Characterization of plaque phenotypes exhibiting an elevated pericoronary adipose tissue attenuation: insights from the REASSURE-NIRS registry

Inflammation has been considered to promote atheroma instability. Coronary computed tomography angiography (CCTA) visualizes pericoronary adipose tissue (PCAT) attenuation, which reflects coronary artery inflammation. While PCAT attenuation has been reported to predict future coronary events, plaque phenotypes exhibiting high PCAT attenuation remains to be fully elucidated. The current study aims to characterize coronary atheroma with a greater vascular inflammation. We retrospectively analyzed culprit lesions in 69 CAD patients receiving PCI from the REASSURE-NIRS registry (NCT04864171). Culprit lesions were evaluated by both CCTA and near-infrared spectroscopy/intravascular ultrasound (NIRS/IVUS) imaging prior to PCI. PCAT attenuation at proximal RCA (PCAT(RCA)) and NIRS/IVUS-derived plaque measures were compared in patients with PCAT(RCA) attenuation ≥ and < -78.3 HU (median). Lesions with PCAT(RCA) attenuation ≥ -78.3 HU exhibited a greater frequency of maxLCBI(4mm) ≥ 400 (66% vs. 26%, p < 0.01), plaque burden ≥ 70% (94% vs. 74%, p = 0.02) and spotty calcification (49% vs. 6%, p < 0.01). Whereas positive remodeling (63% vs. 41%, p = 0.07) did not differ between two groups. On multivariable analysis, maxLCBI(4mm) ≥ 400 (OR = 4.07; 95%CI 1.12–14.74, p = 0.03), plaque burden ≥ 70% (OR = 7.87; 95%CI 1.01–61.26, p = 0.04), and spotty calcification (OR = 14.33; 95%CI 2.37–86.73, p < 0.01) independently predicted high PCAT(RCA) attenuation. Of note, while the presence of only one plaque feature did not necessarily elevate PCAT(RCA) attenuation (p = 0.22), lesions harboring two or more features were significantly associated with higher PCAT(RCA) attenuation. More vulnerable plaque phenotypes were observed in patients with high PCAT(RCA) attenuation. Our findings suggest PCAT(RCA) attenuation as the presence of profound disease substrate, which potentially benefits from anti-inflammatory agents. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10554-023-02907-w.