Abstract

Perimembranous defects are the most frequent types of ventricular septal defect. Spontaneous closure of these defects occurs often in childhood. The mechanism of closure is controversial, but recent pathologic and clinical studies in children suggest that it occurs by reduplication and adhesion of the septal leaflet of the tricuspid valve to the margins of the defect. 1–2 Closure of the defect is frequently associated with the formation of a ventricular septal aneurysm, a term that describes an outpouching in the region of the membranous septum. 3 The adherent tricuspid valve protrudes into the right ventricle during ventricular systole, accounting for its aneurysmal appearance. Less frequently, prolapse of an aortic valve leaflet reduces the size of the defect and can result in aortic insufficiency. 1 Early pathologic studies demonstrated deformity of the tricuspid valve resulting from ventricular septal aneurysm formation. 4 Chordal shortening and fusion, and leaflet deformity have been demonstrated in necropsy examinations of patients with ventricular septal aneurysms. Functional abnormalities resulting from tricuspid valve involvement in the formation of the aneurysm were recently described in pediatric studies.2 However, these abnormalities have not been described in adults, and the use of transesophageal echocardiography for the detection of ventricular septal aneurysms was not previously reported.

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