Focal pericoronary adipose tissue attenuation is related to plaque presence, plaque type, and stenosis severity in coronary CTA

• Type of Material: Article
• Authors: Runlei Ma, University of Groningen; Marly van Assen, Emory University; Daan Ties, University of Groningen; Gert Jan Pelgrim, University of Groningen; Randy van Dijk, University of Groningen; Grigory Sidorenkov, University of Groningen; Peter MA van Ooijen, University of Groningen; Pim van der Harst, University of Groningen; Rozemarijn Vliegenthart, University of Groningen
• Language: English
• Date: 2021-04-16
• Publisher: Springer Verlag
• Publication Version: Final Published Version
• Copyright Statement: © The Author(s) 2021
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1007/s00330-021-07882-1
• Title of Journal or Parent Work: EUROPEAN RADIOLOGY
• Volume: 31
• Issue: 10
• Start Page: 7251
• End Page: 7261
• Grant/Funding Information: The first author of this study has received funding from the China Scholarship Council (CSC).
• Keywords: Computed tomography angiography; Coronary arteries; Atherosclerosis; Adipose tissue
• Research Categories: Health Sciences, Epidemiology; Health Sciences, Radiology

Abstract

Objectives To investigate the association of pericoronary adipose tissue mean attenuation (PCATMA) with coronary artery disease (CAD) characteristics on coronary computed tomography angiography (CCTA). Methods We retrospectively investigated 165 symptomatic patients who underwent third-generation dual-source CCTA at 70kVp: 93 with and 72 without CAD (204 arteries with plaque, 291 without plaque). CCTA was evaluated for presence and characteristics of CAD per artery. PCATMA was measured proximally and across the most severe stenosis. Patient-level, proximal PCATMA was defined as the mean of the proximal PCATMA of the three main coronary arteries. Analyses were performed on patient and vessel level. Results Mean proximal PCATMA was −96.2 ± 7.1 HU and −95.6 ± 7.8HU for patients with and without CAD (p = 0.644). In arteries with plaque, proximal and lesion-specific PCATMA was similar (−96.1 ± 9.6 HU, −95.9 ± 11.2 HU, p = 0.608). Lesion-specific PCATMA of arteries with plaque (−94.7 HU) differed from proximal PCATMA of arteries without plaque (−97.2 HU, p = 0.015). Minimal stenosis showed higher lesion-specific PCATMA (−94.0 HU) than severe stenosis (−98.5 HU, p = 0.030). Lesion-specific PCATMA of non-calcified, mixed, and calcified plaque was −96.5 HU, −94.6 HU, and −89.9 HU (p = 0.004). Vessel-based total plaque, lipid-rich necrotic core, and calcified plaque burden showed a very weak to moderate correlation with proximal PCATMA. Conclusions Lesion-specific PCATMA was higher in arteries with plaque than proximal PCATMA in arteries without plaque. Lesion-specific PCATMA was higher in non-calcified and mixed plaques compared to calcified plaques, and in minimal stenosis compared to severe; proximal PCATMA did not show these relationships. This suggests that lesion-specific PCATMA is related to plaque development and vulnerability.