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BACKGROUND Video-assisted thoracoscopic surgery for patent ductus arteriosus (VATS-PDA) is an alternative surgical procedure to open chest surgery, even in premature infants. This study investigated whether the timing of VATS-PDA has a prognostic impact in premature infants whose operative indication was determined according to the symptomatic PDA and the ineffectiveness of or contraindication to indomethacine therapy. METHODS We studied 49 infants born at or before 28 weeks of gestation who were admitted to the neonatal intensive care unit between January 2004 and June 2016, and who underwent VATS-PDA. The patients were divided into two groups according to median age at the time of surgery (early group, 24 infants who underwent surgery at ≤ 24 days of life; late group, 25 infants who underwent surgery at ≥ 25 days of life). RESULTS No significant differences were found in bodyweight at 30 days of age and 40 weeks of corrected gestational age between the groups. The timing of surgery did not affect the operative procedure or postoperative complications. In addition, no differences were observed between the early and late groups in terms of complications associated with prematurity, including intraventricular hemorrhage, incidence and severity of bronchopulmonary dysplasia, and necrotizing enteropathy. CONCLUSION Video-assisted thoracoscopic surgery for patent ductus arteriosus can be safely performed in premature infants without a preferential timing for the intervention, suggesting that this procedure allows for an elective basis approach after heart failure management with conservative and/or drug therapy in premature infants with PDA.

The aortic root dilation in tetralogy of Fallot (TOF) is a long-term clinical problem, because a severely dilated aorta can lead to aortic regurgitation, dissection, or rupture, which can be fatal, necessitating surgical intervention. The details of the mechanism of aortic root dilation, however, are unclear. We have shown that aortic stiffness is increased in patients with repaired TOF, and may mirror the histological abnormality of elastic fiber disruption and matrix expansion. This aortic stiffness is related closely to the aortic dilation, indicating that aortic stiffness may be a predictor of outcome of aortic dilation. Furthermore, the aortic volume overload is a very important determinant of aortic diameter in TOF patients before corrective surgery. In addition, a chromosomal abnormality and the transforming growth factor-β signaling pathway, a major contributor to aortic dilation in Marfan syndrome, also affect this mechanism. In this way, aortic dilation in TOF patients is suggested to be a multifactorial disorder. The aim of this review was therefore to clarify the mechanism of aortic dilation in TOF, focusing on recent research findings. Studies linking histopathology, mechanical properties, molecular/cellular physiology, and clinical manifestations of aortic dilation facilitate appropriate treatment intervention and improvement of long-term prognosis of TOF.

The patient was an 18-year-old man who had undergone surgical closure of ventricular septal defect at the age of 2 years. The patient was urgently hospitalized due to syncope after longstanding uneventful postoperative course, and diagnosed with atrial flutter. Echocardiography showed poor ventricular motion and markedly dilated both atriums. After termination of atrial flutter, ventricular motion improved remarkably; however, there was little improvement in heart failure. Although we suspected constrictive pericarditis, calcification observed on computed tomography was too localized to fully explain the cause of severe diastolic dysfunction. Based on the waveform of mitral annular tissue Doppler imaging, we were strongly convinced of the underlying physiology of constrictive pericarditis. Pericardial decortications markedly improved heart failure symptoms. This case emphasizes that constrictive pericarditis could be a life-threatening complication in the remote phase after congenital heart surgery. It also emphasizes the importance of functional assessment by echocardiography to identify the cause-effect relation between imaging and clinical symptoms.

Background: Many recent studies suggest that vasopressin deficiency is an important cause of catecholamine-resistant hypotension with vasodilation in adults, but little is known about vasopressin deficiency in children. Methods: To clarify the usefulness of vasopressin administration in pediatric cathecolamine-resistant hypotension with preserved ventricular contractility, urinary output and blood pressure response to vasopressin were retrospectively analyzed in 12 consecutive patients (15 instances) who were treated with vasopressin. The causes of vasodilation were central nervous system disturbance (n = 5), side-effect of drug (n = 5), and infection (n = 5). Plasma vasopressin concentration was measured six times before vasopressin administration and five times during vasopressin administration. Results: Patients were divided into four groups according to their response to vasopressin administration. In group 1 (n = 5), urinary output increased to > 3 mL/kg per h within 3 h after vasopressin administration. In group 2 (n = 4), urinary output increased to > 3 mL/kg per h from 3 to 5 h after vasopressin administration. In group 3 (n = 4), urinary output did not increase to > 3 mL/kg per min within 5 h after vasopressin administration, but systolic blood pressure increased to > 120% of the level at the time of vasopressin administration. All remaining patients were classified into group 4 (n = 3). Plasma vasopressin concentration were low considering the markedly hypotensive state in all six instances. Plasma vasopressin concentration during vasopressin administration were significantly increased compared with before administration (P

Recent studies implicate increased cGMP synthesis as a postreceptor contributor to reduced cardiac sympathetic responsiveness. Here we provide the first evidence that modulation of this interaction by cGMP-specific phosphodiesterase PDE5A is also diminished in failing hearts, providing a novel mechanism for blunted beta-adrenergic signaling in this disorder. In normal conscious dogs chronically instrumented for left ventricular pressure-dimension analysis, PDE5A inhibition by EMD82639 had modest basal effects but markedly blunted dobutamine-enhanced systolic and diastolic function. In failing hearts (tachypacing model), however, EMD82639 had negligible effects on either basal or dobutamine-stimulated function. Whole myocardium from failing hearts had 50% lower PDE5A protein expression and 30% less total and EMD92639-inhibitable cGMP-PDE activity. Although corresponding myocyte protein and enzyme activity was similar among groups, the proportion of EMD82639-inhibitable activity was significantly lower in failure cells. Immunohistochemistry confirmed PDE5A expression in both the vasculature and myocytes of normal and failing hearts, but there was loss of z-band localization in failing myocytes that suggested altered intracellular localization. Thus, PDE5A regulation of cGMP in the heart can potently modulate beta-adrenergic stimulation, and alterations in enzyme localization and reduced synthesis may blunt this pathway in cardiac failure, contributing to dampening of the beta-adrenergic response.