title: Early reintervention on the pulmonary arteries and right ventricular outflow tract after neonatal or early infant repair of truncus arteriosus using homograft conduits.
abstract: Patients with truncus arteriosus often require pulmonary arterial (PA) and/or right ventricular outflow tract (RVOT) reintervention within the first year of repair. However, little is known about the risk factors for early reintervention on the PAs or RVOT in this population. The objective of the present retrospective cohort study was to determine the risk factors for early PA or RVOT reintervention after repair of truncus arteriosus in neonates and young infants. Of 156 patients ascertained (median age at repair 14 days; 143 early survivors), reinterventions on the RVOT and/or PAs were performed in 109. The first reintervention was catheter therapy in 73 patients (conduit dilation/stenting in 29, PA dilation/stenting in 31, both in 13) and conduit reoperation in 36 patients. The freedom from any RVOT or PA reintervention was 68 ± 4% at 1 year and 48 ± 5% at 2 years. The factors associated with early reintervention (shorter 1-year freedom from reintervention) on univariate analysis were repair quartile, neonatal repair, smaller weight at repair, and smaller implanted conduit size. On multivariable analysis, only smaller conduit size remained significant (multivariable hazard ratio 0.66/mm, range 0.53 to 0.83; p <0.001). The freedom from conduit reoperation was 92 ± 3% at 1 year and 76 ± 4% at 2 years. Overall, the left and right PA sizes were modestly larger than normal by the 1-sample t test, and PA Z scores and the PA area index were not associated with the risk of reintervention. Early reintervention for PA and/or RVOT conduit obstruction is common after neonatal and early infant repair of truncus arteriosus using homograft conduits. A smaller conduit size was associated with early RVOT/PA reintervention. The branch PA size was normal before surgery, suggesting that the PA stenosis in these patients resulted from factors other than intrinsic stenosis or hypoplasia.
authors.affiliation: Department of Cardiology, Children's Hospital Boston, Boston, Massachusetts, USA.
authors.forename: Amalia M
authors.initials: AM
authors.lastname: Lund
authors.forename: Melanie
authors.initials: M
authors.lastname: Vogel
authors.forename: Audrey C
authors.initials: AC
authors.lastname: Marshall
authors.forename: Sitaram M
authors.initials: SM
authors.lastname: Emani
authors.forename: Frank A
authors.initials: FA
authors.lastname: Pigula
authors.forename: Wayne
authors.initials: W
authors.lastname: Tworetzky
authors.forename: Doff B
authors.initials: DB
authors.lastname: McElhinney
mesh_terms: D000015:Abnormalities, Multiple / Q000601:surgery*; D001807:Blood Vessel Prosthesis; D004452:Echocardiography; D005500:Follow-Up Studies; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D011651:Pulmonary Artery / Q000601:surgery*; D012086:Reoperation / Q000706:statistics & numerical data*; D012189:Retrospective Studies; D012307:Risk Factors; D013997:Time Factors; D014184:Transplantation, Homologous; D016896:Treatment Outcome; D014339:Truncus Arteriosus, Persistent / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000601:surgery*; D014694:Ventricular Outflow Obstruction / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000601:surgery*