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

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

Morphologic features of the ductus arteriosus after prostaglandin E1administration for ductus-dependent congenital heart defects

Histologic evidence of damage to the ductus arteriosus after the infusion of prostaglandin E1has been reported in neonates with ductus-dependent congenital heart defects. The reported changes suggested structural weakening of the ductus that might render it prone to laceration or rupture. The morphologic features of ductus arteriosi were studied in two groups of neonates with ductus-dependent congenital heart defects. Group 1 (prostaglandin E1group) comprised 12 neonates who received prostaglandin E1and died while receiving it or within 4 days after its administration was discontinued; the mean duration of prostaglandin E1administration was 18 hours (range 30 minutes to 40 hours). Group 2 (control group) comprised 10 neonates who did not receive prostaglandin E1and were matched with group 1 for weight, type of congenital heart defect and age at death.The length of the ductus and its internal diameter at the aortic end were greater in group 1 than in group 2, but the differences were not statistically significant. The internal diameter of the ductus at the pulmonary end was significantly greater in group 1 than in group 2 (p <0.05). Histologic staging of maturation of the ductus (stage 1 being most immature and stage 4 being most mature or functionally closed) showed that the ductus arteriosi of group 1 were significantly more immature than those of group 2. Maturational stage averaged 1.67 ± 0.30 (mean ± standard error of the mean) in group 1 and 3.00 ± 0.29 in group 2 (p <0.0025). Histopathologic abnormalities reported by other investigators were found in only two patients from each group.Cineangiograms obtained at the repeat cardiac catheterization up to 33 months after prostaglandin E1treatment in 28 infants showed no abnormality at the ductus area; in all but 1 infant, the ductus either spontaneously closed or had been surgically ligated uneventfully. In an additional 33 patients, clinical follow-up did not suggest any problems in the ductus. It is concluded that the administration of prostaglandin E1may delay the normal closing process or maturation of the ductus but does not have any significant deleterious morphologic or clinical effect, and that the ductus arteriosus closes normally after prostaglandin E1is discontinued. Prolonged administration of prostaglandin E1)more than 40 hours) may cause the histologic changes observed by others