M. Remsen Behrer

Recurrent coarctation of the aorta after successful repair in infancy

Abstract Twenty unselected infants who survived repair of coarctation of the aorta were restudied an average of 6.2 years postoperatively. Eight patients (40 percent) showed no significant difference in blood pressures between the arms and legs and had normal pressures in their arms. These patients have been followed up for an average of 5.1 years postoperatively. Another 8 patients (40 percent) had moderate blood pressure differences between the upper and lower limbs. These patients have been followed up for an average of 6.6 years postoperatively. Further follow-up of this group will be required to determine how many will need reoperation. Four patients (20 percent), although asymptomatic, had recurrent severe coarctation of the aorta that will require reoperation. These patients have been followed up for an average of 6.9 years postoperatively. The mechanism of the recurrent coarctation is not clear, but there is evidence that the coarctation is incompletely relieved in some and that it develops with growth in others. All infants surviving repair of coarctation of the aorta must be closely followed up for possible recurrent coarctation until they reach adult size.

Nonpenetrating trauma to the heart

This study presents a spectrum of injuries to the heart in 61 individuals from 2 months to 30 years of age who were in automobile accidents. Three patients are presented in detail. One patient died and had severe damage to the left ventricular myocardium. Another patient had severe damage to the tricuspid valve and survived after successful implantation of a Starr-Edwards valve. The third patient had a residual calcified plaque at the base of the left ventricle which was detected 30 years after a childhood automobile accident. Electrocardiographic changes compatible with myocardial injury were found in 29.5 per cent, and 19.6 per cent were found to have suspicious changes. Since the advent of open heart surgery, patients who sustain myocardial tears or rupture of cardiac septa are now potentially curable.

Quantification of the fetal electrocardiogram through LINC computer processing

Abstract A procedure is described for obtaining, through real-time computer processing, estimates of the parameters of the fetal electrocardiogram as recorded from the abdomen. Results include quantification of the P-R interval, QRS amplitude and QRS duration, and the trend of each through gestation. QRS morphology is described according to accepted standards of electrocardiography. Examples of tracings of various qualities and of the averages corresponding to these tracings are included.

Radiocardiography in congenital heart disease

Summary 1. The technique of radiocardiographyhas been employed to study twenty-two children with normal hearts and 100 children with congenital heart disease. 2. Different types of radiocardiograms were obtained in patients with patent ductus arteriosus, tetralogy of Fallot, Eisenmenger complex, and tricuspid atresia. 3. This method may be useful indifferentiating patients with Eisenmenger complex from those with tetralogy of Fallot. 4. Although the exact physiologicalphenomena responsible for the types of curves obtained are not known, preliminary evidence suggests that the radiocardiogram is predominantly a reflection of the blood flow in the right heart.

The microspectrophotometric determination of blood oxygen saturation in infants and children

Summary A rapid and reasonably accurate(within 5 per cent) method for the microspectrophotometric determination of blood oxygen saturation in infants and children is presented. A technique for blood collection simply performed with a minimum of disturbance and cumbersome impedimenta is described.

Artificially produced pulmonary artery stenosis in the dog

The genesis of the obstructive infundibular hypertrophy which is seen in association with pulmonary valvar stenosis, especially beyond infancy, has been explained upon an acquired basis (compensatory) but this has not been substantiated. Also, there are conflicting opinions about the necessity for resecting the infundibular muscle when the pulmonary valve is lysed. Experiments were devised using puppies in which the main pulmonary artery was banded. There was progressive increase in the right ventricular pressure, marked infundibular hypertrophy developed, as demonstrated by angiocardiography, and the cardiac output decreased. After 14 to 22 months, the pulmonary stenosis was relieved surgically and the infundibular region was not resected. After 2 to 10 months there was still significant infundibular hypertrophy. The right ventricular pressure returned to normal levels and the cardiac output increased. These experiments suggest that infundibular hypertrophy is an acquired complication of main pulmonary artery stenosis in the dog. In the human, valvotomy in infancy may prevent the development of infundibular hypertrophy. Valvotomy alone may be all that is needed, when there is an immediate drop in the right ventricular pressure, below 100 mm. Hg, at time of operation.

The two-chambered right ventricle

A relatively rare congenital cardiac malformation is described in nine patients and is characterized by aberrant hypertrophied muscular bands that divide the right ventricular cavity into two chambers. These hypertrophied muscular bands produce an effective stenosis and obstruct the outflow of blood from the right ventricle. An interventricular septal defect is usually seen in association with this abnormality. This cardiac malformation is anatomically distinct from the classic tetralogy of Fallot but may be mistakenly diagnosed as an acyanotic tetralogy of Fallot or an interventricular septal defect. The use of selective angiocardiography in conjunction with right-sided cardiac catheterization will establish the correct diagnosis. This congenital lesion is amenable to surgical correction, and five of the patients in this series were successfully operated upon with the aid of extracorporeal circulation. Surgery has been recommended for the remaining four patients because of the encouraging results.

The treatment of diabetic acidosis: Comparison oftreatment regimes with and without parenteral potassium

Summary 1. The blood chemical determinations and serial electrocardiograms of fifteen juvenile diabetics in moderate to extreme acidosis are reported. 2. These patients were treated according to the Hartmann regime and did not receive added K initially in any instance. The clinical syndrome of hypokaliemia was not observed. 3. No parenteral potassium therapy was necessary since all patients responded rapidly and were taking either liquid or soft diets in the first 24 hours and were ambulatory in 48 hours. 4. A group of seven juvenile diabetics in severe or extreme acidosis received added parenteral K initially and were studied in a similar manner. 5. The serum potassium levels were followed and showed the usual early depressions as in Group I but there seemed to be no correlation with the clinical state of the patient or the serial electrocardiographic findings. 6. No significant differences could be seen in the electrocardiograms of Group I and Group II. 7. There seems to be a reasonabledoubt that the electrocardiographic changes can be attributed solely to hypokaliemia but may be the result of other factors in such a disturbed metabolic state as diabetic acidosis.

Rheumatoid arthritis in children.

HILDREN have rheumatoid arthritis, too. It affects them just as it does adults. Children and adults alike, these patients suffer from a chronic inflammatory disease which may involve any or all of their joints. Their fingers, wrists, elbows, shoulders, hips, knees, ankles, virtually any joint in the body may be affected. The inflammatory process may smolder for as long as 5 to 10 years, its course marked by intermittent acute exacerbations. Fibrotic changes follow the inflammatory process and limit joint motion, sometimes interfering with walking and use of the hands. The muscles waste away because they are not used, general nutrition is poor, and further disability takes place (1,2,3,4). The illustrations in figures 1 to 3 show clearly the effects of this disease on the joints.