Mechanisms of closure of perimembranous ventricular septal defect

Abstract

Although more defects in the muscular ventricular septum close spontaneously than do defects abutting on the membranous septum (perimembranous defects), a good proportion of the latter show a tendency to diminish in size and to close. The mechanism responsible for this closure is usually described as an aneurysm of the membranous septum, although some doubt has been cast as to whether this is the precise mechanism. In this study, 69 unoperated hearts with ventricular septal defect were examined; 26 (38%) showed some evidence of partial closure and none extended exclusively into the outlet part of the septum. Two thirds of the trabecular perimembranous defects, almost half of the inlet defects, and one third of the confluent defects showed signs of partial occlusion. The anatomic structures most frequently responsible were reduplication of tricuspid valve tissue (16 cases), adhesion of tricuspid valve leaflets (6 cases), and prolapse of an aortic valve leaflet (3 cases). Only in 2 cases were subaortic tissue tags observed which might have originated from the remnant of the membranous septum. The present study shows that although anatomic evidence of partial closure was present in two fifths of the hearts studied, only rarely was it due to so-called aneurysm of the membranous septum.