Association of CT-derived body composition with coronary plaque components and vascular inflammation

To investigate the relationship of body composition with coronary plaque components and vascular inflammation.

This retrospective study included 412 individuals who underwent computed tomography angiography scan between August 2024 and July 2025. Body composition including both muscle and adipose components was analyzed. Plaque characteristics and pericoronary fat attenuation index (FAI) were quantified. The associations between body composition, plaque burden, and FAI were examined using correlation and multivariable linear regression analyses. Furthermore, we explored the mediating roles of specific body composition metrics in the relationship between body mass index (BMI) and plaque burden, as well as the potential mediation by FAI in the association linking body composition to plaque burden.

Of all-subjects, 269 (65.29%) were male. The average age was 62.85 ± 13.81 years old. Correlation analyses revealed significant moderate to strong positive associations of BMI, visceral adipose tissue (VAT), intermuscular adipose tissue (IMAT), and fatty muscle fraction (FMF) with lipid plaque burden. Additionally, BMI was moderately positively correlated with calcified plaque burden, while skeletal muscle (SM) was weakly negatively correlated with it. Specifically, in a multivariable-adjusted model, higher BMI (β= 0.053) were independently associated with greater lipid plaque burden. Higher BMI (β = 0.909) and lower SM (β = -0.004) were associated with an increased calcified plaque burden. Moreover, higher BMI (β = -0.547), subcutaneous adipose tissue (SAT) (β = -0.004), and SM (β = -0.001), as well as lower VAT (β = 0.005), epicardial adipose tissue (EAT) (β = 0.041), IMAT (β = 0.061), and FMF (β = 0.075) remained independently associated with decreased FAI. Mediation analysis revealed that SM and VAT mediated -29.555% and 56.489% of the association between BMI and calcified plaque burden and lipid plaque burden, respectively. Furthermore, FAI mediated 40.426% of the effect of VAT and 30.909% of the effect of IMAT on lipid plaque burden.

Different body composition metrics exert divergent effects on various components of coronary plaque. Our study suggests that VAT and IMAT may contribute to lipid plaque formation, potentially mediated by a state of increased vascular inflammation as captured by FAI, while a higher muscle mass may protect against the progression of calcified plaque. These findings highlights the necessity of precise body composition analysis in cardiovascular risk assessment.