STUDY OF CARDIAC ENLARGEMENT IN INFANCY WITH CASE REPORTS OF REVERSIBLE ENLARGEMENT

Abstract

The heart was considerably enlarged in 16 of 1,000 infants subjected to roentgenographic examination in the neonatal period. Seven of this group died shortly. Seven of the surviving cases continued under observation for several years: five had some congenital malformation of the heart, but in the remaining two cases the cardiac enlargement receded and no sign of any organic defect remained. Etiology of Cardiac Enlargement in Neonates Coming to Autopsy It was considered that autopsy examination would provide the most accurate information concerning the etiology of all types of cardiac enlargement, including reversible forms. Accordingly, records and pathologic material were examined from 200 consecutive autopsies on infants born alive at the Boston Lying-in Hospital but dying in the neonatal period. Criteria based on weight are more reliable than those based on size, even though cases with pure dilatation may be excluded. Cases were selected from this series in which the heart weighed more than 25 gm. This figure of 25 gm. was selected to avoid inclusion of borderline cases, due to variations in technic and slight differences in age. A considerable number of cases with enlargement of lesser degree were thereby excluded. In 29 of the 200 cases reviewed, the heart weighed more than 25 gm. The causes of death are listed in Table II. It would be anticipated that intrauterine aspiration or atelectasis might be complicated by supervening infection, and in most cases a combination of more than one of the conditions enumerated occurred. Separation into individual types was therefore impracticable. In the tissue sections from this group, the cardiac muscle fibers were not hypertrophied, but in every case changes due to congestion and edema were apparent. These changes did not necessarily correspond in intensity to the degree of cardiac enlargement; thus, in the largest heart of the series (weight, 54 gm.), from a case of intrauterine aspiration with minimal pneumonic changes, cardiac congestion and edema were only slight. [See Table II in source PDF] Group 2 calls for no further description. Cardiac enlargement in fatal cases of erythroblastosis (Group 3) has long been recognized, but it is interesting to speculate whether it occurs to any significant degree in cases which survive. Among the miscellaneous cases (Group 4), one had previously been labelled "idiopathic cardiac hypertrophy"; microscopic changes associated with aspiration were, however, present in the lungs, though to a slight extent, and this case should more correctly be included in Group 1. Three cases are described in which cardiac enlargement in infants receded over a considerable period. In two of these cases, cardiac hypertrophy appeared to originate in association with pulmonary infection. Some other possible causes of reversible cardiac enlargement are discussed. To determine the incidence of all forms of cardiac enlargement, including reversible enlargement, 1,000 infants were examined roentgenologically in the neonatal period. In 16 patients, considerable cardiac enlargement was present. Of these, seven died shortly. Among the nine survivors, two were lost sight of, five had a congenital malformation of the heart and two recovered with an apparently normal heart. To investigate the etiology of neonatal cardiac enlargement, the material from 200 consecutive autopsies was reviewed. In 29 cases considerable hypertrophy of the heart was found: in eight of these a congenital malformation of the heart was present, six were cases of erythroblastosis fetalis and in five some miscellaneous cause produced the cardiac enlargement: In the remaining 10 cases some pathologic condition of the lungs was present. It is suggested that some cases of cardiac hypertrophy are associated with pathologic lung conditions occurring before, during or after birth. The association is not necessarily fatal and the cardiac enlargement may prove reversible.