Ongoing vascular inflammation evaluated by 18F-fluorodeoxyglucose positron emission tomography in patients long after
Kenji Suda1,2, Nobuhiro Tahara3,4, Munehisa Bekki5
1Department of Pediatrics and Child Health, Kurume University School of Medicine, Kurume, Japan. suda_kenji@med.kurume-u.ac.jp.
Insights
Ongoing vascular inflammation persists long after Kawasaki disease (KD), particularly in patients with giant coronary artery aneurysms (gCAAs). This highlights the need for continued monitoring in severe KD cases.
Area of Science:
- Cardiovascular Medicine
- Pediatric Cardiology
- Nuclear Medicine
Background:
- Kawasaki disease (KD) can lead to coronary artery aneurysms (CAAs).
- The presence of ongoing vascular inflammation in KD patients with CAAs is not fully understood.
- Severe KD may result in giant CAAs (gCAAs).
Purpose of the Study:
- To investigate persistent vascular inflammation in patients with Kawasaki disease-associated coronary artery aneurysms (CAAs).
- To compare vascular inflammation levels between patients with giant CAAs (gCAAs) and smaller CAAs (smCAAs).
Main Methods:
- 26 KD patients (15 gCAA, 11 smCAA) underwent CT and 18F-FDG PET.
- Coronary and thoracic aorta target-to-background ratios (CaTBR, TaTBR) were measured.
- Vascular inflammation markers were correlated with CAA size and metabolic risk factors.
Main Results:
- CaTBR and TaTBR were significantly higher in gCAA patients compared to smCAA patients.
- Elevated vascular inflammation was observed even in patients without metabolic risk factors.
- Acute phase CAA size positively correlated with both CaTBR and TaTBR.
Conclusions:
- Ongoing vascular inflammation is present long after Kawasaki disease, especially in severe cases with gCAAs.
- Vascular inflammation markers correlate with initial aneurysm severity.
- These findings suggest the need for continued surveillance in KD patients with significant CAAs.
Background:
This study aimed to determine whether ongoing vascular inflammation presents in patients who had coronary artery aneurysms (CAAs) caused by Kawasaki disease (KD).
Methods:
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.
Results:
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).
Conclusions:
Ongoing vascular inflammation may present long after KD, especially in patients with severe inflammation expressed as gCAA in the acute phase.
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