Longitudinal changes in epicardial adipose tissue attenuation significantly improved the prediction of coronary plaque progression independent of LDL-C lowering (likelihood ratio test P=0.012).
Cohort (n=313)
Do longitudinal changes in epicardial adipose tissue attenuation predict coronary plaque progression independent of LDL-C lowering in asymptomatic, statin-naive patients?
Serial changes in epicardial adipose tissue attenuation are associated with coronary plaque remodeling independent of LDL-C lowering, suggesting a role for EAT inflammation in residual risk.
Effect estimate: ΔAkaike information criterion -4.8
p-value: p=0.012
BACKGROUND: Coronary plaque progression persists in some patients despite effective low-density lipoprotein cholesterol (LDL-C) lowering. Epicardial adipose tissue (EAT) is a metabolically active visceral fat depot that may influence coronary atherosclerosis through inflammatory signaling. The authors hypothesized that longitudinal changes in EAT would influence plaque progression. METHODS: Plaque and EAT quantification with paired baseline and follow-up coronary computed tomography angiography was attainable in 313 asymptomatic, statin-naive participants (aged 58.8 ± 6.8 years, 44% female) in the CAUGHT-CAD (Coronary Artery calcium score: Use to Guide management of Hereditary Coronary Artery Disease) trial. Associations between longitudinal changes in EAT volume and attenuation (ΔEAT) and coronary plaque outcomes were evaluated using analysis of covariance models, with adjustment for baseline plaque burden, treatment allocation, and changes in cardiometabolic risk factors. Exploratory analyses evaluated the relationship between ΔEAT attenuation and Δpericoronary adipose tissue (PCAT) attenuation. An LDL-C-based reference model of achieved LDL-C (reference 1.8 mmol/L >70 mg/dL) was used, and incremental discrimination with ΔEAT attenuation was assessed using nested model comparison and likelihood ratio testing. RESULTS: ), the addition of ΔEAT attenuation to LDL-C-based analysis of covariance models resulted in a statistically significant improvement in model fit (ΔAkaike information criterion -4.8; likelihood ratio test P = 0.012). In exploratory analyses, ΔEAT attenuation was also associated with increasing PCAT attenuation (β = 2.44 HU per SD; P < 0.001), suggesting that changes in PCAT may partly explain the observed association with plaque progression. CONCLUSIONS: The association of serial changes in EAT attenuation with coronary plaque remodeling, independent of LDL-C lowering, supports a potential mechanistic role for EAT inflammation in residual plaque progression.
Khanna et al. (Wed,) conducted a cohort in Asymptomatic, statin-naive with hereditary coronary artery disease risk (n=313). Longitudinal changes in epicardial adipose tissue (EAT) attenuation vs. LDL-C-based reference model alone was evaluated on Coronary plaque progression (improvement in model fit) (ΔAkaike information criterion -4.8, p=0.012). Longitudinal changes in epicardial adipose tissue attenuation significantly improved the prediction of coronary plaque progression independent of LDL-C lowering (likelihood ratio test P=0.012).