Association between changes in pericoronary adipose tissue attenuation and compositional plaque progression as assessed by coronary computed tomography angiography

Background Pericoronary adipose tissue (PCAT) attenuation quantified from coronary computed tomography angiography (CCTA) reflects local coronary inflammation. While prior reports have shown this biomarker to associate with changes in coronary plaque burden on the per-patient level, the relationship between changes in PCAT attenuation and progression of plaque composition in individual coronary lesions has not been well studied. Purpose To examine the association between per-lesion level changes in PCAT attenuation and progression of total and compositional plaque volume in patients with stable coronary artery disease (CAD) undergoing serial CCTA. Methods Retrospective study of consecutive patients who underwent clinically indicated serial CCTA at an interscan interval of ≥2 years in a single tertiary centre between 2011-2023. Quantitative plaque analysis was performed using automated research software, with calculation of volumes of total plaque, calcified plaque (CP), and noncalcified plaque (NCP) on the per-lesion level. Following this, volumetric PCAT attenuation was automatically measured within a radial distance from the vessel wall equal to the average diameter of the vessel. Linear mixed models with random intercept were used to examine the relationship between temporal change in PCAT attenuation and change in plaque volumes, with adjustment for patient demographics, cardiovascular risk factors, statin treatment, and tube voltage. Results In total, 1123 coronary lesions were included in 402 patients (mean age 59.2 ± 10.1 years; 53.0% male; mean interscan interval 4.9 ± 2.4 years; 62.9% statin-treated). There was a reduction in mean per-lesion PCAT attenuation between baseline and follow-up scans (−82.1 ± 11.7 HU vs. −86.8 ± 10.0 HU; p<0.001). Per-lesion total plaque volume increased from baseline to follow-up (31.4 ± 42.4 mm³ vs. 43.4 ± 53.3 mm³), resulting from increases in volumes of CP (6.1 ± 18.2 mm³ vs. 12.7 ± 27.8 mm³) and NCP (25.3 ± 33.2 mm³ vs. 30.7 ± 36.5 mm³; all p<0.001). In adjusted models, a temporal decrease in PCAT attenuation was associated with progression of CP volume (β −0.13 per HU; 95%CI −0.20 to −0.06; p<0.001) and total plaque volume (β = −0.18 per HU; 95%CI −0.29 to −0.07; p=0.001). Meanwhile, there was a trend toward a positive association between increasing PCAT attenuation and NCP volume progression (β = 0.08; 95% CI −0.01 to 0.16; p=0.068). Conclusions In patients with stable CAD undergoing CCTA, a decreasing PCAT attenuation is associated with calcified volume progression, independently of cardiovascular risk factors and statin use. These findings support the potential use of PCAT attenuation as an imaging biomarker to monitor compositional plaque change and plaque stabilisation in response to therapies.