arterial inflammation in asymptomatic individuals?
Higher cholesterol efflux capacity is inversely associated with early, non-calcified subclinical atherosclerosis and arterial inflammation in asymptomatic individuals.
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Abstract Background Impaired cholesterol efflux capacity (CEC) has been linked to incident atherosclerotic cardiovascular disease (ASCVD) events independent of high-density lipoprotein cholesterol (HDL-C) levels or other traditional risk factors1. However, association of CEC with subclinical atherosclerosis is unknown. Purpose Investigate whether CEC associates with arterial plaque and inflammation in multiple vascular beds among asymptomatic participants without known cardiovascular disease (CVD). Methods CEC was measured in a subset of participants from the Progression of Early Subclinical Atherosclerosis (PESA) study undergoing subclinical atherosclerosis assessment by 2 and 3D-vascular ultrasound (VUS) and coronary artery calcium score (CACS), and arterial inflammation evaluation by 18F-fluorodeoxyglucose positron emission tomography/magnetic resonance imaging (FDG PET/MRI.) Number of plaques and FDG arterial uptake were assessed in 7 vascular territories (bilateral carotid/iliac/femoral arteries and abdominal aorta). Plaque extension was assessed by PESA score (0-6 by presence in 5 territories and CAC,) 3DVUS territories (bilateral carotid and femoral,) and global plaque volume (GPV; sum of 3DVUS plaque volumes in mm3). CEC was assessed in blood samples measuring the efflux of radiolabeled cholesterol from J774 macrophages to apolipoprotein B–depleted participant plasma. Demographic and clinical characteristics, atherosclerosis, and inflammation were evaluated across CEC quartiles and as a continuous variable per unit of standard deviation (SD) using linear regression. Univariate/multivariate models were adjusted for SCORE2, diabetes, and body mass index (BMI.) Results Among 1,149 participants (median age 51.7 years, 84% male, mean HDL-C 47.4 mg/dL), 793 had vascular 18F-FDG PET/MRI imaging. In adjusted models, CEC was inversely associated with plaque number (B=-0.33 per 1 SD increase in CEC, -0.60- -0.06) and extension as defined by PESA score (OR=0.84 , 95%CI 0.73-0.96,) as well as FDG uptake in femoral (B=-0.012, -0.023 - -0.001) and carotid (-0.020, -0.033 -0.007) territories and globally (B=-0.012, -0.023, -0.001.) GPV decreased across increasing quartiles of CEC (p=0.013,) but the trend lost statistical significance in the adjusted model. There was no association between CEC and CACS. Conclusion This is the largest study of CEC in asymptomatic participants with data on multi-territorial subclinical atherosclerosis and vascular inflammation from FDG-PET. We show that CEC inversely correlates with atherosclerotic plaque number, plaque extension (PESA score,) and arterial inflammation on FDG-PET. The association with plaque number and inflammation but not with CACS suggests that the role of CEC may impact atherosclerosis at earlier (non-calcified) stages2.Participant data by CEC quartile Influence of CEC in adjusted models
Skoza et al. (Sat,) reported a other. Higher cholesterol efflux capacity inversely correlates with plaque number (B=-0.33/SD), plaque extension (OR=0.84), and arterial inflammation in early subclinical atherosclerosis.