PET/CT evaluation of ^sup 18^F-FDG uptake in pericoronary adipose tissue in patients with stable coronary artery disease: Independent predictor of atherosclerotic lesions' formation?

Background Inflammatory infiltrations in EAT which releases inflammatory cytokines correspond anatomically to the atheromatous plaques in underlying coronary vessels. However, it is unknown whether inflammatory activity of pericoronary adipose tissue (PCAT) promotes coronary atherosclerosis. Methods...

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Published inJournal of nuclear cardiology Vol. 24; no. 3; p. 1075
Main Authors Mazurek, Tomasz, Kobylecka, Magorzata, Zielenkiewicz, Magdalena, Kurek, Aleksandra, Kochman, Janusz, Filipiak, Krzysztof J, Mazurek, Krzysztof, Huczek, Zenon, Królicki, Leszek, Opolski, Grzegorz
Format Journal Article
LanguageEnglish
Published New York Springer Nature B.V 01.06.2017
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Abstract Background Inflammatory infiltrations in EAT which releases inflammatory cytokines correspond anatomically to the atheromatous plaques in underlying coronary vessels. However, it is unknown whether inflammatory activity of pericoronary adipose tissue (PCAT) promotes coronary atherosclerosis. Methods and Results 35 non-diabetic patients with confirmed CAD and 35 non-CAD controls matched for age and BMI underwent 18F-FDG-PET/CT. Maximal SUV normalized by LA blood activity was measured on the sections corresponding to the respective coronaries (RCA, LCX, LAD), as well, as in subcutaneous fat, visceral fat, and epicardial fat. Extent of CAD was determined by % stenosis in segments corresponding to 18F-FDG-PET/CT sections in coronarography using quantitative coronary analysis. PCAT SUV was significantly greater than SUV in other fat locations, as well as PCAT SUV in the controls. In CAD patients with BMI >25, PCAT SUV was positively related to % stenosis of a respective coronary artery (RCA: 0.43; P < .05; LCX 0.58; P < .05; LAD 0.65; P < .05). PCAT SUV was the only independent predictor of coronary stenosis of LAD and RCA. Conclusions Inflammatory activity of PCAT is greater than in other fat locations, in CAD is greater than in non-CAD controls, and is independently associated with coronary stenosis. In overweight patients, PCAT SUV correlates with the extent of CAD.
AbstractList Background Inflammatory infiltrations in EAT which releases inflammatory cytokines correspond anatomically to the atheromatous plaques in underlying coronary vessels. However, it is unknown whether inflammatory activity of pericoronary adipose tissue (PCAT) promotes coronary atherosclerosis. Methods and Results 35 non-diabetic patients with confirmed CAD and 35 non-CAD controls matched for age and BMI underwent 18F-FDG-PET/CT. Maximal SUV normalized by LA blood activity was measured on the sections corresponding to the respective coronaries (RCA, LCX, LAD), as well, as in subcutaneous fat, visceral fat, and epicardial fat. Extent of CAD was determined by % stenosis in segments corresponding to 18F-FDG-PET/CT sections in coronarography using quantitative coronary analysis. PCAT SUV was significantly greater than SUV in other fat locations, as well as PCAT SUV in the controls. In CAD patients with BMI >25, PCAT SUV was positively related to % stenosis of a respective coronary artery (RCA: 0.43; P < .05; LCX 0.58; P < .05; LAD 0.65; P < .05). PCAT SUV was the only independent predictor of coronary stenosis of LAD and RCA. Conclusions Inflammatory activity of PCAT is greater than in other fat locations, in CAD is greater than in non-CAD controls, and is independently associated with coronary stenosis. In overweight patients, PCAT SUV correlates with the extent of CAD.
Author Kurek, Aleksandra
Filipiak, Krzysztof J
Królicki, Leszek
Mazurek, Tomasz
Zielenkiewicz, Magdalena
Kochman, Janusz
Opolski, Grzegorz
Huczek, Zenon
Kobylecka, Magorzata
Mazurek, Krzysztof
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SubjectTerms Atherosclerosis
Cardiovascular disease
Coronary vessels
Title PET/CT evaluation of ^sup 18^F-FDG uptake in pericoronary adipose tissue in patients with stable coronary artery disease: Independent predictor of atherosclerotic lesions' formation?
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