Characterization of Plaque Phenotypes Exhibiting an Elevated Pericoronary Adipose Tissue Attenuation: Insights from the REASSURE-NIRS Registry

Overview

Journal Int J Cardiovasc Imaging

Publisher Springer

Specialty Radiology

Date 2023 Jun 28

PMID 37380905

Authors

Satoshi Kitahara

Yu Kataoka

Hiroyuki Miura

Tatsuya Nishii

Kunihiro Nishimura

Kota Murai

Takamasa Iwai

Hideo Matama

Satoshi Honda

Masashi Fujino

Shuichi Yoneda

Kensuke Takagi

Fumiyuki Otsuka

Yasuhide Asaumi

Yusuke Fujino

Kenichi Tsujita

Rishi Puri

Stephen J Nicholls

Teruo Noguchi

Affiliations

Soon will be listed here.

Abstract

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) and NIRS/IVUS-derived plaque measures were compared in patients with PCAT attenuation ≥ and < -78.3 HU (median). Lesions with PCAT attenuation ≥ -78.3 HU exhibited a greater frequency of maxLCBI ≥ 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 ≥ 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 attenuation. Of note, while the presence of only one plaque feature did not necessarily elevate PCAT attenuation (p = 0.22), lesions harboring two or more features were significantly associated with higher PCAT attenuation. More vulnerable plaque phenotypes were observed in patients with high PCAT attenuation. Our findings suggest PCAT attenuation as the presence of profound disease substrate, which potentially benefits from anti-inflammatory agents.

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