Infants born to mothers with disseminated lupus erythematosus occasionally have transient manifestations of the maternal disease. In six infants with congenital heart block born to mothers with systemic lupus erythematosus we postulated a causative relation. In one of the infants a post-mortem study of the conduction system suggested faulty embryonic development of the atrioventricular node with an abnormally thick annulus fibrosus and the effects of early inflammatory changes. Two of the infants had a cardiomyopathy and three, associated congenital heart disease.

To determine the effects of increased cerebrospinal fluid (CSF) pressure on neuronal morphology, obstructive hydrocephalus was induced by injecting kaolin into the fourth ventricle and cisterna magna of 1-day-old rats. The animals were sacrificed 10 to 12 days later, at which time severe ventriculomegaly and cortical thinning were apparent in the parieto-occipital region. Tissue from this area was processed by rapid Golgi methods. Well impregnated pyramidal neurons were examined by light microscopy, and their somatic and dendritic features compared to those of age-matched littermate controls. The somata of medium pyramidal neurons were unaffected, but their basilar dendrites had fewer branches and those that remained were shorter. A variable reduction in dendritic spines occurred, such that some branches were totally denuded while others exhibited spine densities similar to those seen in control animals. The most striking alteration was the occurrence of frequent dendritic varicosities. These enlargements of the dendritic shaft separated by extremely thin constrictions gave the affected segment a beaded appearance. Both dendritic spine loss and varicosity formation were most notable on distal portions of individual branches and within regions of the dendritic tree closest to the ventricular and meningeal surfaces. These alterations are consistent with other reports of dendritic changes associated with aging, mental retardation, and alcohol exposure. These observations suggest that hydrocephalus causes dendritic deterioration or retardation of dendritic maturation. The fact that neuronal morphology was not more severely affected may indicate that these effects are reversible.

The superior vena cava and adjacent right atrium containing the sinoatrial node in each of five human hearts was studied histologically in serial scction. The tissue block of a 41 year old man was reconstructed in four colors to provide a three-dimensional model of the sinoatrial node, atrial relations, blood supply and nodal configuration. The resulting model demonstrated the curved course of the compact sinoatrial node and the mural relations of its tapered superior and inferior ends.Microscopic measurements of the boundaries of the five human nodes yielded an epicardial to endocardial mean thickness in the compact body of the node of 1.6 mm, that of the lower node was 0.6 mm. The mean length of the five nodes was 7.3 mm. Such microscopic delineation of the node is more accurate than gross measurements and indicates that the size of this vital mass of pacemaker tissue in man is smaller than the larger meafiurements usually given in the literature. Small strands of nodal muscle fibers follow longer or shorter courses before they become continuous with the larger more darkly stained atrial cardiac muscle fibers. We found no histologic evidence within the human node, or along its periphery, of continuity between the small nodal fibers and very large atrial fibers.

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The right atrioventricular junction and A-V node area in each of five human hearts was studied histologically in serial sections. The A-V node of a 54-year old female was reconstructed in four colors to provide a three-dimensional model of cardiac relationships, blood supply, and nodal configuration. The nodal fibers demonstrated two laminations. A superficial layer was composed of longitudinally oriented fibers, whereas a deeper layer was composed of oblique and transversely directed fibers. The atrioventricular bundle fibers were always continuous with nodal fibers of the deeper portion of the A-V node. Atrionodal fiber junctions occur along the superior, endocardia1 and inferior borders of the A-V node and impart to these surfaces a spiked appearance. The potential significance of A-V node structure to atrial cardiac conduction is presented.