INTRAUTERINE CLOSURE OF MEMBRANOUS VENTRICULAR SEPTAL-DEFECTS - MECHANISM OF CLOSURE IN 2 AUTOPSY SPECIMENS

Citation
A. Nir et al., INTRAUTERINE CLOSURE OF MEMBRANOUS VENTRICULAR SEPTAL-DEFECTS - MECHANISM OF CLOSURE IN 2 AUTOPSY SPECIMENS, Pediatric cardiology, 15(1), 1994, pp. 33-37
Citations number
25
Categorie Soggetti
Cardiac & Cardiovascular System",Pediatrics
Journal title
ISSN journal
01720643
Volume
15
Issue
1
Year of publication
1994
Pages
33 - 37
Database
ISI
SICI code
0172-0643(1994)15:1<33:ICOMVS>2.0.ZU;2-8
Abstract
Anatomic evidence of intrauterine closure of ventricular septal defect s (VSDs) has been reported rarely. Between 1985 and 1990, 112 autopsie s were performed at the Mayo Clinic on third trimester stillborns and infants who died during the first week of life. There were 21 (19%) ca ses of congenital heart disease. VSD was found in 12 (11%) cases: in e ight (7%) as a part of a more complex heart defect and in four (4%) as an isolated lesion. Two cases with membranous VSDs with tricuspid val ve tissue partially occluding-the ventricular septal defect were found . A 2280-g female infant (case 1) with trisomy t8 died at 4 days of ag e. Autopsy revealed bilateral superior venae cavae, a large atrial sep tal defect, cor triatriatum, an atypical tricuspid valve with large se ptal leaflet partially obstructing a large membranous VSD, a hypoplast ic right ventricle, and severe pulmonic stenosis. A 2610-g female infa nt (case 2), born with congenital heart block died at 4 days of age. A utopsy revealed cor triatriatum dexter obstructing the tricuspid orifi ce, a large membranous VSD partially obstructed by the septal leaflet of the tricuspid valve, four small muscular VSDs, and pulmonic stenosi s. These cases suggest that closure of membranous VSDs may begin in ut ero and the mechanism of closure is similar to that reported postnatal ly.