Kaiyu Tao

Perventricular Device Closure of Ventricular Septal Defects: Six Months Results in 30 Young Children

BACKGROUND Both surgical repair and transcatheter closure of isolated ventricular septal defects are known to have limitations in children. This report describes the short-term results of perventricular device closure of nonmuscular ventricular septal defects without cardiopulmonary bypass in young children. METHODS Thirty patients who had nonmuscular ventricular septal defects underwent perventricular closure by minimally invasive technique without cardiopulmonary bypass. A subxiphoid minimally invasive incision was performed. Under the continuous guidance of transesophageal echocardiography, the free wall of the right ventricle was punctured and a guidewire was introduced into the left ventricle through the defect. A delivery sheath was advanced over the wire and through the defect into the left ventricle. The device was released. RESULTS Closure was successful in 27 patients (90%). There was no mortality or atrioventricular block perioperatively or during the entire follow-up period. Three patients developed incomplete right bundle branch blocks and seven patients developed new trace or mild tricuspid regurgitation after the closure. The mean hospital stay was 3.6 +/- 0.7 days (range, 3 to 5 days) and no patient needed any blood or blood products. Follow-up at 6 months showed that two of the three patients had persistent incomplete right bundle branch block and three of the seven patients had persistent closure-related trace or mild tricuspid regurgitation. CONCLUSIONS Perventricular device closure of isolated ventricular septal defects without cardiopulmonary bypass appeared to be safe and efficacious in selected young children. The outcomes of short-term follow-up are acceptable.

Perventricular device closure of perimembranous ventricular septal defects in 61 young children: Early and midterm follow-up results

OBJECTIVES Perventricular device closure of perimembranous ventricular septal defect as a novel technique has recently been described in several small series with initial experience. Further studies with larger cohorts and longer-term follow-up are needed to confirm the validity of this new approach. This report describes our recent experience with perventricular device closure of perimembranous ventricular septal defects on beating hearts in 61 young children with over 1 year of follow-up. METHODS Between April 2007 and April 2008, 61 patients with perimembranous ventricular septal defects were enrolled for a prospective study of perventricular device closure of their defects. The hospital course and the immediate and midterm complications during follow-up were herein reported. RESULTS The defects were closed successfully with devices in 57 (93.4%) patients without mortality or major morbidity. Four (6.6%) patients were converted to surgical repair when device closure was deemed unsuccessful; the failure of device closure was associated with the subaortic rim (odds ratio = 21.471; P = .038). Residual shunt was observed in 4 (6.6%) patients during the procedure. One of them was converted into surgical repair, and the residual shunt of the other 3 resolved during the 6-month follow-up period. Two (3.3%) patients had complete atrioventricular block develop in the operating room or during follow-up. One was converted into surgical repair and the other patient converted to sinus rhythm after treatment with steroids. CONCLUSIONS Perventricular device closure of ventricular septal defect is a safe and efficacious treatment option with acceptable midterm outcomes. For infants with poor vascular access, it might be the procedure of choice.

Perventricular device closure of muscular ventricular septal defects on beating hearts: Initial experience in eight children

OBJECTIVE The conventional surgical repair and transcatheter closure of muscular ventricular septal defects are known to have undesirable limitations. This communication describes the short-term results of perventricular device closure of muscular ventricular septal defects with the heart beating in 8 children with 15 muscular ventricular septal defects, with or without other congenital malformations. METHODS A subxiphoid minimally invasive incision was used in 3 children with isolated muscular ventricular septal defects whereas standard full median sternotomies were used in the other 5 children who required subsequent correction of coexisting malformations. Under the continuous guidance of transesophageal echocardiography, the free wall of the right ventricle was punctured, and a guidewire was introduced into the left ventricle through the defect. A delivery sheath was advanced over the wire and through the defect into the left ventricle. The device was released. RESULTS A total of 14 muscular ventricular septal defects were successfully closed perventricularly without cardiopulmonary bypass. There was no mortality perioperatively or during the entire follow-up period. At 6-month follow-up, there was no detectable residual shunt, arrhythmia, or new mitral or tricuspid insufficiency. Other than 5 children with the coexisting malformations, none of the other children required any blood or blood products. The average hospital stay was 7.9 +/- 2.2 days (range, 5-11 days). CONCLUSION Perventricular device closure of muscular ventricular septal defects with or without coexisting congenital malformations appeared to be safe and efficacious. The outcomes of short-term follow-up are acceptable.

