Histopathological study on Kawasaki disease with special reference to the relation between the myocardial sequelae and regional wall motion abnormalities of the left ventricle.

Yonesaka, Susumu; Takahashi, Toru; Matubara, Toru; Nakada, Toshimasa; Furukawa, H; Tomimoto, Kazuhiko; Oura, Hiroaki

doi:10.1253/jcj.56.352

Cited by 29 publications

(16 citation statements)

References 8 publications

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“…The inflammatory process began in the adventitia and was accentuated in the microvasculature, especially the capillaries. This is identical with the early histopathological changes seen in human KD, with initiation of the inflammatory process in the adventitia with involvement of the vasovasorum (55)(56)(57)(58)(59). Coronary inflammation continued, with maximum cellular infiltrates at day 28 post-LCWE injection (Fig.…”

Section: Persistent Inflammatory Infiltrate In Affected Cardiac Tissuesupporting

confidence: 79%

Presence of IFN-γ Does Not Indicate Its Necessity for Induction of Coronary Arteritis in an Animal Model of Kawasaki Disease

Chan

Duong

Yeung

2004

The Journal of Immunology

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Kawasaki disease is the most common cause of vasculitis affecting children, and the leading cause of acquired heart disease in the developed world. To date, studies on the role of IFN-γ in the pathogenesis of Kawasaki disease have focused on peripheral production of IFN-γ, and have yielded conflicting results. Affected heart tissue is not available from children with Kawasaki disease. In this study, we use an animal model of Kawasaki disease, Lactobacillus casei cell wall extract (LCWE)-induced coronary arteritis, to examine the role of IFN-γ in the development of coronary artery lesions. We report the presence of IFN-γ, both at the mRNA and protein levels, in the affected vessels. Its biphasic expression, first at days 3–7 and again at days 28–42 post-LCWE injection, corresponds to the first appearance of inflammatory infiltrate in coronary arteries, and later to vascular wall disruption and aneurysm formation, respectively. Interestingly, ablation of IFN-γ expression did not dampen the inflammatory response, and IFN-γ-deficient lymphocytes proliferated more vigorously in response to LCWE than those of wild-type animals. Of more importance, the incidence of coronary arteritis was the same in IFN-γ-deficient and wild-type mice. Taken together, our findings demonstrate that IFN-γ regulates the immune response during development of coronary arteritis, but is not required for the induction of coronary artery disease.

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Section: Persistent Inflammatory Infiltrate In Affected Cardiac Tissuesupporting

confidence: 79%

Presence of IFN-γ Does Not Indicate Its Necessity for Induction of Coronary Arteritis in an Animal Model of Kawasaki Disease

Chan

Duong

Yeung

2004

The Journal of Immunology

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“…Early biopsy studies suggested the presence of myocardial abnormalities, but the relationship to the acute illness and coronary artery abnormalities was unclear. [294][295][296] In a more recent study of 16 patients with giant aneurysms, initial biopsy samples showed myocyte degeneration, hypertrophy, and inflammatory cell infiltration, whereas follow-up biopsy specimens showed myocyte disarray, interstitial fibrosis, and ongoing inflammatory cell infiltration. 297 The pathogenesis of the abnormalities was not clear, but the sites of the aneurysms were not related to the biopsy findings.…”

Section: Myocardial Abnormalitiesmentioning

confidence: 99%

Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease: A Scientific Statement for Health Professionals From the American Heart Association

McCrindle¹,

Rowley²,

Newburger³

et al. 2017

Circulation

2,863

4,124

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BACKGROUND:Kawasaki disease is an acute vasculitis of childhood that leads to coronary artery aneurysms in ≈25% of untreated cases. It has been reported worldwide and is the leading cause of acquired heart disease in children in developed countries. METHODS AND RESULTS:To revise the previous American Heart Association guidelines, a multidisciplinary writing group of experts was convened to review and appraise available evidence and practice-based opinion, as well as to provide updated recommendations for diagnosis, treatment of the acute illness, and long-term management. Although the cause remains unknown, discussion sections highlight new insights into the epidemiology, genetics, pathogenesis, pathology, natural history, and longterm outcomes. Prompt diagnosis is essential, and an updated algorithm defines supplemental information to be used to assist the diagnosis when classic clinical criteria are incomplete. Although intravenous immune globulin is the mainstay of initial treatment, the role for additional primary therapy in selected patients is discussed. Approximately 10% to 20% of patients do not respond to initial intravenous immune globulin, and recommendations for additional therapies are provided. Careful initial management of evolving coronary artery abnormalities is essential, necessitating an increased frequency of assessments and escalation of thromboprophylaxis. Risk stratification for long-term management is based primarily on maximal coronary artery luminal dimensions, normalized as Z scores, and is calibrated to both past and current involvement. Patients with aneurysms require life-long and uninterrupted cardiology follow-up. CONCLUSIONS:These recommendations provide updated and best evidence-based guidance to healthcare providers who diagnose and manage Kawasaki disease, but clinical decision making should be individualized to specific patient circumstances. K awasaki disease (KD) is an acute, self-limited febrile illness of unknown cause that predominantly affects children <5 years of age. When initially described, the potential for coronary artery complications was not appreciated. KD is now the most common cause of acquired heart disease in children in developed countries. In the absence of pathognomonic tests, the diagnosis continues to rest on the identification of principal clinical findings and the exclusion of other clinically similar entities with known causes. Timely initiation of treatment with intravenous immunoglobulin (IVIG) has reduced the incidence of coronary artery aneurysms defined from absolute luminal dimensions from 25% to ≈4%. Ongoing studies with additional therapies have not substantially reduced this residual risk. The long-term prognosis is determined by the initial and current level of coronary artery involvement. Certain subsets of patients are at risk for myocardial ischemia from coronary artery thrombosis and stenoses. Medical management of such patients hinges on judicious use of thromboprophylaxis and vigilance to identify evolving stenoses. Invasive revascul...

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“…Our adult KD data suggest that these levels do, in fact, normalize in patients without giant aneurysms at some time point beyond one year. Multiple studies of endomyocardial biopsies have documented that myocardial inflammation is a universal feature of acute KD [4,5]. Of the more than 200 subjects studied by different investigators, approximately one-third also had changes of myocardial fibrosis.…”

Section: Discussionmentioning

confidence: 99%

“…Thrombosis of these aneurysms or stenosis due to luminal myofibroblastic proliferation can lead to myocardial infarction, ischemic heart disease, or sudden death. Myocarditis is associated with coronary artery vasculitis in the majority of KD cases based on histologic studies of autopsies and endomyocardial biopsies [3][4][5]. Emerging recognition of the long-term significance of myocardial fibrosis in young adults following KD is based largely on case reports from cardiac transplantation and small series of autopsy cases [6].…”

mentioning

confidence: 99%

Galectin-3 is a marker of myocardial and vascular fibrosis in Kawasaki disease patients with giant aneurysms

Numano

Shimizu

Jimenez-Fernandez

et al. 2015

International Journal of Cardiology

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Histopathological study on Kawasaki disease with special reference to the relation between the myocardial sequelae and regional wall motion abnormalities of the left ventricle.

Cited by 29 publications

References 8 publications

Presence of IFN-γ Does Not Indicate Its Necessity for Induction of Coronary Arteritis in an Animal Model of Kawasaki Disease

Presence of IFN-γ Does Not Indicate Its Necessity for Induction of Coronary Arteritis in an Animal Model of Kawasaki Disease

Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease: A Scientific Statement for Health Professionals From the American Heart Association

Galectin-3 is a marker of myocardial and vascular fibrosis in Kawasaki disease patients with giant aneurysms

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