Key result
High pericoronary adipose tissue attenuation linked to ~4-fold higher odds of vulnerable plaque phenotypes.
Why the study?
While PCAT attenuation predicts future coronary events, plaque phenotypes exhibiting high PCAT attenuation remain to be fully elucidated.
Does high pericoronary adipose tissue (PCAT) attenuation correlate with vulnerable plaque phenotypes in patients with CAD?
Observational (n=69)
No
Does high pericoronary adipose tissue (PCAT) attenuation correlate with vulnerable plaque phenotypes in patients with CAD?
High pericoronary adipose tissue attenuation on CCTA is significantly associated with vulnerable plaque phenotypes on NIRS/IVUS, suggesting its utility as a non-invasive marker for profound disease substrate.
Hypothesis-generating for PCAT attenuation as a CCTA marker; prospective validation required before clinical adoption.
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.
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Kitahara et al. (2023) conducted an observational in Coronary artery disease (n=69). High PCAT RCA attenuation (≥ -78.3 HU) vs. Low PCAT RCA attenuation (< -78.3 HU) was evaluated on maxLCBI4mm ≥ 400 (OR 4.07, 95% CI 1.12-14.74, p=0.03). High pericoronary adipose tissue attenuation (≥ -78.3 HU) was independently associated with vulnerable plaque phenotypes, including a maximum lipid core burden index ≥ 400 (OR 4.07).
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