Histopathological characteristics of myocarditis in acute‐phase Kawasaki disease

Harada, M; Yokouchi, Yuki; Oharaseki, Toshiaki; Matsui, Kotoko; Tobayama, Hisako; Tanaka, Noboru; Akimoto, Katsumi; Takahashi, Ken; Kishiro, Masahiko; Shimizu, Toshiaki; Takahashi, Kei

doi:10.1111/j.1365-2559.2012.04332.x

Cited by 89 publications

(89 citation statements)

References 17 publications

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“…Myocarditis in KD likely improves rapidly as the inflammatory process subsides because it results from interstitial edema and inflammation and only rarely from myocardial cell necrosis. 73,122 Infrequently, acute myocardial inflammation is associated with overt ventricular ectopy, although recent information indicates more common repolarization impact than may be clinically apparent (see Long-Term Management, Arrhythmias). The exception to the more typical short-term impact of mild myocarditis in KD is the KD shock syndrome.…”

mentioning

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

2,606

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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mentioning

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

2,606

4,124

View full text Add to dashboard Cite

show abstract

“…Of the more than 200 subjects studied by different investigators, approximately one-third also had changes of myocardial fibrosis. Harada et al conducted histological studies of myocardial tissues from 29 KD patients who died within 40 days from KD onset and included eight cases with no evidence of CAA [3], inflammatory cell infiltration in the myocardium was seen in all cases. From our histologic study of the myocardium from patients who had a history of KD but who died from non-cardiac causes, we observed neither myocardial fibrosis nor Gal-3 expression with the exception of Case N-1 who died of sepsis and had infiltrating inflammatory cells expressing Gal-3.…”

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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“…RVSV was determined as the longed myocarditis due to Kawasaki disease. 4 All patients were diagnosed as anatomically normal with normal RV and left ventricular (LV) function after a complete examination. In patients who complained of chest pain, the causes of chest pain were confirmed to be non-cardiac origin such as intercostal neuralgia on complete medical examination.…”

Section: Rv/lv Diameter Ratiomentioning

confidence: 99%

Alternation of Right Ventricular Contraction Pattern in Healthy Children

Hashimoto

Watanabe

2014

Circ J

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Histopathological characteristics of myocarditis in acute‐phase Kawasaki disease

Abstract: In KD, myocarditis develops even earlier than epicardial coronary arteritis; it peaks by disease day 10 and then disappears gradually after day 20. The myocarditis is distributed unevenly, ranging from the entire heart to the epicardial layer of the base of the heart.

Cited by 89 publications

References 17 publications

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

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

Alternation of Right Ventricular Contraction Pattern in Healthy Children

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