Actin Filament Reorganization Is a Key Step in Lung Inflammation Induced by Systemic Inflammatory Response Syndrome

Acute lung injury (ALI) induced by systemic inflammatory response syndrome (SIRS) is characterized by deterioration in pulmonary function and leukocyte-associated lung inflammation. Actin fragment (F-actin) reorganization is required for leukocyte activation, adhesion, and transcription of inflammatory factors. We tested the hypothesis that F-actin plays a central role in SIRS-induced ALI. ALI was produced in a rat model with extracorporeal circulation. Cytochalasin B (CB) pretreatment to block F-actin reorganization improved oxygenation and reduced BAL inflammatory factors and pulmonary neutrophil sequestration, but did not reduce the adhesive molecules of blood leukocytes. We challenged blood neutrophils with TNF-α in vitro to explore the underlying mechanisms. Upon activation, neutrophils became polarized and formed a protrusive leading edge, with an aggregation of CD11b molecules. This effect could be blocked by CB, leading to reduced neutrophil adhesion. In addition, after LPS challenge, we observed F-actin reorganization and the up-regulation of inflammatory factors in pulmonary monocytes, which could also be blocked by CB pretreatment. F-actin reorganization initiates lung inflammation via increased blood neutrophil adhesion and migration, and by the production of inflammatory factors by pulmonary monocytes. Thus, blocking F-actin reorganization may potentially prevent and treat SIRS-induced ALI.

Modified Cavoatrial Anastomosis in Warden Procedure

The Warden procedure was introduced for surgical repair of partial anomalous pulmonary venous connection to the higher portion of the superior vena cava in an attempt to decrease the incidence of postoperative sinoatrial node dysfunction and pulmonary venous obstruction. However, postoperative cavoatrial channel stenosis and obstruction up to 20% and 10%, respectively, requiring catheter intervention has been reported. In this article, we describe a modified cavoatrial anastomotic technique to avoid postprocedural superior vena cava stenosis.

Which is better to preserve pulmonary function: Short-term or prolonged leukocyte depletion during cardiopulmonary bypass?

OBJECTIVES Neutrophils are crucial in the development of acute lung injuries during cardiopulmonary bypass. However, the efficacy of leukocyte depletion on pulmonary protection remains controversial, possibly owing to different filtration strategies used in the literature. In this study, we investigated whether short-term leukocyte depletion strategy is more efficacious than prolonged leukocyte depletion in preserving pulmonary function. METHODS Eighteen adult dogs were randomized equally into 3 groups. Leukocyte-depleting filters were used for 10 minutes in the LD-S group, throughout cardiopulmonary bypass in the LD-T group, and not used in the control group. Neutrophil counts, elastase, and interleukin-8 concentrations in plasma, myeloperoxidase and interleukin-8 concentrations in pulmonary tissue, and pulmonary vascular resistance and oxygen index were determined to evaluate the inflammatory response and damage to pulmonary function. RESULTS Although the neutrophil count and pulmonary parenchymal myeloperoxidase contents were significantly lower in both LD-S and LD-T groups than that in the control group, lower pulmonary parenchymal interleukin-8 level, lower pulmonary vascular resistance (113 +/- 33 dyne x s/cm(5)), higher oxygen index (366 +/- 82.3 mm Hg), and thinner alveolus wall thickness were seen only in the LD-S group, and the pulmonary parenchymal interleukin-8 levels were also lower in the LD-S group after cardiopulmonary bypass. The plasma elastase and interleukin-8 levels were significantly lower in the LD-S group, but they were significantly higher in the LD-T group compared with the control group after cardiopulmonary bypass. CONCLUSIONS Short-term rather than prolonged leukocyte depletion during cardiopulmonary bypass appears to be more efficacious in protecting pulmonary function via attenuation of the extracorporeal circulation-induced inflammatory response.

