Closure Of Muscular Ventricular Septal Defects Research Articles

Periventricular closure of ventricular septal defects without cardiopulmonary bypass

Background. Minimally invasive techniques are currently in use to close atrial and ventricular septal defects (VSD). Cardiopulmonary bypass (CPB) is instituted via the femoral vessels, which may cause injury to these vessels, especially in younger patients. The objectives of this study were to demonstrate the feasibility of periventricular closure of muscular VSD (MVSD) and paramembranous VSD (PVSD) without CPB, using the Amplatz VSD device.Methods. Five Yucatan pigs with naturally occurring PVSD (3- to 7-mm diameter) and 5 dogs with surgically created MVSD (6- to 14-mm diameter) were subjects of this study. The VSDs were closed intraoperatively with a 7-French delivery sheath inserted through the free wall of the right (n = 5) or left ventricle (n = 5), under epicardial echocardiogram guidance. The animals were followed for 3 months.Results. There was no operative mortality. All MVSD closed after placement of the device. Closure rate of PVSD was 4 of 5 after placement and 3 of 5 after 3 months. One pig developed aortic incompetence at the last follow-up.Conclusions. Perventricular closure of MVSD and PVSD is feasible. Avoidance of CPB can decrease recovery time, its complications, and trauma to the femoral vessels.

Transcatheter closure of muscular ventricular septal defects with the amplatzer ventricular septal defect occluder: initial clinical applications in children

OBJECTIVESThe aim of this study was to close muscular ventricular septal defects (MVSDs) in children, with a new device, the Amplatzer ventricular septal defect occluder (AVSDO).BACKGROUNDThe design of previously used devices for transcatheter closure of MVSDs is not ideal for this purpose and their use has been limited by several drawbacks.METHODSSix patients, aged 3 to 10 years, with MVSDs underwent transcatheter closure using the AVSDO. The device is a modified self-centering and repositionable Amplatzer device that consists of two low profile disks made of Nitinol wire mesh with a 7-mm connecting waist. The prosthesis size (connecting waist diameter) was chosen according to the measured balloon stretched VSD diameters. A 6-F or 7-F sheath was used for the delivery of the AVSDO. Fluoroscopy and transesophageal echocardiography were utilized for optimal guidance.RESULTSThe location of the defect was midmuscular in five patients and beneath the pulmonary valve in one. The balloon stretched MVSD diameter ranged from 6 to 11 mm. Device placement was successful in all patients, and complete occlusion occurred in all six patients (95% confidence interval 54.06% to 100%). Two patients developed transient complete left bundle branch block. No other complications were observed.CONCLUSIONSThis encouraging initial clinical success indicates that the AVSDO is a promising device for transcatheter closure of MVSDs in children. Further clinical trials and longer follow-up are needed before the widespread use of this technique can be recommended.

Intraoperative closure of muscular ventricular septal defect in a canine model and application of the technique in a baby

J Thorac Cardiovasc Surg 1998;115:1374-6

Pediatric lung transplantation for pulmonary hypertension and congenital heart disease

Five children underwent lung transplantation for endstage pulmonary hypertension and respiratory insufficiency associated with congenital heart disease. One (17 mo) had pulmonary hypertension with a patent ductus arteriosus and required two periods of preoperative extracorporeal membrane oxygenation before successful bilateral sequential lung transplantation. One (21 mo) required bilateral lung transplantation for pulmonary hypertension and bronchopulmonary dysplasia associated with iatrogenic injury to the left pulmonary artery. This child also had patent ductus arteriosus ligation and preoperative catheter closure of an atrial septal defect. Extracorporeal membrane oxygenation was required for early postoperative pulmonary support. One child underwent right single-lung transplantation and closure of an atrial septal defect for pulmonary hypertension. Two patients had single-lung transplantation for Eisenmenger's syndrome: 1 with muscular inlet ventricular septal defect closure, atrial septal defect closure, and right single-lung transplantation; 1 with ventricular septal defect closure, patent ductus arteriosus ligation, right ventricular outflow tract patch repair, and single-lung transplantation. All patients survived operation, with one late death (lymphoproliferative disease). The 4 survivors are all ambulatory without oxygen and have evidence of normal pulmonary artery pressure 9 to 12 months after transplantation.

Left ventriculotomy for closure of muscular ventricular septal defects. Treatment of choice.

Closure of muscular ventricular septal defects (VSDs) through the right atriotomy or right ventriculotomy may be difficult. These VSDs are often located behind the hypertrophied trabeculae carnae or papillary muscle. Residual or recurrent VSD may result from the difficult approach. Between March 1971 and December 1975, we have used the left ventriculotomy near the apex for closure of muscular VSDs in ten children. The patients' ages ranged from five months to eight years and three months. The diagnosis was established by cardiac catheterisation and left ventricular angiocardiogram in all patients. Six patients had multiple VSDs; in four patients VSD in the muscular septum was present (three apical, one midseptal). Operations were performed on cardiopulmonary bypass with moderate hypothermia and intermittent anoxic arrest. VSDs in the membranous septum were closed through the right atrium. Muscular VSDs were approached through a small vertical incision in the left ventricle near the apex. The postoperative course was uneventful in eight patients. Two patients, aged 16 months and eight years, died; histology showed grade IV pulmonary vascular disease in both. All survivors are well four months to five years after the operation, without clinical evidence of residual or recurrent VSD.