A voltage-triggered system for adaptive sampling in body surface mapping.
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Biomedical subjects
Publications and source records attributed to M S Spach.
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Using a system for obtaining body surface potential distributions from 150 sites on the anterior and posterior torso, 43 body surface maps were evaluated in 31 normal infants, ages 15 hours to 10 months. Serial maps were obtained at 0.6-msec intervals during QRS and at 2.4-4-msec intervals throughout the ST-T wave. We found an orderly evolution of both QRS and ST-T wave maps during the first year of life. In the newborn, the patterns during the latter half of QRS were consistent with early completion of depolarization of the left ventricle and prolonged depolarization of the right ventricle. The patterns changed gradually such that by 5-6 months of age, the maps demonstrated simultaneous effects of both right and left ventricles during the latter half of QRS. By 9 months, the QRS patterns were similar to those of older children and adults. The changes in the ST-T-wave maps were consistent with the idea that age-related changes in the sequence of ventricular activation.
Forty-nine patients with Wolff-Parkinson-White syndrome, ages 7 weeks to 51 years, were studied with isopotential body surface maps during normal sinus rhythm, atrial pacing or induced atrial fibrillation. The location of the accessory pathway was determined by multicather electrophysiologic study or surgical ablation of the accessory pathway. When fusion was minimized and ventricular activation primarily controlled by a single accessory pathway, the distribution of positive and negative potentials on the anterior and posterior torso during QRS (observed at 40 msec) and the ST segment were an excellent index of the location of the site of the accessory pathway. The relationship between a specific sequence of QRS-T wave body surface maps and a specific preexcitation site was similar from patient to patient in the presence of marked differences in age, size, and different cardiac status due to structural congenital cardiac defects. The localization of the site of the accessory pathway using distributions too early in QRS (before 40 msec) was unreliable because the early distributions varied from patient to patient for the same preexcitation site; however, the potential distributions during the ST segment were both stable and consistent from patient to patient for the same preexcitation site. The presence of significant fusion of ventricular activation initiated via a single accessory pathway and the normal conduction system or via multiple accessory pathways complicated the interpretation of body surface distributions. Thus, one can predict accurately at least seven preexcitation sites by the combined use of QRS and ST-segment body surface maps.
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Propagation velocities of action potentials were measured simultaneously along the longitudinal and transverse axes of cardiac fibers in ventricular muscle. The anisotropic distribution of propagation velocities was found to be altered transiently and in the steady state by the rate and pattern of stimulation and by ouabain. The relative amount of velocity change varied with the direction of propagation and was greatest in the direction perpendicular to the long fiber axis. None of the variables usually associated with the membrane ionic mechanism of depolarization--resting potential, Vmax, and taufoot--showed enough variation to account for the observed changes in velocity. A simplified anisotropic propagation model representing the internal current pathway as an alternating sequence of cytoplasmic and junctional resistance is presented, taking into account the larger contribution to the internal resistance made by the cell couplings in the transverse direction than in the longitudinal direction. On the basis of this model, it was concluded that the observed changes in velocity were due to changes in cell coupling. Both transient and steady state velocity changes were found to correspond to changes in the action potential duration, suggesting that there is a common factor, such as the internal calcium and/or sodium concentrations, linking the control of the action potential duration and the coupling resistance between cardiac cells.
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A 10-month-old infant with multiple muscular ventricular septal defects, congestive heart failure, Wolff-Parkinson-White syndrome, and supraventricular tachycardia is presented. The site of ventricular pre-excitation was predicted by analysis of ST-T wave isopotential body surface maps to be in the posterior free wall of the right ventricle. The site was confirmed by epicardial mapping of the ventricles during surgery. The pathyway was cryoblated and the ventricular defects were closed. The patient has been free of pre-excitation and supraventricular tachycardia for over two years since surgery.
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This is a report of a 10-year-old child who underwent surgery for complex congenital heart disease consisting of corrected transposition of the great vessels, ventricular septal defect, patent ductus arterisus, severe left-sided atrioventricular (AV) valve insuffieicney (Ebstein's deformity) and Wolff-Parkinson-White syndrome. The site of his accessory AV connection was localized preoperatively at a left anterolateral site by isopotential body surface maps and by intracardiac electrophysiologic studies. He successfully underwent surgery for closure of the ventricular septal defect, ligation of the patent ductus arteriosus, replacement of the left-sided AV valve, and interruption of the accessory AV pathway. Unavoidable complete AV block acquired at surgery required subsequent permanent pacemaker therapy.
Total body surface potential distributions were recorded from 20 normal young adults, 20-35 years old, during multistage maximal exercise testing on a bicycle ergometer. Using a system for measuring total body surface potential distributions from measurements at 24 locations, high-quality potential maps were obtained during exercise without requiring wave form averaging or special modes of exercise. Serial maps recorded at 1-msec intervals throughout QRS-T during exercise and during recovery from exercise were compared with corresponding maps recorded with the subjects at rest. During and after exercise, consistent changes appeared in the map patterns during early QRS and the ST segment and in the magnitude of the T-wave potentials. Increases in QRS duration (0-10 msec) also appeared during exercise. The changes in map patterns during early QRS in exercise strongly suggested changes in the initial sequence of activation in the ventricles. The results demonstrate the importance of analyses of total body surface potential distributions in understanding ECG changes during exercise.
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This paper considers a quantitative description of intracellular and transmembrane currents in anisotropic muscle, with emphasis on the factors that determine the extracellular potentials. Although Vmax of the intracellular action potential had no relation to changes in conduction velocity in anisotropic tissue with constant membrane properties, the extracellular waveforms were quite sensitive to velocity changes. Large amplitude biphasic deflection occurred in the fast areas, and in the slow areas the waveforms were of lower amplitude and triphasic in shape; i.e., negative potentials preceded the biphasic positive-negative deflection. The extracellular potentials were simulated on the bases of a model of intracellular currents, and the theoretical and measured results showed good agreement. In tissue with anisotropic conductivity, the relationship between the spatial intracellualr potential gradient and the magnitude of the extracellular potential of the excitation wave was opposite to the classical relationship in isotropic tissue. Due to the influence of the effective intracellular conductivity on the spread of intracellular currents and on conduction velocity, in anisotropic tissue the extracellular potential decreased as the intracellular potential gradient increased. The peak values of the positive and negative potentials and the spatial distribution of the potential gradients varied considerably along the activation front. These findings were accounted for by differences in the distribution and spatial extent of the transmembrane currents, which were determined by the intracellular currents. The theoretical analysis showed that intracellular and transmembrane currents were proportional to the local conduction velocities of the wavefront. Thereby, it was not possible to have a "uniform layer" of current when there were differences in conduction velocity along the length of the excitation wave. The implications of the analysis are considerable, since the gratifying agreement between the theoretical and measured results indicates that the details of the extracellular waveforms can be explained on the basis of the distribution of intracellular currents; i.e., extracellular potentials provide a sensitive index of intracellular current flow.
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