Aprotinin combined with nitric oxide and prostaglandin E1 protects the canine kidney from cardiopulmonary bypass-induced injury

OBJECTIVE Aprotinin is frequently used to reduce blood loss during cardiac surgery; however, it also causes renal injury. Since aprotinin reduces nitric oxide (NO) and prostaglandin I(2) (PGI(2)), and both cause vasodilation and inhibit activation of neutrophils and platelets, their reduction may be responsible for the injury. This study was to determine whether the combination of aprotinin with NO and prostaglandin E(1) (PGE(1), an analogue of PGI(2)) can attenuate renal injury associated with aprotinin during cardiopulmonary bypass (CPB). METHODS Thirty mongrel dogs were equally divided into five groups, with each group receiving CPB and aprotinin, NO, PGE(1), a combination of the three or no treatment (control). Serum creatinine and creatinine clearance were determined. To elucidate the mechanism, neutrophil, platelet and thrombin activations were also assessed. RESULTS After CPB, serum creatinine increased and creatinine clearance decreased in all dogs. These changes were similar among the NO, PGE(1), aprotinin and control groups, but were significantly smaller in the combination group. Similarly, myeloperoxidase activities in tissues, CD11b expression, plasma elastase, prothrombin fragment (PTF) 1+2 and platelet activation factor were lower, whereas neutrophil and platelet counts were higher in the combination group than in the other groups (P<0.05). CONCLUSIONS Aprotinin combined with NO and PGE(1) produced synergistic protective effects and improved renal function, due partly to inhibition of platelet and neutrophil activation and suppression of thrombin formation.

An asymptomatic lipoma of the right atrium in a neonate.

A 1-month-old boy was incidentally found to have a mass in the right atrium without any symptoms. The tumor was resected uneventfully 2 years later. Histologic examination showed intramyocardial lipoma, which is very rare in children. To date, cardiac lipoma has not been reported in neonates. We describe such a case herein.

Long-Term Leukocyte Filtration Should Be Avoided during Extracorporeal Circulation

Filtration during extracorporeal circulation (ECC) not only removes but also activates leukocytes; therefore, long-term leukocyte filtration may cause adverse effects. In the present study, we tested this hypothesis by priming ECC with 300 mL of canine blood and examining filtration effects in 3 groups (n = 6 each) during 60 min ECC. In the control group (Group C) blood was filtrated with an arterial filter for 60 min; in long-term (Group L) and short-term (Group S) groups, blood was filtrated with a leukocyte filter for 60 and 5 min. We found that about 90% of leukocytes were removed after 5 min of filtration in both Groups L and S. Although leukocyte count continued to reduce, mean fluorescent intensities of CD11/CD18, free hemoglobin, and neutrophil elastase increased in Group L and were higher than those in Groups C and S at 60 min. Leukocyte rupture, cytoplasmic leakage, and circulating naked nuclei were also found in Group L. The data support our hypothesis that long-term filtration can induce inflammation and lead to leukocyte destruction.

Perventricular Device Closure of Patent Ductus Arteriosus: A Secondary Chance

Transcatheter closure is the mainstay of treatment for patent ductus arteriosus (PDA) in the pediatric patient but it is technically challenging and does not always succeed, especially in a younger age child with a large PDA. We present a technique of using a transesophageal echocardiogram-guided minimally invasive perventricular closure for the pediatric patient with a large PDA who failed transcatheter closure.