Ongoing vascular inflammation evaluated by 18F-fluorodeoxyglucose positron emission tomography in patients long after Kawasaki disease

• Published in: Journal of Nuclear Cardiology Vol. 30; no. 1; pp. 264 - 275
• Main Authors: Suda, Kenji, Tahara, Nobuhiro, Bekki, Munehisa, Nakamura, Tomohisa, Honda, Akihiro, Kishimoto, Shintaro, Kagiyama, Yoshiyuki, Iemura, Motofumi, Fujimoto, Kiminori, Abe, Toshi, Fukumoto, Yoshihiro
• Format: Journal Article
• Language: English
• Published: Cham Elsevier Inc 01.02.2023; Elsevier BV; Springer International Publishing; Springer Nature B.V
• Subjects: CAD; Cardiology; Imaging; Inflammation; Kawasaki disease; Medicine; Medicine & Public Health; Metabolism; Nuclear Medicine; Original Article; others; PET; Radiology; Tomography; CT; CAA; gCAA; inflammation; SUV; TBR; CAD; FDG; KD; PET; others; smCAA
• ISSN: 1071-3581; 1532-6551; 1532-6551
• DOI: 10.1007/s12350-022-03041-1

This study aimed to determine whether ongoing vascular inflammation presents in patients who had coronary artery aneurysms (CAAs) caused by Kawasaki disease (KD). Subjects were 26 patients with a history of KD; 15 had giant CAA (gCAA) ≥ 8.0 mm and 11 had smaller CAA (smCAA) < 8 mm in the acute phase. They underwent X-ray computed tomography and 18F-fluorodeoxyglucose positron emission tomography. We determined the maximum coronary target-to-background ratio (CaTBR) and the mean thoracic aorta TBR (TaTBR) in each patient. They were compared between groups, and their correlation with various variables was determined. CaTBR and TaTBR were significantly higher in gCAA than in smCAA (P < .005 for both values) and were significantly higher even in patients without any metabolic risk factor (P < .05 for both values). The CAA size in acute phase significantly positively correlated with CaTBR (R2 = 0.32) as well as TaTBR (R2 = 0.28). Also, TaTBR significantly positively correlated with CaTBR (R2 = 0.32) as well as cumulative number of metabolic risk factors (trend, P = .03). Ongoing vascular inflammation may present long after KD, especially in patients with severe inflammation expressed as gCAA in the acute phase.