The Use of Echocardiography in Pediatric Interventional Cardiac Catheterization Procedures

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/74658/1/j.1540-8183.1995.tb00584.x.pd

Influence of Echocardiographic Guidance on Positioning of the Buttoned Occluder for Transcatheter Closure of Atrial Septal Defects

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73381/1/j.1540-8175.1996.tb00878.x.pd

The Early “Unnatural” History Following Surgical Repair of Ventricular Septal Defects

Introduction Surgical outcomes for simple ventricular septaldefects (VSD) have been excellent in the past three decades. Forthis project, the timing of resolution of left-sided dilation and mitralregurgitation (MR) following VSD repair was assessed. Methods Echocardiographic data surrounding surgery of 42 consecutivechildren who underwent surgical patch repair of a VSD werereviewed. The echocardiograms were reviewed up to a mean of 12months post-operatively (range 9 - 14 months). Quantitative dataindexed to body surface area including left atrial (LA) volume, mitralvalve annulus diameter, and left ventricular end-diastolic dimension(LVEDD) was analyzed. Results The majority of our pre-surgical cohort had only trace(44%) or no MR (31%), with a small proportion having mild (16%)or moderate MR (9%). No patients had moderate or greater MR followingrepair at follow-up. The median mitral valve annular Z-scorewas 1.8 (SD 1.6; range: -1.2 to 4.1) pre-operatively, improving to a 0.6(range: -1.7 to 2.4; p < 0.001) at follow-up. LA dilation was present in70% of patients, with a median LA volume Z-score of 1.1 (range: -2.6to 15.5), decreasing to 13% median Z-score -1.2 (range: -3.5 to 2.9; p< 0.001) at follow-up. LV dilation was present in 81% of pre-operativepatients with a median LVEDD Z-score of 3.0 (range: -2.0 to 7.9).There was significant improvement in qualitative assessment of LVenlargement (25%) with a median LVEDD Z-score of 0.5 (range:-2.1 to 2.9; p < 0.001) at follow-up. Discharge echocardiogram wasperformed at a mean of 5.7 days (range: 3 - 12 days) following surgery. Conclusions Normalization of LA, mitral valve annulus, and LV sizeoccurred within the first three months in the majority of patients, withsignificant changes occurring within the first post-operative weekfollowing surgical repair for VSD

The Abnormal Contralateral Atrioventricular Valve in Mitral and Tricuspid Atresia in Neonates: An Echocardiographic Study

Abnormalities of the mitral valve (MV) or the tricuspid valve (TV) morphology and/or function in patients with functional single ventricle may result in early morbidity and death. The purpose of this study was to determine the incidence of contralateral atrioventricular valve (AVV) pathologies in mitral valve atresia (MA) and tricuspid valve atresia (TA). We retrospectively reviewed the echocardiographic data of 50 neonates with MV and 20 with TA. Appearance of the papillary muscles, chordae tendinae, and valve leaflets was assessed. AVV regurgitation was semiquantitated by color-flow Doppler and the AVV annulus diameter was measured and indexed to body surface area. MV abnormalities were found in 9 of 20 (45%) of patients with TA. The MV was myxomatous in 9 patients, the leaflets were redundant in 5 patients, and prolapsing occurred in 4 patients. Mild regurgitation was found in 2 patients. In 18 of 20 (90%) patients MV annulus size was larger than 95% of predicted normal values. TV abnormalities were found in 12 of 50 (24%) patients with MA. The TV was myxomatous in 4 patients, prolapsing in 2, and redundant in 3, and moderate TV regurgitation was found in 3 patients. In 29 of 50 (58%) patients TV annulus size was larger than 95% of predicted normal values. Contralateral AVV abnormalities in tricuspid and mitral valve atresia are common and should be assessed carefully before surgical procedures.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42381/1/246-20-3-200_20n3p200.pd

The Influence of a Restrictive Atrial Septal Defect on Pulmonary Vascular Morphology in Patients with Hypoplastic Left Heart Syndrome

Hypoplastic left heart syndrome (HLHS) with a restrictive atrial septal defect (ASD) is a form of congenital heart disease with considerable morbidity and mortality. This morphologic analysis assesses the pulmonary vasculature in this patient population. Pulmonary arteries, the persistence of high-resistance fetal arterioles, pulmonary veins, and lymphatics from multiple lung sections from each of five patients with HLHS and a restrictive ASD were compared to those of five patients with HLHS and nonrestrictive ASD. Lung sections from each patient were qualitatively graded in severity of pathology from 0 to 3 for each of the structures described previously, with the pathologist blinded to the status of the ASD. Patients with a restrictive ASD exhibited more significant pulmonary venous thickening and lymphatic dilatation (p = 0.02), with a tendency toward persistence of high-resistance fetal vessels (p = 0.2), compared to patients with a nonrestrictive ASD. These findings imply that patients with HLHS and a restrictive ASD possess pulmonary vascular abnormalities that place them at higher risk for the current surgical interventions available compared to patients with a nonrestrictive ASD.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42386/1/246-23-2-146_20230146.pd

Stent redilation in canine models of congenital heart disease: Pulmonary artery stenosis and coarctation of the aorta

In a canine puppy model, pulmonary artery stenosis was created by banding the left pulmonary artery to 30–40% of its original diameter. Animals underwent right heart catheterization and angiography 1–2 mo later, and Palmaz P308 stents were implanted. Stent redilation was performed 3–5 mo later. One mo postredilation, the animals were restudied and sacrificed. Coarctations of the aorta were created by transverse aortic incision and longitudinal repair. P308 stent implantation was performed 2–3 mo later. Stent redilation was performed after 6–10 mo, and the animals were restudied and sacrificed 1–2 mo later. Stent implantation was performed in 6 puppies with pulmonary artery stenosis, as 2 animals developed postoperative pulmonary arterial hypoplasia, precluding stenting. The stenosis diameter increased from 4.8 ± 0.5 mm to 7.4 ± 0.6 mm (mean ± SE) following stenting ( P = 0.005), and increased further to 9.2 ± 0.7 mm following redilation ( P < 0.001). There were no significant vessel tears or ruptures. Coarctation stenting was performed in 8 animals. The coarctation was dilated from 5.8 ± 0.9 mm to 9.8 ± 0.6 mm ( P < 0.001), and to 13.5 ± 0.5 mm at redilation ( P = 0.002). Redilation could not be performed in 1 animal. Aortic rupture and death occurred in 2 of 7 animals at redilation. Stent implantation and redilation in experimental pulmonary artery stenosis appears safe and effective. Though stent implantation for coarctation of the aorta appears safe, there was a 28% aortic rupture rate at stent redilation in this model. © 1996 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/38176/1/24_ftp.pd

Amplatzer Closure of Atrial Septal Defect and da Vinci Robot-Assisted Repair of Vascular Ring

Technology for minimally invasive approaches to congenital heart disease is a rapidly evolving field. This case report reviews a novel approach to combining two of the newer technologies available to treat a pediatric patient with an atrial septal defect (ASD) and a vascular ring. This report is the first to describe the use of the da Vinci surgical system to assist in a thoracoscopic procedure for a pediatric patient. The da Vinci assisted division of the vascular ring, joined with an Amplatzer closure of the ASD, demonstrates how maximum benefit can be obtained for patients by combining emerging technologies.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/48103/1/246_2003_Article_537.pd

Influence of Echocardiographic Guidance on Positioning of the Buttoned Occluder for Transcatheter Closure of Atrial Septal Defects

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73381/1/j.1540-8175.1996.tb00878.x.pd