OBJECTIVE: Kawasaki disease (KD) is a diffuse necrotizing vasculitis with predominant involvement of coronary arteries. Endothelial dysfunction has been implicated as an important event in the pathogenesis of arteriosclerosis, coronary vasoconstriction, hypertension, and myocardial ischemia. We examined the presence of endothelial dysfunction in North Indian children (of Caucasoid ethnicity) with KD without overt coronary artery involvement. METHODS: Twenty children (mean age 8.4+/-2.3 years; range 4.5-12.1 years) in the convalescent phase of KD were studied. All had received intravenous immunoglobulin during the acute phase of the disease. The interval between acute episode and enrolment ranged from 3 to 78 months (mean 25.3+/-20.1 months). High-resolution ultrasonography was used to analyze brachial artery responses to reactive hyperemia (with increased flow causing endothelium-dependent dilatation) and sublingual nitroglycerine (causing endothelium-independent dilatation). Flow-mediated dilatation was also studied in an equal number of healthy age- and sex-matched controls. Carotid artery stiffness index (SI) was calculated and compared in all subjects using previously published equations. RESULTS: Significant differences were observed between the percent flow mediated dilatation in children with KD (5.7+/-9.2%) compared with controls (12.2+/-8.9%, p=0.017). Sublingual nitroglycerine-mediated dilatation in children with KD was 28.5+/-12.3%. Carotid artery SI was higher in children with KD (2.81+/-0.77 U) when compared to controls (2.32+/-0.80 U), but it failed to meet statistical significance (p=0.058). CONCLUSION: Brachial arteries of children with KD show evidence of endothelial dysfunction. This may point towards possibility of preclinical arteriosclerosis in children with KD even in the absence of coronary artery abnormalities.
OBJECTIVE:Kawasaki disease (KD) is a diffuse necrotizing vasculitis with predominant involvement of coronary arteries. Endothelial dysfunction has been implicated as an important event in the pathogenesis of arteriosclerosis, coronary vasoconstriction, hypertension, and myocardial ischemia. We examined the presence of endothelial dysfunction in North Indian children (of Caucasoid ethnicity) with KD without overt coronary artery involvement. METHODS: Twenty children (mean age 8.4+/-2.3 years; range 4.5-12.1 years) in the convalescent phase of KD were studied. All had received intravenous immunoglobulin during the acute phase of the disease. The interval between acute episode and enrolment ranged from 3 to 78 months (mean 25.3+/-20.1 months). High-resolution ultrasonography was used to analyze brachial artery responses to reactive hyperemia (with increased flow causing endothelium-dependent dilatation) and sublingual nitroglycerine (causing endothelium-independent dilatation). Flow-mediated dilatation was also studied in an equal number of healthy age- and sex-matched controls. Carotid artery stiffness index (SI) was calculated and compared in all subjects using previously published equations. RESULTS: Significant differences were observed between the percent flow mediated dilatation in children with KD (5.7+/-9.2%) compared with controls (12.2+/-8.9%, p=0.017). Sublingual nitroglycerine-mediated dilatation in children with KD was 28.5+/-12.3%. Carotid artery SI was higher in children with KD (2.81+/-0.77 U) when compared to controls (2.32+/-0.80 U), but it failed to meet statistical significance (p=0.058). CONCLUSION: Brachial arteries of children with KD show evidence of endothelial dysfunction. This may point towards possibility of preclinical arteriosclerosis in children with KD even in the absence of coronary artery abnormalities.