A neonatal survivor of group B beta-hemolytic streptococcal endocarditis.
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Biomedical subjects
Publications and source records attributed to M Dick.
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Recent interest in cardiac arrhythmias in children has been stimulated by a growing awareness of primary rhythm disorders in children, by the appearance of rhythm disorders following repair of many congenital heart defects, and by recent developments in clinical electrophysiology. This chapter focuses on developmental clinical cardiac electrophysiology, the spectrum of tachycardias in children, and the frequency, mechanism, and therapeutic decisions regarding cardiac arrhythmias in children who have had surgery for congenital heart disease.
To determine the acute and chronic effects of vasodilator therapy in children, vasodilator therapy was evaluated in 13 children (aged 0.2 to 14.5 years) with severe left ventricular dysfunction or mitral regurgitation. In seven children, nitroprusside increased cardiac index by an average of 33% (P less than .01) and increased stroke index by 29% (P less than .01). In eight children, hydralazine caused a 31% increase in cardiac index (P less than .01) and a 27% increase in stroke index (P less than .02). Ten children received chronic oral vasodilator therapy and were followed for 5.7 +/- 1.4 (SEM) months. Early clinical improvement was observed in every child. Symptoms of heart failure diminished in all, and five children became entirely asymptomatic. A significant (P less than .05) improvement was noted in growth velocity, respiratory rate, heart size, and incidence of gallop rhythm after 1 month of therapy. The duration of the beneficial response to vasodilator therapy varied considerably, however, and significant improvement for the group was not found after 1 month. Four children had sustained clinical improvement for 6 months or longer, but the others experienced recurrent heart failure within 1 to 4 months.
Each of seven infants 1 to 9 days old and weighing 2.1 to 3.3 kg with truncus arteriosus underwent repair of their defects with a right ventricular-to-pulmonary artery valveless conduit. Congestive heart failure and cyanosis were present before surgery in each. Five patients survived surgery and one of these subsequently died. Comparison between preoperative hemodynamics of the survivors and nonsurvivors disclosed similar peak systolic pulmonary arterial and aortic pressures, and pulmonary (Rp) or systemic resistance (Rs) in the groups. However, the mean Rp/Rs ratio in survivors (0.15) was significantly less than in nonsurvivors (0.63) (p = .001). The four remaining survivors are asymptomatic 7 months to 5.5 years after operation. Postoperative cardiac catheterization in three patients disclosed proximal conduit obstruction of 10 to 20 mm Hg in each, distal conduit obstruction of 35 mm Hg in two, and mild truncal valve stenosis and moderate truncal regurgitation in one each. We recommend the use of a valveless conduit for the symptomatic neonate with truncus arteriosus and a low Rp/Rs ratio (less than or equal to 0.03).
Addition of 125I-thyroxine to serum allows autoradiography for thyroxine-binding globulin microheterogeneity to be carried out after isoelectric focusing has been performed to display (by protein stain) the heterogeneous bands of the alpha 1-antitrypsin (PI) system. Comparison of the protein stain for PI with the autoradiograph for thyroxine-binding globulin indicates that these two systems are interrelated with the major bands of the PI system corresponding to the bands on the autoradiograph. This correspondence holds for PI variants other than the common M type and in particular it holds for the deficient Z type in which the autoradiograph for thyroxine-binding globulin is strikingly different from normal. We conclude that the major cause of microheterogeneity of TBG is due to an association with the PI system under the conditions of isoelectric focusing as normally performed. Precipitation experiments with antisera to PI and TBG suggest that the complex between these biologically important globulins may occur under conditions other than isoelectric focusing, but further work will be needed to examine this possibility.
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The presence of what we believe is a unique variant of thyroxine-binding globulin in a high proportion of Australian Aborigines causes difficulty in the interpretation of thyroid function tests in such subjects. We present reference ranges for the common tests of thyroid function and a suitable combination of tests for the laboratory investigation of thyroid function in Aborigines. We suggest that the thyroid status of Aborigines previously diagnosed as hypothyroid should be reviewed.
Epicardial and left ventricular endocardial activation were assessed in 5 patients (aged 4 months to 9.5 years) with endocardial cushion defect (ECD) during surgical repair. Epicardial activation was recorded from 40 to 47 sites over the epicardium; left ventricular endocardial activation was measured at 3 sites immediately after institution of cardiopulmonary bypass. Compared with the reported activation sequence in normal hearts, the pattern of excitation in hearts of patients with ECD was abnormal; epicardial excitation began at the left ventricular diaphragmatic surface and spread laterally and anteriorly over the anterobasal left ventricle. It then merged with right ventricular wavefronts ending along the right ventricular anterior atrioventricular groove and outflow tract. Left ventricular endocardial activation also occurred earliest in the diaphragmatic segment of the left ventricle with later wavefronts recorded laterally and anteriorly. This study demonstrates, for the first time in human subjects, correlation between left ventricular epicardial and endocardial activation in patients with ECD. The data indicate that earliest endocardial and epicardial activation occurs at the left ventricular diaphragmatic segments of the heart, and are consistent with the known posterior and inferior displacement of the specialized atrioventricular conduction system in patients with ECD.
