Abstract
I have studied some 100 abnormal pig embryo hearts—equivalent in development to human embryos of the first trimester—which exhibit early stages of persisting truncus arteriosus, complete transposition, aortic and pulmonary stenosis, as well as other anomalies. Persisting truncus and complete transposition are caused by an arrest in the downgrowth of the aorticopulmonary septum, so that it either fails to reach the bulbus or reaches it too late to connect the aorta and pulmonary artery with their proper heart inlets. Aortic and pulmonary stenosis are the secondary result of an arrest in the development of the atrioventricular endocardial cushions. I have studied some 100 abnormal pig embryo hearts—equivalent in development to human embryos of the first trimester—which exhibit early stages of persisting truncus arteriosus, complete transposition, aortic and pulmonary stenosis, as well as other anomalies. Persisting truncus and complete transposition are caused by an arrest in the downgrowth of the aorticopulmonary septum, so that it either fails to reach the bulbus or reaches it too late to connect the aorta and pulmonary artery with their proper heart inlets. Aortic and pulmonary stenosis are the secondary result of an arrest in the development of the atrioventricular endocardial cushions.
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