Participant-level pericoronary adipose tissue attenuation predicts changes in plaque composition: a 1-year prospective study in asymptomatic individuals with type 2 diabetes mellitus

Abstract Background Individuals with type 2 diabetes mellitus (T2DM) have a two- to fourfold increased risk of coronary artery disease (CAD). This increased risk is partly attributed to shared inflammatory pathways involved in the pathogenesis of both conditions. Pericoronary adipose tissue attenuation (PCATa), measured by coronary computed tomography angiography (CCTA), reflects the inflammatory activity within the coronary arteries and shows potential as a biomarker for cardiovascular risk assessment. Purpose This study investigated whether a participant-level baseline PCATa predicts changes in compositional plaque volumes and burden over a year in asymptomatic individuals with T2DM, who had neither symptoms nor a prior diagnosis of CAD. Methods This prospective longitudinal study included 200 asymptomatic participants with T2DM. Participants underwent CCTA scans at baseline and after one year to measure PCATa and quantify compositional plaque volumes and burden. PCATa represents the adipose tissue located within a radial distance from the outer coronary vessel wall equivalent to the vessel diameter, with an attenuation range of -190 to -30 Hounsfield units (HU). PCATa was measured along the proximal 40 mm of each coronary vessel, and the values were averaged to calculate participant-level PCATa. High PCATa were determined using the validated cut-off of -70.1 HU. Changes in plaque compositional volumes were quantified from the differences between baseline and one-year CCTA, and compositional plaque burden was calculated as the normalized atheroma volume. Multivariable linear and logistic regressions evaluated baseline PCATa associations with compositional plaque changes. Results Participants mean age was 61 ±9.4 years, 72% were male, and the mean body mass index was 30.5 ±4.5 kg/m². Over a years follow-up, compositional plaque volumes and burden increased, while PCATa remained stable. After multivariable adjustments, baseline PCATa was significantly associated with changes in total plaque volume (β=0.005, p=0.005), non-calcified plaque volume (β=0.006, p=0.007), total plaque burden (β=1.7, p=0.007), and non-calcified plaque burden (β=2.0, p=0.006). No significant associations were observed between baseline PCATa and changes in calcified plaque volume or burden. High baseline PCATa ( -70.1 HU) was observed in 44 participants (22%) and was the only independent predictor of non-calcified plaque burden progression (odds ratio 3.5, p=0.002). Conclusions Baseline PCATa was significantly associated with increased total and non-calcified plaque volumes and burden over a year in asymptomatic participants with T2DM. High PCATa predicts non-calcified plaque burden progression, suggesting that PCATa may serve as a marker for subclinical atherosclerosis progression. This supports further investigation into the role of PCATa in cardiovascular risk stratification, particularly in high-risk populations such as T2DM.Central Figure Changes in plaque compositions by PCATa