TY - JOUR
T1 - Association Between Changes in Perivascular Adipose Tissue Density and Plaque Progression
AU - Lee, Sang Eun
AU - Sung, Ji Min
AU - Andreini, Daniele
AU - Al-Mallah, Mouaz H.
AU - Budoff, Matthew J.
AU - Cademartiri, Filippo
AU - Chinnaiyan, Kavitha
AU - Choi, Jung Hyun
AU - Chun, Eun Ju
AU - Conte, Edoardo
AU - Gottlieb, Ilan
AU - Hadamitzky, Martin
AU - Kim, Yong Jin
AU - Lee, Byoung Kwon
AU - Leipsic, Jonathon A.
AU - Maffei, Erica
AU - Marques, Hugo
AU - de Araújo Gonçalves, Pedro
AU - Pontone, Gianluca
AU - Shin, Sanghoon
AU - Kitslaar, Pieter H.
AU - Reiber, Johan H.C.
AU - Stone, Peter H.
AU - Samady, Habib
AU - Virmani, Renu
AU - Narula, Jagat
AU - Berman, Daniel S.
AU - Shaw, Leslee J.
AU - Bax, Jeroen J.
AU - Lin, Fay Y.
AU - Min, James K.
AU - Chang, Hyuk Jae
N1 - Publisher Copyright:
© 2022 American College of Cardiology Foundation
PY - 2022/10
Y1 - 2022/10
N2 - 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 mm3 (19.2 ± 44.8 mm3 of calcified PV and 28.9 ± 51.0 mm3 of noncalcified PV). On multivariate analysis (adjusted for clinical risk factors, medication use, change in lipid levels, total PV at baseline, luminal HU attenuation, location of lesions, and tube voltage), the increase in PVAT density was positively associated with the progression of total PV (estimate = 0.275 [95% CI: 0.004-0.545]; P = 0.047), driven by the association with fibrous PV (estimate = 0.245 [95% CI: 0.070-0.420]; P = 0.006). Calcified PV progression was not associated with the increase in PVAT density (P > 0.050). Conclusions: Increase in vessel inflammation represented by PVAT density is independently associated with the progression of the lipid component of coronary atherosclerotic plaques.
AB - 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 mm3 (19.2 ± 44.8 mm3 of calcified PV and 28.9 ± 51.0 mm3 of noncalcified PV). On multivariate analysis (adjusted for clinical risk factors, medication use, change in lipid levels, total PV at baseline, luminal HU attenuation, location of lesions, and tube voltage), the increase in PVAT density was positively associated with the progression of total PV (estimate = 0.275 [95% CI: 0.004-0.545]; P = 0.047), driven by the association with fibrous PV (estimate = 0.245 [95% CI: 0.070-0.420]; P = 0.006). Calcified PV progression was not associated with the increase in PVAT density (P > 0.050). Conclusions: Increase in vessel inflammation represented by PVAT density is independently associated with the progression of the lipid component of coronary atherosclerotic plaques.
KW - coronary artery atherosclerosis
KW - coronary artery disease
KW - coronary computed tomography angiography
KW - perivascular adipose tissue
KW - vessel inflammation
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U2 - 10.1016/j.jcmg.2022.04.016
DO - 10.1016/j.jcmg.2022.04.016
M3 - Article
C2 - 36202455
AN - SCOPUS:85138408377
SN - 1936-878X
VL - 15
SP - 1760
EP - 1767
JO - JACC: Cardiovascular Imaging
JF - JACC: Cardiovascular Imaging
IS - 10
ER -