Biomedical subjects
Publications and source records attributed to T D King.
A 17-year-old girl had clinical and cardiac catheterization findings compatible with a secundum atrial septal defect. During cardiac catheterization, the atrial septal defect was sized and closed using a transvenous umbrella technique.
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Most congenital heart anomalies now can be surgically corrected in a neonate or very young infant. Because their hearts are so small, it is advantageous to work in a bloodless and motionless operative field. Deep hypothermia with circulatory arrest provides this setting. Physiologic problems associated with hypothermia are minimized by inducing general vasodilatation with large doses of methylprednisolone. Surface cooling is done with ice blankets and small sandwich bags filled with crushed ice. The patient's temperature gradually falls to 75.2 F (24 C). After median sternotomy, core cooling can be used to bring the patient's temperature to the desired 68 F (20 C). Circulatory arrest is produced by draining blood into the reservoir and cross-clamping the great vessels and venae cavae. It can be maintained for up to 60 minutes. In infants over six months and over 6 kg (13.2 lb), moderate hypothermia 77 F (25 C) and low perfusion (1/4-1/3 of normal) with short periods (10 to 15 minutes) of circulatory arrest improve operative conditions and allow correction of the most complicated congenital heart defects.
Case histories of 8 consecutive patients who underwent surgical correction of Type C complete atrioventricular (A-V) canal at the Ochsner Medical Center over the past 2 years were analyzed. Ages ranged from 1 1/3 to 14 years. Before bypass, the level to which the common leaflets ascend and the arc that they inscribe are determined by palpation to ensure their proper reconstitution on the canal patch. The major area of closure is usually allocated to the ventricular portion. Mapping the conduction system and tying sutures with the heart beating in high-risk conduction areas prevent heart block. Precise marking and splitting of the valve leaflets and reattachment with interrupted felt-buttressed sutures avoid disruption. All patients survived the operation and have shown clinical improvement. At recatheterization, 7 of 8 patients have shown a definite decrease in mitral insufficiency. Right ventricular pressures returned toward normal and there were no significant residual shunts. Associated anomalies or previous operations have not been a contraindication, and since we have begun using the present technique, we have achieved consistently good results without prosthetic valves.
Efforts to close left-to-right shunts at Ochsner Medical Institutions have been directed toward atrial septal defects (ASD) and patent ductus arteriosus (PDA). PDA's were constructed in dogs by interposing a segment of jugular vein between the aorta and main pulmonary artery. Five dogs in which the PDA was closed by a plug device inserted through the femoral vessels were put to death at 6 to 12 months. Histologic sections showed good fibrous ingrowth with endothelial covering on the aorta and pulmonary artery sides. There were no migrations redidual shunts. At cardiac catherterization, 18 patients had ASD's sized and located as to position in the septum. The sized ranged from 13 to greater than 30 mm. in diameter. The ASD sizes in patients who underwent standard operative closure were compared to the measurements at catheterization, and the variation was insignificant. In 5 patients, centrally positioned secundum ASD's were closed with double umbrella devices, 25 to 35 mm. in diameter. Anatomic contraindications for umbrella closure include ASD's greater than 30mm. in diameter, anomalous pulmonary venous connection, common atrium, inferiorly or superioly located secrumdum ASD, and sinus venosus ASD. Follow-up studies from 6 to 12 months on 5 patients with umbrella closure have revealed no hemolysis, arrhythmias, thromboembolism, migration, or other untoward effects.
A 5-year-old boy had clinical, cardiac catheterization, and operative findings of a thoracic arteriovenous fistula arising from the right subclavian artery. The venous connection was to the paravertebral plexus with eventual drainage into the inferior vena cava through the right common iliac vein. To our knowledge, this type of fistula has not been reported previously and is believed to represent embryological defects of the first or second posterior intercostal arteries as well as maldevelopment of the venous connections of azygos vein to the superior vena cava, which resulted in the observed caudal venous pathways becoming operative.
Allotype suppression is held to be an example of T-cell suppressor function. Failure of generalized suppressor T-cell function is considered to be responsible for the chronic and progressive disease of the NZB. The possible association of allotype suppression and autoimmune disease has been investigated here in a group of NZB mice, transplanted and born from BALB/c recipients whilst producing anti-NZB allotype. In this situation it was anticipated that if allotype suppression should fail this would coincide with the development of autoimmune disease; both processes reflecting failure of T-cell suppressor function. However, in spite of the fact that allotype suppression was not achieved, certain observations seem important. The fact that NZB born the BALB/c were in no way different from normally derived NZB confirms that the cause of the NZB disease is established prior to the stage of implantation. Maternal influence at or beyond this stage appears of little consequence in terms of effecting the development or progression of the NZB disease. The failure to induce allotype suppression in the NZB is important. In this context this strain appears to be no different from the majority of other strains that have been tested as homozygotes. The suppression obtained with (BALB/c X SJL/J)F1 hybrids in which chronic suppression has been achieved therefore seems to represent an exceptional situation and this suggests that it is perhaps unwise to base general assumptions as to the universal adaptability of T-cell control mechanisms upon unusual findings. It must be remembered that only homozygotes were examined here. Earlier attempts to induce allotype suppression in homozygotes also failed, even in the SJL/J. Since allotype suppression has only been demonstrated in heterozygote mice there is a distinct possibility that this phenomenon never occurs in the homozygote situation. The significance of this possibility is discussed.
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