Outcome of coronary artery aneurysms after Kawasaki disease

Akagi, Teiji; Rose, Vera; Benson, Lee; Newman, Alice; Freedom, Robert M.

doi:10.1016/s0022-3476(05)81894-3

Cited by 190 publications

(116 citation statements)

References 21 publications

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“…Every patient underwent regular echocardiography examinations, beginning during the acute stage of KD, at 2 months and 6 months after disease onset, and once a year thereafter. A CAA was identified when either the right coronary artery or the left coronary artery showed a dilated diameter of Ն3 mm in children younger than 5 years or Ն4 mm in children older than 5 years (38).…”

Section: Methodsmentioning

confidence: 99%

HLA–E gene polymorphism associated with susceptibility to kawasaki disease and formation of coronary artery aneurysms

Lin¹,

Wan²,

Wu³

et al. 2009

Arthritis & Rheumatism

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Objective. Kawasaki disease (KD) is a pediatric systemic vasculitis of unknown cause for which a genetic influence is supposed. The purpose of this study was to identify possible genetic variants in the major histocompatibility complex (MHC) region that are associated with KD and the development of coronary artery aneurysms (CAAs) in a Taiwanese population.Methods. The 168 genetic variants covering the MHC locus were analyzed in an association study of a Taiwanese cohort of 93 KD patients and 680 unrelated healthy children matched for sex and age with the study patients.Results. Eleven single-nucleotide polymorphisms (SNPs) were associated with the occurrence of KD. The SNP located at the 3 -untranslated region of HLA-E (rs2844724) was highly associated (P < 1 ؋ 10 ؊7 ). In addition, the frequency of the C allele was higher in KD patients without CAAs than in controls (P < 0.001) due to a significantly increased frequency of the CC and CT genotypes. Plasma levels of soluble HLA-E were significantly higher in KD patients than in controls regardless of the presence of CAAs. Furthermore, there was a trend toward higher plasma levels of soluble HLA-E in KD patients with the CT and TT genotypes of the HLA-E gene polymorphism.Conclusion. Our results suggest that the HLA-E gene polymorphism may play a role in the pathogenesis of KD.

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Section: Methodsmentioning

confidence: 99%

HLA–E gene polymorphism associated with susceptibility to kawasaki disease and formation of coronary artery aneurysms

Lin¹,

Wan²,

Wu³

et al. 2009

Arthritis & Rheumatism

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“…All patients met the criteria for the diagnostic guidelines of Kawasaki disease (http://www.kawasaki-disease.org/diagnostic/ index.html). A CAL was defined as the lumen diameter being at least 3 mm (4 mm in cases of the patients' age older than 5 y) or the internal diameter of one or more segments at least 1.5 times larger than that of the adjacent normal-size segments (16). Informed consent was obtained from patients or their parents.…”

Section: Methodsmentioning

confidence: 99%

Genetic Analysis of MMP Gene Polymorphisms in Patients With Kawasaki Disease

et al. 2008

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Kawasaki disease (KD) is an acute febrile disorder characterized by systemic vasculitis primarily occurring in coronary arteries. Matrix metalloproteinases (MMPs) have been considered to play pathophysiologic roles in the development of coronary artery lesions (CALs); therefore, an evaluation of the genetic contributions of the MMP genes to the development of CALs in KD patients would be beneficial for the prediction of CAL formation. We focused on the known functional single nucleotide polymorphisms (SNPs) in the MMP genes (MMP-2-735CϾT, MMP-3-1612 5A/6A, MMP-9-1562CϾT, and performed the association study between these SNPs and CAL formation in KD. The study population consisted of 44 KD patients with CALs and 92 without CALs and 175 healthy controls. As a result, allele and genotype frequencies of MMP-13-77AϾG showed significant differences between KD patients with CALs and without CALs (p ϭ 0.00989 and p ϭ 0.00551, respectively). The estimated frequencies of the G-C haplotype in the MMP-13 gene promoter were significantly lower in KD patients with CALs than in those without CALs. There was no association between other MMP genes and CAL formation. In conclusion, the genetic evaluation by association study demonstrated that the MMP-13 gene, at least in part, contributed to the development of CALs in KD. K awasaki disease (KD) is an acute febrile disorder characterized by systemic vasculitis predominantly occurring in infants and young children. Although the administration of i.v. immunoglobulin (IVIG) in the acute phase of the disease significantly reduces the development of coronary artery lesions (CALs), 2%-15% of KD patients still suffer from this complication (1,2). There is a strong inflammatory predilection for the coronary arteries, and the inflammation in subendothelial layers includes striking edema and infiltration of CD8ϩ T cells, monocytes, and macrophages with little or no fibrinoid necrosis and few polymorphonuclear cells (3). Inflammatory cells infiltrating from the lumen and from the adventitia to the media appear to mediate transmural damage to the arteries, followed by the development of coronary aneurysms.The inability to obtain affected coronary arteries has precluded a comprehensive understanding of the mechanism how the pathologic changes in the vessel wall evolve. As a substitute for pathologic evaluation of the affected tissues, the measurements of cytokines in serum and gene expression levels in peripheral blood cells were studied for the prediction of CAL formation (4). In previous studies, serum vascular endothelial growth factor (VEGF) and hepatocyte growth factor levels in patients with KD were remarkably high in the acute phase and were major risk factors for the occurrence of CALs, probably by an increasing permeability in vessels to cause vascular edema (4 -6). A significant elevation of serum matrix metalloproteinase (MMP)-9 levels and a remarkably high expression of the MMP-9 mRNA in the leukocytes were detected during the acute phase of KD (7), suggesting that MMP-9...

