Refractory chylothorax, a postoperative complication of CHD, is difficult to manage and sometimes fatal. Herein, we report the case of a 10-month-old infant with 22-mosaic trisomy and a coarctation complex, who developed refractory chylothorax after cardiac repairs and was successfully treated with midodrine, an oral alpha-1-adrenoreceptor agonist. Midodrine may be used as adjunctive therapy for postoperative refractory chylothorax.
View Article and Find Full Text PDFBackground: Intimal smooth muscle cells (SMCs) play an important role in the vasculitis caused by Kawasaki disease (KD). Lipoprotein receptor 11 (LR11) is a member of the low-density lipoprotein receptor family, which is expressed markedly in intimal vascular SMCs and secreted in a soluble form (sLR11). sLR11 has been recently identified as a potential vascular lesion biomarker.
View Article and Find Full Text PDFObjectives: The aim of this study was to characterize the range of management issues raised by adults with cardiovascular sequelae from Kawasaki disease (KD) in childhood.
Background: Aneurysms resulting from vascular inflammation associated with KD in childhood may remain clinically silent until adulthood. Adults with large aneurysms, unstable angina, or myocardial infarction following KD in childhood present unique challenges to interventional cardiologists and cardiothoracic surgeons.
Objective: Coronary artery lesions (CALs) and a risk for early onset of atherosclerosis are major concerns following Kawasaki disease (KD). Intimal smooth muscle cells (SMCs) have an important role in vascular lesions in KD. It is known that soluble LR11 (sLR11) is a novel biomarker for vascular lesions and LR11 is markedly expressed in intimal SMCs in atherosclerotic lesions.
View Article and Find Full Text PDFCoronary artery inflammation and aneurysm formation are the most common complications of Kawasaki disease (KD). Valvulitis and myocarditis are also well described and may lead to valvar regurgitation and left ventricular dysfunction. However, functional changes in the right heart have rarely been reported.
View Article and Find Full Text PDFBackgrounds: Galectin-3 (Gal-3) is a multifunctional matricellular protein associated with heart failure and cardiovascular events. Gal-3 is required for transforming growth factor-β pathway-mediated myofibroblast activation that is a key process in coronary artery aneurysm formation in Kawasaki Disease (KD). Autopsies from young adults late after KD onset (AKD) have demonstrated bridging fibrosis throughout the myocardium and arteries.
View Article and Find Full Text PDFInferior vena cava injuries are highly lethal. We experienced a case of retrohepatic inferior vena cava injury as a result of blunt trauma in a three-year-old female. Because the site of bleeding of the IVC was identified, we repaired it with running sutures.
View Article and Find Full Text PDFThe present patient was delivered at a gestational age of 27 weeks. She had abdominal bloating with symptoms of respiratory distress. We suspected Hirschsprung disease (HD) or small intestinal stricture, but examinations were not definitive.
View Article and Find Full Text PDFTwo cases of coronary aneurysm developed in the late period after Kawasaki disease (KD). Case 1 involved a 13-year-old boy who had aneurysms develop after a diagnosis of complete regression. Case 2 involved a 29-year-old man who had a new aneurysm develop after he was older than 20 years.
View Article and Find Full Text PDFAn 8-year-old boy suffered from an unconsciousness attack and torsade de pointes arrhythmia during sleep or at rest. His electrocardiogram showed prolonged QT intervals, but the T wave morphology was atypical for type 1, 2 or 3 congenital long-QT syndrome (LQTS). Intravenous epinephrine slightly prolonged the QT interval whereas mexiletine infusion shortened the QT interval.
View Article and Find Full Text PDFBackground: The second derivative of the photoplethysmogram (SDPTG) has been verified as a useful method for analyzing pulse wave form in adults; however, there have been few studies on the SDPTG in children.
Methods: We examined age-related alteration of SDPTG (study 1) and the SDPTG response to a vasodilator (study 2). The subjects in study 1 were 36 healthy children aged 0.