Key result
High EAT in nonobstructive CAD links to total plaque regression but increased vulnerable hypodense plaque.
Why the study?
Inflammation drives atherosclerosis and plaque vulnerability and is associated with epicardial adipose tissue accumulation, but its link to compositional plaque progression in nonobstructive CAD remains unexplored.
Does high baseline epicardial adipose tissue volume associate with compositional plaque progression and vulnerability in patients with nonobstructive CAD?
Cohort (n=31)
Does high baseline epicardial adipose tissue volume associate with compositional plaque progression and vulnerability in patients with nonobstructive CAD?
In patients with nonobstructive CAD, high epicardial adipose tissue volume may be associated with a transformation into a vulnerable plaque phenotype over time, despite a tendency for total plaque volume regression.
Answers are grounded in this paper and cite their sources.
Should not yet alter management in nonobstructive CAD; leaves open epicardial adipose tissue as a vulnerability marker.
BACKGROUND: Inflammation is a driver of atherosclerosis and plaque vulnerability. Epicardial adipose tissue (EAT) accumulation is associated with inflammation. The aim of this study was, therefore, to explore the association between EAT volume, compositional plaque progression, and vulnerability in nonobstructive coronary artery disease (CAD). METHODS: We identified 31 individuals [median age 58 (52, 68) years, 42% women] from the Norwegian Registry of Invasive Cardiology with nonobstructive CAD undergoing clinically indicated serial cardiac computed tomography (CT) and coronary CT angiography (CCTA). EAT volume was measured at baseline by a semiautomatic analysis software. Patients were grouped according to lower or higher than median baseline EAT (b-EAT) volume. Plaque progression was quantified by CCTA as annual change in total and compositional plaque volume. Hypodense plaques were adjudicated as vulnerable plaques. RESULTS: Patients with high b-EAT volume had numerically lower calcium score, coronary artery segment involvement score, total coronary plaque burden, and increased prevalence of vulnerable plaques compared with patients with low EAT volume at baseline and follow-up, even if it did not reach statistical significance. Compared with patients with low b-EAT volume, patients with high b-EAT volume tended to have an annual regression in total plaque volume, while the proportion of vulnerable hypodense plaque volume increased. CONCLUSION: In nonobstructive CAD, patients with high b-EAT volume tended to have a regression of total plaque volume, but a transformation into a vulnerable plaque phenotype during follow-up. Whether lifestyle changes may improve prognosis in nonobstructive CAD needs to be confirmed in larger trials.
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Khan et al. (2025) conducted a cohort in Nonobstructive coronary artery disease (CAD) (n=31). High baseline epicardial adipose tissue (EAT) volume vs. Low baseline EAT volume was evaluated on Annual change in total and compositional plaque volume. High baseline epicardial adipose tissue volume in nonobstructive CAD tended to be associated with regression of total plaque volume but an increase in vulnerable hypodense plaque volume.
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