In 31 adults with stable coronary artery disease, pericoronary adipose tissue (PCAT) attenuation measured on CT angiography showed no significant association with transcoronary or transcardiac gradients of interleukin-6 or interleukin-1β. Regression analyses across all three major coronary territories returned near-zero R² values and p-values above 0.40 for IL-6. IL-1β was undetectable in 81% of participants, precluding meaningful gradient analysis. Results held in plaque-free vessel subgroups.
PCAT attenuation has gained traction as a non-invasive cardiovascular risk marker, with the fat attenuation index (FAI) even forming the basis of commercial risk tools like CaRi-Heart. The underlying assumption has been that inflamed perivascular fat reflects active, cytokine-driven coronary inflammation — a biologically intuitive but mechanistically underexplored claim. These findings directly challenge that assumption for stable disease, raising the possibility that PCAT attenuation captures structural or chronic remodeling changes in adipose tissue rather than acute inflammatory signaling. The study's small cohort of 31 patients is a significant limitation, reducing statistical power to detect modest associations, and the stable-disease-only design deliberately excludes the acute inflammatory states where PCAT biomarker performance is strongest. Assay sensitivity for IL-1β also appears insufficient for this clinical context. As a preprint posted on medRxiv and not yet peer-reviewed, these results must be treated as preliminary. If replicated in larger cohorts, they would meaningfully constrain the mechanistic interpretation of PCAT-based cardiac risk scores and could reshape how clinicians contextualize CT-derived inflammation signals.