"Pericoronary adipose tissue attenuation as a marker of global coronary inflammation rather than lesion-specific...

Pericoronary adipose tissue (PCAT) attenuation is a non-invasive imaging marker of coronary vascular inflammation. However, its relationship with clinical outcomes and its relevance at different levels of analysis remain incompletely understood. This study aimed to investigate the association between PCAT attenuation and major adverse cardiovascular events (MACE), with a focus on its role as a marker of coronary inflammatory burden at the lesion and patient levels.

In this retrospective cohort study, 772 participants were included (56.6% men). Lesions from patients who experienced MACE exhibited higher (less negative) PCAT attenuation compared with those without events. PCAT attenuation was assessed at the patient and lesion levels. Associations with MACE were analyzed using logistic regression and mixed-effects models. ROC analysis evaluated predictive performance. Linear mixed-effects models showed lesion-level mean and maximum PCAT attenuation were higher in patients with MACE (ΔHU = -1.941, 95% CI -3.563 to -0.320; p = 0.019, and ΔHU = -2.899, 95% CI -4.838 to -0.961, p = 0.003, respectively), including after adjustment for cardiovascular risk factors. However, lesion-level PCAT attenuation was not associated with MACE in generalized linear mixed-effects models. At the patient level, higher PCAT attenuation values were consistently associated with increased hazard of MACE during follow-up in both univariable (HR 1.046, 95% CI 1.013-1.081; p = 0.006) and multivariable analyses (HR 1.014, 95% CI 1.004-1.024; p = 0.006). Despite these associations, discriminatory performance of PCAT attenuation was modest (AUC 0.591, 95% CI 0.534-0.644), indicating limited ability to distinguish individuals at risk.

PCAT attenuation is associated with adverse cardiovascular outcomes at the patient level, supporting its role as a marker of global coronary inflammatory burden, with stronger, more consistent associations at the patient level than at the lesion level. While it reflects biologically relevant inflammatory processes, its limited discriminatory performance suggests that PCAT attenuation is best interpreted as a complementary marker within the broader context of clinical and imaging risk assessment.