Lee, Sang-Eun; Sung, Ji Min; Andreini, Daniele; Al-Mallah, Mouaz H; Budoff, Matthew J; Cademartiri, Filippo; Chinnaiyan, Kavitha; Choi, Jung Hyun; Chun, Eun Ju; Conte, Edoardo; Gottlieb, Ilan; Hadamitzky, Martin; Kim, Yong Jin; Lee, Byoung Kwon; Leipsic, Jonathon A; Maffei, Erica; Marques, Hugo; de Araújo Gonçalves, Pedro; Pontone, Gianluca; Shin, Sanghoon; Kitslaar, Pieter H; Reiber, Johan H C; Stone, Peter H; Samady, Habib; Virmani, Renu; Narula, Jagat; Berman, Daniel S; Shaw, Leslee J; Bax, Jeroen J; Lin, Fay Y; Min, James K; Chang, Hyuk-Jae     «

Lee, Sang-Eun; Sung, Ji Min; Andreini, Daniele; Al-Mallah, Mouaz H; Budoff, Matthew J; Cademartiri, Filippo; Chinnaiyan, Kavitha; Choi, Jung Hyun; Chun, Eun Ju; Conte, Edoardo; Gottlieb, Ilan; Hadamitzky, Martin; Kim, Yong Jin; Lee, Byoung Kwon; Leipsic, Jonathon A; Maffei, Erica; Marques, Hugo; de Araújo Gonçalves, Pedro; Pontone, Gianluca; Shin, Sanghoon; Kitslaar, Pieter H; Reiber, Johan H C; Stone, Peter H; Samady, Habib; Virmani, Renu; Narula, Jagat; Berman, Daniel S; Shaw, Leslee J; Bax, J...     »

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. (Progression of AtheRosclerotic PlAque DetermIned by Computed TomoGraphic Angiography Imaging [PARADIGM]; NCT02803411).      «

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...     »