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After obtaining samples at open heart surgery, serum and right atrial digoxin concentrations were measured in 25 children by a nonspecific, direct radioimmunoassay method (NS) and by a specific method in which digoxin was separated from its metabolites by HPLC before radioimmunoassay was applied to the digoxin fraction (S). Digoxin was detectable by S assay (sensitivity 0.1 ng/g) in 16 heart specimens and 22 serum samples. The mean and range of the S/NS ratio was 0.74 (0.23 to 2.63) for serum and 0.81 (0.068 to 1.38) for atrial tissue. By NS assay the mean and range of the atrial/serum ratio was 78.1 (2.4 to 340, n = 21) and by S assay the corresponding values were 100 (10.7 to 318, n = 15). A multiple linear regression indicated that 72.5% of the variance of the heart digoxin concentrations measured by S assay were accounted for by the variables height, body weight, daily digoxin dose before operation, plasma digoxin concentration by S assay, and BUN.
We analyzed the sequence of ventricular emptying using the phase image in 10 patients with accessory pathways and in 15 normal subjects. In normal subjects, the earliest emptying occurred in ventricular septal, apical and left basal segments. Eight patients had manifest preexcitation; the earliest emptying occurred ectopically in the right ventricle in one of these patients and in the left ventricle in five. The remaining two patients had normal phase maps. Two patients had concealed left-sided pathways. Their phase maps showed earliest emptying in left basal segments. Six of the 10 patients underwent electrophysiologic mapping. There was complete agreement between phase and electrophysiologic maps. Transesophageal atrial pacing increased preexcitation in one patient, normalized the ECG in another and precipitated narrow QRS tachycardia in four patients. Phase maps then showed enlargement, reduction and loss of the ectopic earliest emptying segments, respectively. We conclude that this technique in conjunction with pacing is successful in lateralizing accessory pathways.
To examine the excitation of the double chamber right ventricle and the possibility that it results from a displaced, hypertrophied moderator band, seven patients with double chamber right ventricle were studied. All seven had pre- and postoperative electrocardiograms. Intraoperative right ventricular epicardial maps were obtained in three; right ventricular endocardial activation maps performed at postoperative catheterization were obtained in four. In the three patients studied at operation the breakthrough point of right ventricular epicardial activation was demonstrated in a normal inferior location well below the obstructing muscle band. Two patients with right bundle branch block after operation and two others with only right ventricular conduction delay on postoperative electrocardiogram demonstrated high normal right ventricular time with prolongation of activation in the right ventricular outflow or inflow region, or both, suggesting only peripheral injury. These data suggest that activation of the double chamber right ventricle is similar to that of the normal heart. In addition, the observed normal activation sequence militates against the hypothesis that the moderator band is the obstructing bundle.
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Ventricular pacing was performed in forty-one children ranging from one day to twenty years of age (median age = 10). Weight of the recipient at implant ranged from 2 kg. to 86 kg. Indications included presyncope, syncope, dyspnea on exertion, congestive heart failure, postoperative infra-Hisian heart block, and inadequate cardiac rate during pharmacotherapy. Four patients died during follow-up, but no deaths were attributable to pacemaker management. In contrast, 66% of the patients required more than one pacemaker related-operative procedure, and 43% of leads implanted failed by 48 hours. Indications for permanent cardiac pacing in this population at this time are symptomatic congenital AV block, symptomatic sinus node disease, and AV block in the postoperative period. Technological developments which might reduce complications seen in this population and electrophysiologic techniques which may better define indications for pacing in children are also reviewed.
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During a 31/2 year period, 11 consecutive infants with total anomalous pulmonary venous connection younger than 6 months of age underwent repair at our institution. Early mortality was 19% (one of 11) and long-term mortality 18% (two of 11), yielding an overall survival of 73%. One late death was due to bradyarrhythmia and the other was due to recurrent pulmonary venous obstruction. Postoperative catheterization in seven of eight survivors and in three additional patients disclosed normal or nearly normal pulmonary artery pressure and pulmonary arteriolar resistance. Left ventricular diastolic volume was normal before operation (n = 5) and on follow-up study (n = 9). Mild left ventricular outflow obstruction or coarctation or both developed during follow-up in two patients. Sinus node function was normal in all seven late survivors studied, and atrioventricular conduction was normal in three of four. This experience indicates that total anomalous pulmonary venous connection can be repaired early in infancy, with preservation of normal hemodynamics and electrophysiologic state.
We have recently described a major variation from the normal levels of serum thyroxine-binding globulin in many Australian Aborigines [1]. Subsequently we presented evidence that affected individuals were widely distributed throughout Australia, that "low values of thyroxine-binding globulin were not caused by environmental or health factors, but were inherited in an autosomal dominant fashion [2]. Refetoff [3] has shown that the cause of genetically determined low thyroxine-binding globulin levels in Caucasians is alteration in synthesis rate without any structural variation of the protein. Since however the "low" thyroxine-binding globulin of Aborigines is vastly more prevalent and genetically distinct from the X-linked type, we investigated the possibility that this may be a structural variant. Evidence suggestive of this includes results from heat inactivation, competitive binding of thyroxine to thyroxine-binding globulin to measure affinity, and use of a radioimmunoassay different from that used in the original work. The "Low thyroxine-binding globulin of Aborigines may be a protein with a structural variation at or near the binding site for thyroxine, resulting in low affinity for thyroxine and hence "low" results with assay methods which depend upon the thyroxine binding site. Since the Australoid peoples, to whom Australian Aborigines are racially related, are distributed widely throughout the southern hemisphere it is important to establish whether this variant is found outside Australia in order to avoid the likelihood of misdiagnosis of thyroid disease in such subjects.