The perennial interest in heart anomalies has produced a variety of discordant explanations for them. Transposition of the great vessels poses an especially difficult problem. One explanation for it, widely accepted by pathologists, is that of Spitzer. Of Spitzer's several papers, the one published in 1923 deals most comprehensively with his theory. This paper has been honored with an extensive paraphrase by Harris and Farber ('39), and recently has been translated and republished by Lev and Vass ('51). Abbott ('36) adopts Spitzer's teaching in her well known Atlas.Spitzer assumes that the hearts of all vertebrates above amphibia evolved from a primitive amniote heart furnished with a small pulmonary artery and two aortae. These higher vertebrates, Spitzer states, led a more and more active life and needed an increasingly efficient respiration. To make this possible, the primitive amniote vessels were modified. In reptiles the pulmonary artery and the left ventricular aorta were enlarged and the right ventricular aorta reduced; in the still more active birds and mammals the right ventricular aorta was done away with altogether. In addition, the interventricular foramen of birds and mammals was closed, thus completely dividing the pulmonary from the general circulation. The evolution of the pulmonary circulation was impelled and directed by teleological and phylogenetic forces, which dominate the ontogeny of the bird and mammal embryo. The abnormal transposition of the aorta of man, in Spitzer's view, is an atavistic revival of the suppressed right ventricular aorta of reptiles.Embryologists have either ignored or opposed Spitzer's theory. For one thing, they have grown wary of mixtures of teleology, phylogeny, and ontogeny. Furthermore, embryologists no longer consider the normal development of an embryo to be a simple recapitulation of ancestral adult forms. De Beer ('58) has amassed evidence for other factors at work within the embryo. The embryos of all higher vertebrates do start with a common structure. But after this common beginning each kind of embryo goes its own way; it may invert the succession of later structures, may introduce novel deviations, may accelerate the growth of some part, or may retain primitive structures lost in other forms, all without regard for adult ancestors. The embryo is much more than a passive register of adult ancestral forms; it has its own spontaneous mutations that produce novel adult structures. All such strictly embryonic factors of development are ignored by Spitzer and his followers.The comparative development of the hearts of the Crocodilia, mammals, and birds offers a good field for the older and newer schools of embryological thought to contend in. The embryos of these three groups start with very similar hearts and arterial arches. All three groups -and they alone -achieve adult hearts with completely divided ventricles and completely separated pulmonary and systemic circulations. Nevertheless, the adult hearts of all three differ considerably, and pass through diff...

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Four kinds of abnormal pulmonary and three kinds of abnormal semilunar valves are described from pig and human embryos of an age equivalent to the first human trimester. The pulmonary valves include bicuspid forms resulting from the absence of an anterior cusp, from the fusion of left and anterior cusps and from the fusion of left and right cusps; also dome-shaped valves. The aortic valves include bicuspid forms resulting from the absence of the non-coronary cusp and from the fusion of right and left cusps. All are discussed in the light of accompanying heart anomalies and a re-examination of normal cusp development. Embryonic abnormal pulmonary valves are generally linked with early stages of Fallot's tetralogy. They are caused by a n arrest in heart development and the changed hemodynamic conditions that result from it. Embryonic abnormal aortic valves are caused by a n arrest in heart development and an abnormal degree of coarctation of the aorta. The evidence from embryos supports the general belief that abnormal pulmonary cusps of all ages, when not caused by infection, are of congenital origin. Some aortic abnormal valves are also of congenital origin, but are hard to distinguish from similar ones produced after birth by postnatal coarctation.Many abnormal semilunar valves thought to be congenital have been reported from the hearts of infants and older persons. Abnormal pulmonary valves may be bicuspid, or dome-shaped; they may have extra cusps or no cusps at all. Abnormal aortic valves fall into the same categories, except that there seems to be no record of a complete absence of aortic cusps.Pulmonary bicuspid valves in infants and older persons occur so often with a patent interventricular foramen and other signs of arrested heart development that a congenital origin may always be suspected (Koletsky, '41a). The comprehensive surveys of Dilg (1883) and of all later writers attest this. Just which cusp is defective in bicuspid pulmonary valves is not always clear, thanks to confusing terminology and lack of critical detail. Bicuspid pulmonary valves may result from a simple absence of the anterior cusp ( fig. I ) , or from a fusion of the anterior cusp with either the right or left cusps; a fusion of the right and left cusps is the least frequent anomaly. Dome-shaped pulmonary valves are often found with isolated pulmonary stenosis (Friedberg, '56). Some quadricuspid valves appear in hearts with other congenital anomalies ( Kissin, '36).Campeau et al. ('61) cite 15 cases of complete absence of pulmonary cusps linked with Fallot's tetralogy and presumably congenital in origin.Authorities differ over the congenital origin of aortic bicuspid valves, especially of those in older persons (Gross, '37; Koletsky, '41b). Bicuspid aortic valves are very often combined with coarctation (Reifenstein e t al., '47). Since the coronary arteries label the right and left cusps, the cusps involved are easily recognized. All agree that bicuspid valves from a fusion of the two coronary cusps is the most frequent an...

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