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2b-1. Ventricular septal defect, moderate left to right shunt.  (Legend.)

A. PA chest radiograph demonstrates cardiomegaly, the pulmonary outflow tract is convex and the pulmonary arterial markings are increased.

B. Right anterior oblique view demonstrates posterior displacement of the esophagus indicating left atrial dilation in addition to bi-ventricular enlargement. Hilar dance was noted at flouroscopy.

2b-2. Ventricular septal defect, large left to right shunt.

A. PA chest radiograph demonstrates moderate cardiomegaly with the left ventricular apex extending to the left chest wall. The pulmonary vascular markings are bilaterally symmetrically increased and the pulmonary outflow tract is convex. The patient has had a sternotomy.

2b-3. Ventricular septal defects, large left to right shunt.

A. PA chest radiograph demonstrates marked cardiomegaly with bilaterally increased pulmonary arterial markings. Air trapping is appreciable in the right middle lobe.

B. Right anterior oblique film and barium swallow demonstrates left atrial compression of the esophagus confirming left atrial dilation.

Ventricular Septal Defect (VSD)

VSDs represent the commonest form of congenital heart disease. This lesion was first described by Roger in 1879 giving his name to small asymptomatic ventricular septal defects "maladie de Roger". With the advent of cardiac catheterization and real time 2D echocardiography a classification system of VSDs evolved.

Incidence: This lesion accounts for approximately 20% of patient visits to the cardiology clinic with a reported incidence of 1.5-2 per 1000 live births.


  1. Supracristal VSD (type I): occur beneath the pulmonary valve and communicate with the right ventricular outflow tract above the the supraventricular crest. Often associated with prolapse of a coronary cusp and associated aortic regurgitation. Account for 5% of VSDs in the U.S. and 30% in Japan.
  2. Perimembranous VSD (type II): occur infracristal referring to the crista supraventricularis, a muscular region in the normal heart which seperates the tricuspid from the pulmonary valve and the pulmonary from the aortic valve. Perimembranous (also termed membranous) defects are further classified into three groups related to anatomcial position; peerimembranous inlet which lie posterior to the septal leaflet of the tricuspid valve, perimembranous trabecular (commonest) and perimembranous outlet. Naturally there may be some degree of overlap of the VSD with extension from one portion to another of the septum. All perimembranous VSDs are subaortic by virtue of their proximity to the membranous septum.
  3. AV canal VSD (type III): occur beneath the septal leaflet of the tricuspid valve, in the posterior region of the septum. These account for approximately 8-10% of VSDs and are often associated with left-axis deviation on the ECG.
  4. Muscular VSD (type IV): occur within the muscular septum and are subclassified as inlet, trabecular and infundibular. These defects account for 5-20% of lesions. Muscular trabecular defects may be multiple and described as Swiss cheese defects.

Perimembranous inlet may be associated with malaignment of the ventricular septum with the atrial septum, and perimembranous outlet defects with malalignment of the ventricular and infundibular septum (often in association with conotruncal defects including tetralogy of Fallot and truncus arteriosus).

Embryology: Formation of the interventricular septum occurs by fusion of endocardial cushion tissue, from the conus septum, with the superior portion of the muscular septum and a portion of the right superior endocardial cushion. Defects involving the outlet septum are thought to arise from failure of fusion of components of the conus septum. Defects of the inlet septum from failure of fusion of the right superior endocardial cushion tissue with the muscular septum. Muscular defects (particularly trabecular) are probably secondary to excessive excavation of septum during ventricular growth or inadequate merging of the medial walls of the ventricles.