title: Regional myocardial perfusion and metabolism assessed by positron emission tomography in children with Kawasaki disease and significance of abnormal Q waves and their disappearance.
abstract: To clarify the significance of newly appearing abnormal Q waves and their disappearance in patients with Kawasaki disease, regional myocardial perfusion and glucose metabolism at rest in the fasting condition were assessed by positron emission tomography (PET) with 13N-ammonia and 18F-fluorodeoxyglucose (FDG), and regional wall motion by left ventriculography in regions with persistent and transient abnormal Q waves in 14 patients. PET identified 3 groups of abnormal myocardial segments: segments with hypoperfusion without increased FDG uptake, those with hypoperfusion and increased FDG uptake, and those with normal perfusion and increased FDG uptake. Almost all the segments with persistent or transient abnormal Q waves had abnormal PET findings. PET demonstrated evidence of metabolic activity in 57% of segments with persistent abnormal Q waves and 67% of those with transient abnormal Q waves. Regional wall motion, scored from 0 (normal) to 4 (dyskinesia), was not significantly different between segments with persistent and transient abnormal Q waves (2.3 +/- 1.3 vs 2.2 +/- 1.2). The persistence of abnormal Q waves on serial electrocardiograms was significantly shorter in metabolically active than in inactive segments (19 +/- 17 vs 92 +/- 27 months). In conclusion, in patients with Kawasaki disease, the new appearance of abnormal Q waves is a reliable clue to the presence of ischemic myocardial injury and a high proportion of them are associated with metabolically active myocardial regions. The disappearance of abnormal Q waves does not necessarily mean the normalization of regional myocardial perfusion, metabolism or function, and their early disappearance may imply "viability" in the associated myocardial region.
authors.affiliation: Department of Pediatrics, Kyoto University School of Medicine, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Yoshibayashi
authors.forename: N
authors.initials: N
authors.lastname: Tamaki
authors.forename: K
authors.initials: K
authors.lastname: Nishioka
authors.forename: M
authors.initials: M
authors.lastname: Matsumura
authors.forename: T
authors.initials: T
authors.lastname: Ueda
authors.forename: S
authors.initials: S
authors.lastname: Temma
authors.forename: Y
authors.initials: Y
authors.lastname: Yonekura
authors.forename: K
authors.initials: K
authors.lastname: Yamashita
authors.forename: J
authors.initials: J
authors.lastname: Konishi
authors.forename: H
authors.initials: H
authors.lastname: Mikawa
mesh_terms: D000293:Adolescent; D000641:Ammonia; D002648:Child; D002675:Child, Preschool; D017023:Coronary Angiography; D003326:Coronary Circulation / Q000502:physiology*; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D003847:Deoxyglucose / Q000031:analogs & derivatives; D004562:Electrocardiography; D005260:Female; D005462:Fluorine Radioisotopes; D019788:Fluorodeoxyglucose F18; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008297:Male; D009080:Mucocutaneous Lymph Node Syndrome / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D009590:Nitrogen Radioisotopes; D015635:Radionuclide Ventriculography; D014055:Tomography, Emission-Computed; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D005462:Fluorine Radioisotopes; D009590:Nitrogen Radioisotopes; D019788:Fluorodeoxyglucose F18; D000641:Ammonia; D003847:Deoxyglucose; D005947:Glucose