Henry Ford Hospital Medical Journal


The generally accepted and most common mechanism of the pathogenesis of VSD is the failure of fusion of the conus ridges, atrioventricular cushions and the ventricular muscular septum. Our findings in a study of serial sections of the hearts of newborn gerbils (Meriones unguiculatus) leads us to hypothesize a second, less common, mechanism for the development of VSD, i.e., an exaggeration of the normal process of resorption and atrophy which undermines the septal cusp of the tricuspid valve, thus separating it from the muscular septum. This hypothesis can explain an instance of high membranous VSD in the form of a tortuous canal undermining the septal cusp of the tricuspid valve and opening into the left ventricle just above the crest of the muscular septum. It is probable that in this case the process of tissue atrophy and resorption has extended abnormally through the septum just below the cusp, thus forming a high membranous VSD. The technique of serial section of the heart is relatively simple and is particularly useful in studying the effects of teratogenic agents on the development of small mammalian hearts.