Evidence of endothelial damage in acute KD

Although the cause of Kawasaki disease (KD) is unknown, endothelial dysfunction is a key event in atherogenesis associated with KD. Systemic endothelial dysfunction in KD in reflected by flow-mediated dilation of the brachial artery, particularly in children with coronary artery lesions. Nitric oxide has a key role in maintaining the vascular wall, especially endothelial cells. Nitric oxide synthase (NOS) function is disrupted in patients with KD, and a genetic link exists in the form of NOS gene polymorphisms. Levels of endothelial microparticles, circulating markers of endothelial cell damage, are significantly higher during acute KD and lower during convalescence of KD. Levels of endothelial progenitor cells, which contribute to endothelial repair and neovascularization, are lower in KD patients with coronary artery lesions. These measures of endothelial function yield important evidence regarding vascular biology in KD and may help uncover the mechanisms of and new therapies for KD.