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“…12 Regardless of treatment methods, resolution of large coronary artery aneurysms does not seem to occur. 2,10,13,14 In addition, long-term follow-up studies suggest functional coronary artery abnormalities with significantly reduced vasodilating capability despite a relatively normal angiographic appearance of the vessels. 15,16 Agents that promote vascular remodeling have recently received a great deal of attention in the adult literature.…”

Section: Discussionmentioning

confidence: 99%

Does Abciximab Enhance Regression of Coronary Aneurysms Resulting From Kawasaki Disease?

et al. 2002

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ABSTRACT. Objective. Acute Kawasaki disease can result in the development of large coronary artery aneurysms that may persist. Abciximab, a platelet glycoprotein IIb/IIIa receptor inhibitor, is associated with resolution of thrombi and vascular remodeling in adults with acute coronary syndromes. The purpose of this study was to compare changes in aneurysm diameter at early follow-up in patients who had Kawasaki disease and received abciximab in addition to standard therapy with those who were treated with standard therapy alone.Methods. Patients with Kawasaki disease and large aneurysms were divided into 2 groups on the basis of acute therapy: 1) abciximab in addition to standard therapy and 2) standard therapy alone. Echocardiograms were reviewed for coronary aneurysms (lumen diameter 1.5 times that of the adjacent vessel). Maximum aneurysm diameter was determined during the acute/subacute phase of Kawasaki disease (<6 weeks) and at early follow-up (4 -6 months). Regression of the aneurysm was defined as a decrease in lumen diameter, and resolution was defined as normalization of the vessel.Results. Six patients had 20 aneurysms in the abciximab group, and 9 patients had 30 aneurysms in the standard therapy group. Early follow-up data were available for 19 of the 20 aneurysms in the abciximab group and 19 of the 30 aneurysms in the standard therapy group. Patients who were treated with abciximab demonstrated greater regression in aneurysm size at early follow-up than patients who were treated with standard therapy alone (percentage decrease: 41 ؎ 19% vs 17 ؎ 27%). In the abciximab group, 68% (13 of 19) of aneurysms resolved at early follow-up compared with 35% (7 of 19) in the standard therapy group.Conclusions. Patients who were treated with abciximab demonstrated greater regression in aneurysm diameter at early follow-up than patients who received standard therapy alone. These findings suggest that treatment with abciximab may promote vascular remodeling in this population and warrants further study. Pediatrics 2002;109(1). URL: http://www.pediatrics.org/ cgi/content/full/109/1/e4; Kawasaki disease, coronary artery abnormalities, abciximab.

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Outcome of coronary artery aneurysms after Kawasaki disease

Cited by 190 publications

References 21 publications

HLA–E gene polymorphism associated with susceptibility to kawasaki disease and formation of coronary artery aneurysms

HLA–E gene polymorphism associated with susceptibility to kawasaki disease and formation of coronary artery aneurysms

Genetic Analysis of MMP Gene Polymorphisms in Patients With Kawasaki Disease

Does Abciximab Enhance Regression of Coronary Aneurysms Resulting From Kawasaki Disease?

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