18 research outputs found
Redilation of endovascular stents in congenital heart disease: factors implicated in the development of restenosis and neointimal proliferation
AbstractOBJECTIVESWe sought to determine the incidence of and risk factors for the development of restenosis and neointimal proliferation after endovascular stent implantation for congenital heart disease (CHD).BACKGROUNDRisk factors for the development of restenosis and neointimal proliferation are poorly understood.METHODSThis was a retrospective review of patients who underwent endovascular stent redilation between September 1989 and February 2000.RESULTSOf 368 patients who had 752 stents implanted, 220 were recatheterized. Of those 220 patients, 103 underwent stent redilation. Patients were classified into three groups: 1) those with pulmonary artery stenosis (n = 94), tetralogy of Fallot/pulmonary atresia (n = 72), congenital branch pulmonary stenosis (n = 9), status post-Fontan operation (n = 6), status post-arterial switch operation (n = 7); 2) those with iliofemoral venous obstruction (n = 6); and 3) those with miscellaneous disorders (n = 3). The patients’ median age was 9.9 years (range 0.5 to 39.8); their mean follow-up duration was 3.8 years (range 0.1 to 10). Indications for stent redilation included somatic growth (n = 67), serial dilation (n = 27) and development of neointimal proliferation or restenosis, or both (n = 9). There was a low incidence of neointimal proliferation (1.8%) and restenosis (2%). There were no deaths. Complications included pulmonary edema (n = 1), hemoptysis (n = 1) and contralateral stent compression (n = 2).CONCLUSIONSRedilation or further dilation of endovascular stents for CHD is effective as late as 10 years. The risk of neointimal proliferation (1.8%) and restenosis (2%) is low and possibly avoidable. Awareness of specific risk factors and modification of the stent implantation technique, including avoidance of minimal stent overlap and sharp angulation of the stent to the vessel wall and avoidance of overdilation, have helped to reduce the incidence of restenosis
721-6 Pulmonary Balloon Valvuloplasty: Effective Palliation for Infants with Tetralogy of Fallot and Small Pulmonary Arteries
Infants with tetralogy of Fallot (TOF) and small pulmonary arteries (PAs) may need palliation to improve pulmonary blood flow and allow growth of the PAs prior to complete repair. Shunts may become occluded, distort the PAs or cause pulmonary overcirculation. As an alternative palliation, we performed pulmonary balloon valvuloplasty (PBV) on infants with TOF and small PAs.20 infants, ages 1.8±1.5 mo and weights 4.1±1.6kg, undervvent PBV as initial palliation for persistent cyanosis or “spells”. 4/20 pts were intubated prior to or for PBV All pts had pre and post-PBV angiograms. In all pts, single balloon valvuloplasty was performed. The ratio of balloon: pulmonary valve annulus (PVA) diameter was 1.51±0.32. Post-PBV, there was no change in the PYA diameter (5.2±1.1mm vs 5.6 + 1.1mm; p=0.1) or PA branch diameter(4.1±1.6mm vs 4.5±1.7mm, p>0.05). The systemic 02 saturation increased from 81±8% to 93±6%. (p<0.001)7/20 pts undervvent follow-up (F/U) cath 8.2±2.4 mo post-PBV Compared to pre-PBV measurements, the PYA diameter increased from 5.2 ± 1.1mm to 7.1±1.4mm (p<0.03) and the McGoon ratio increased from 1.4±0.4 to 2.1±0.3 (p<0.02).Of the 20 pts, 11 pts undervvent corrective surgery 8.0±3.1 mo post-PBV with no surgical deaths; 5 pts remain in stable condition awaiting surgery; 3 pts required shunt placement 9-66 days post-PBV; 1 pt died due to other congenital anomalies.ConclusionsPulmonary balloon valvuloplasty promotes growth of the PAs and PYA in infants with TOF and small PAs, offering a safe and effective alternative palliation for infants who are not yet candidates for complete repair
Vascular endothelial growth factor and basic fibroblast growth factor in children with cyanotic congenital heart disease
AbstractObjective: Vascular endothelial growth factor and basic fibroblast growth factor are potent stimulators of angiogenesis. Children with cyanotic congenital heart disease often experience the development of widespread formation of collateral blood vessels, which may represent a form of abnormal angiogenesis. We undertook the present study to determine whether children with cyanotic congenital heart disease have elevated serum levels of vascular endothelial growth factor and basic fibroblast growth factor. Methods: Serum was obtained from 22 children with cyanotic congenital heart disease and 19 children with acyanotic heart disease during cardiac catheterization. Samples were taken from the superior vena cava, inferior vena cava, and a systemic artery. Vascular endothelial growth factor and basic fibroblast growth factor levels were measured in the serum from each of these sites by enzyme–linked immunosorbent assay. Results: Vascular endothelial growth factor was significantly elevated in the superior vena cava (P = .04) and systemic artery (P = .02) but not in the inferior vena cava (P = .2) of children with cyanotic congenital heart disease compared to children with acyanotic heart disease. The mean vascular endothelial growth factor level, determined by averaging the means of all 3 sites, was also significantly elevated (P = .03). Basic fibroblast growth factor was only significantly elevated in the systemic artery (P = .02). Conclusion: Children with cyanotic congenital heart disease have elevated systemic levels of vascular endothelial growth factor. These findings suggest that the widespread formation of collateral vessels in these children may be mediated by vascular endothelial growth factor. (J Thorac Cardiovasc Surg 2000;119:534-9
Spontaneous aberrant right subclavian arterio-oesophageal fistula in a previously healthy child
Reproducing Patient-Specific Hemodynamics in the Blalock–Taussig Circulation Using a Flexible Multi-Domain Simulation Framework:Applications for Optimal Shunt Design
For babies born with hypoplastic left heart syndrome, several open-heart surgeries are required. During Stage I, a Norwood procedure is performed to construct an appropriate circulation to both the systemic and the pulmonary arteries. The pulmonary arteries receive flow from the systemic circulation, often using a Blalock–Taussig (BT) shunt between the innominate artery and the right pulmonary artery. This procedure causes significantly disturbed flow in the pulmonary arteries. In this study, we use computational hemodynamic simulations to demonstrate its capacity for examining the properties of the flow through and near the BT shunt. Initially, we construct a computational model which produces blood flow and pressure measurements matching the clinical magnetic resonance imaging (MRI) and catheterization data. Achieving this required us to determine the level of BT shunt occlusion; because the occlusion is below the MRI resolution, this information is difficult to recover without the aid of computational simulations. We determined that the shunt had undergone an effective diameter reduction of 22% since the time of surgery. Using the resulting geometric model, we show that we can computationally reproduce the clinical data. We, then, replace the BT shunt with a hypothetical alternative shunt design with a flare at the distal end. Investigation of the impact of the shunt design reveals that the flare can increase pulmonary pressure by as much as 7% and flow by as much as 9% in the main pulmonary branches, which may be beneficial to the pulmonary circulation
Interventional Radiology in the Treatment of the Complications of Organ Transplant in the Pediatric Population—Part 1: The Kidneys, Heart, Lungs, and Intestines
Transplants continue to be the preferred treatment for end-stage organ disease in children. Transplants in children vary from adults due to the different indications and diseases leading to transplant, the smaller body size of children, and the different surgical techniques. These differences have led to a set of complications often seen in the transplanted child as well as interventional solutions tailored to their special needs. This paper will examine each transplanted solid organ (with the exception of the liver) and their associated complications. The interventional technique for each key procedure will be described