No abstract

We speculate that endothelial dysfunction in former KD patients is affected by the febrile period of the acute phase, and antiplatelet drugs may improve endothelial function. The increased arterial stiffness of patients caused by post-inflammatory fibrotic changes in the arterial wall indicates that adults with a history of KD have an increased risk of developing atherosclerosis.

Background: It remains controversial whether Kawasaki disease (KD) is a risk factor for the onset of atherosclerosis. An imbalance of peroxisome proliferator-activated receptor g (PPARg) and adiponectin appears to play a role in the onset of atherosclerosis in adults, and we therefore examined PPARg mRNA expression and adiponectin profiles in the peripheral white blood cells obtained from KD patients. Methods: A total of 50 subjects were studied: nine patients with acute KD, 20 patients with convalescent KD, and 21 age-matched controls. The gene expression of PPARg, monocyte chemoattractant protein-1, and CC chemokine receptor 2 present in the blood were quantified. The relative gene expression, adiponectin levels, and the three adiponectin isoforms were compared among the subjects. Results:The abundance of PPARg and CC chemokine receptor 2 mRNA was significantly increased in convalescent KD patients. The monocyte chemoattractant protein-1 level was also increased in convalescent KD patients. The level of high-molecular-weight adiponectin was significantly lower in convalescent patients compared to controls. The PPARg transcription levels negatively correlated with apolipoprotein A-I levels in acute KD patients. Conclusions:The transcript abundance of PPARg and low levels of high-molecular-weight adiponectin in KD patients may have important clinical implications on the development of premature atherosclerosis. Because the potential risk for developing atherosclerosis has not yet been verified, long-term observation is important, even in convalescent KD patients without coronary artery lesions.

The outcome of stent implantation for pulmonary vein stenosis (PVS) in children remains poor. Several reports describe placing drug-eluting stents to treat PVS, but their effectiveness remains unknown. In this study, three bare-metal stents (BMSs) and three sirolimus-eluting stents (SESs) were implanted in 1-month-old pigs. The pigs were killed 8 weeks later to compare in-stent stenosis rates. The extent of neointimal thickness, as measured by injury score, was significantly less in the SES group than in the BMS group (injury score 1: BMS 0.351 + or - 0.033 vs SES 0.226 + or - 0.031 mm; P < 0.01; injury score 2: BMS 1.232 + or - 0.244 vs SES 0.609 + or - 0.208 mm; P < 0.01). The pathologic findings showed confluence of inflammatory cells around the stent wires in BMS-treated areas and granuloma formation. Granuloma formation was not seen with SES. The degree of in-stent stenosis was significantly reduced in the SES group, suggesting that the use of drug-eluting stents is an effective treatment for PVS. Because of the small sample size and the considerable variation in injury scores and balloon-to-vein ratios, future studies with larger samples are necessary.

Pacemaker implantation in infants during the early postnatal period is difficult because of their small body size and susceptibility to infection. We describe the successful pacemaker implantation for complete heart block in an infant weighing 803 g.