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Clinical and Histopathological Studies in Children with Giant Coronary Aneurysm of Long-standing Kawasaki Disease with Special Reference to Myocardial Changes Susumu Yonesaka 1 , Toru Takahashi 2 , Sumito Sato 2 , Shuji Eto 2 , Kota Ichinose 2 , Makoto Koda 2 , Katuki Otani 2 , Takumi Sato 2 , Manabu Kinjo 2 1Division of Internal Medicine, Chousei Municipal Hospital 23rd Department of Internal Medicine, Chiba University School of Medicine Keyword: 川崎病 , 心筋生検 , 巨大冠動脈瘤 , Kawasaki disease , endomyocardial biopsy , giant coronary artery aneurysm pp.809-815
Published Date 2001/8/15
DOI https://doi.org/10.11477/mf.1404902336
  • Abstract
  • Look Inside

 Since Kawasaki disease (KD) was first reported 30 years ago. many studies focused on coronary arterial lesions (CAL) have been reported, but there have been only a few reports of pathological studies on myocardial after-effects of KD using endomyocardial biopsy (EMB).

 With this in mind, we attempted to investigate the long-standing myocardial abnormalities and the relationship between CAI and myocardial damage by serial coronary arteriography and EMB in patients with KD.

 Their ages ranged from 6 months to 11 years and 6months in the first study, 6 years and 1 monh to 19 years in the subsequent study. and the male to female ratio was 14 : 5 in 19 patients with G-AN.

 The interval between the first study and the second one was more than 2 years and 6 months. Epicardial coronary arterial lesions were analyzed semiquantatively with MIPRONTRM and histopathology using histomorphometric methods to calculate the percent area of myocytes, fibrous tissue and fatty tissue and small vessel changes.

 In the subsequent study, progression of CAL was noticed in 21%, unchanged condition in 63% and regression in 16%. Myocardial changes of second EMB in patients treated with intravenous high dose γ-globulin treatment were fibrosis in 100%, degeneration in 57%. One of the cases with KD, who had CAL, revealed massive inflammatory cell infiltration and mvocvtolysisin the subsequent study performed 7 years, after onset, which suggested chronic myocarditis.

 Myocardial changes in patients with G-AN were relatively mild when viewed on light microscope, but still remained and there were ultrastructural changes such as microangiopathy in the late stage without relation to γ-globulin administration. The relatively high incidence of myocardial damage in KD with G-AN might possibly result in a cardiomyopathy-like state over a long-term period. Further approaches are mandatory to clarify the significance of the myocardial sequelae of KD with close attention not only to CAL but also to the myocardial changes in long-standing cases of the disease.


Copyright © 2001, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 1882-1200 印刷版ISSN 0452-3458 医学書院

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