Association Between Changes in Perivascular Adipose Tissue Density and Plaque Progression.
Adipose Tissue
/ diagnostic imaging
Aged
Computed Tomography Angiography
/ methods
Coronary Angiography
/ methods
Coronary Artery Disease
/ diagnostic imaging
Coronary Vessels
/ diagnostic imaging
Disease Progression
Female
Humans
Inflammation
/ pathology
Lipids
Male
Middle Aged
Plaque, Atherosclerotic
Predictive Value of Tests
Prospective Studies
coronary artery atherosclerosis
coronary artery disease
coronary computed tomography angiography
perivascular adipose tissue
vessel inflammation
Journal
JACC. Cardiovascular imaging
ISSN: 1876-7591
Titre abrégé: JACC Cardiovasc Imaging
Pays: United States
ID NLM: 101467978
Informations de publication
Date de publication:
10 2022
10 2022
Historique:
received:
19
08
2021
revised:
11
04
2022
accepted:
19
04
2022
entrez:
6
10
2022
pubmed:
7
10
2022
medline:
12
10
2022
Statut:
ppublish
Résumé
The association between the change in vessel inflammation, as quantified by perivascular adipose tissue (PVAT) density, and the progression of coronary atherosclerosis remains to be determined. The purpose of this study was to explore the association between the change in PVAT density and the progression of total and compositional plaque volume (PV). Patients were selected from a prospective multinational registry. Patients who underwent serial coronary computed tomography angiography studies with ≥2-year intervals and were scanned with the same tube voltage at baseline and follow-up were included. Total and compositional PV and PVAT density at baseline and follow-up were quantitatively analyzed for every lesion. Multivariate linear regression models using cluster analyses were constructed. A total of 1,476 lesions were identified from 474 enrolled patients (mean age 61.2 ± 9.3 years; 65.0% men). The mean PVAT density was -74.1 ± 11.5 HU, and total PV was 48.1 ± 83.5 mm Increase in vessel inflammation represented by PVAT density is independently associated with the progression of the lipid component of coronary atherosclerotic plaques. (Progression of AtheRosclerotic PlAque DetermIned by Computed TomoGraphic Angiography Imaging [PARADIGM]; NCT02803411).
Sections du résumé
BACKGROUND
The association between the change in vessel inflammation, as quantified by perivascular adipose tissue (PVAT) density, and the progression of coronary atherosclerosis remains to be determined.
OBJECTIVES
The purpose of this study was to explore the association between the change in PVAT density and the progression of total and compositional plaque volume (PV).
METHODS
Patients were selected from a prospective multinational registry. Patients who underwent serial coronary computed tomography angiography studies with ≥2-year intervals and were scanned with the same tube voltage at baseline and follow-up were included. Total and compositional PV and PVAT density at baseline and follow-up were quantitatively analyzed for every lesion. Multivariate linear regression models using cluster analyses were constructed.
RESULTS
A total of 1,476 lesions were identified from 474 enrolled patients (mean age 61.2 ± 9.3 years; 65.0% men). The mean PVAT density was -74.1 ± 11.5 HU, and total PV was 48.1 ± 83.5 mm
CONCLUSIONS
Increase in vessel inflammation represented by PVAT density is independently associated with the progression of the lipid component of coronary atherosclerotic plaques. (Progression of AtheRosclerotic PlAque DetermIned by Computed TomoGraphic Angiography Imaging [PARADIGM]; NCT02803411).
Identifiants
pubmed: 36202455
pii: S1936-878X(22)00250-9
doi: 10.1016/j.jcmg.2022.04.016
pii:
doi:
Substances chimiques
Lipids
0
Banques de données
ClinicalTrials.gov
['NCT02803411']
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1760-1767Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Funding Support and Author Disclosures This work was supported by the Korea Medical Device Development Fund grant funded by the Korea government (the Ministry of Science and ICT; the Ministry of Trade, Industry and Energy; the Ministry of Health and Welfare, Republic of Korea, the Ministry of Food and Drug Safety) (Project Number: 202016B02). The study was also funded in part by a grant from the Dalio Foundation. Dr Leipsic has served as a consultant for and holds stock options in HeartFlow and Circle CVI. Drs Kitslaar and Reiber are employees of Medis Medical Imaging. Dr Samady has served on the scientific advisory board of Philips; has equity interest in Covanos Inc; and has received a research grant from Medtronic. Dr Lin has received grant support from GE Healthcare. Dr Min has received funding from GE Healthcare; has served on the scientific advisory board of Arineta and GE Healthcare; and has an equity interest in and is an employee of Cleerly, Inc. Dr Chang has received funding from the Leading Foreign Research Institute Recruitment Program through the National Research Foundation (NRF) of Korea funded by the Ministry of Science and ICT (MSIT) (Grant No. 2012027176). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.