Mary Jo Burgess

Influence of sympathetic tone on ventricular fibrillation threshold during experimental coronary occlusion.

The effects of increased and decreased cardiac sympathetic tone and coronary occlusion on ventricular fibrillation were determined in 14 open chest dogs anesthetized with sodium pentobarbital. Heart rate was kept constant by pacing the right atrium at cycle lengths of 500 msec. Ventricular fibrillation threshold was measured by delivering 350 msec trains of constant current stimuli with a frequency of 100 hertz and 2 msec duration. The minimal current of the train that induced fibrillation was taken as the ventricular fibrillation threshold. In seven animals, the effects of stellate stimulation were studied. Ventricular fibrillation threshold was measured during control periods, after 2 minutes of cornoary occlusion, after 2 minutes of stellate stimulation and after 2 minutes of stellate stimulation and coronary occlusion. Coronary occlusion alone decreased ventricular fibrillation threshold an average of 35 percent of control valvues and stellate stimulation alone decreased the threshold an average of 42 percent of control values. The combination of both these interventions decreased ventricular fibrillation threshold an average of 63 percent of control values. The effects of stellate ablation were studied in seven animals. Ventricular fibrillation threshold was measured during control periods, and during coronary occlusion before and after stellate ganglionectomy. Stellectomy increased the threshold an average of 31 percent above control values. After stellectomy, coronary occlusion decreased ventricular fibrillation threshold by only 11 percent of control values, a value 26 percent higher than the threshold during coronary occlusion before stellectomy. These findings may have therapeutic implications for the management of arrhythmias in patients with acute myocardial infarction or some forms of central nervous system disease.

The sequence of normal ventricular recovery

Abstract Functional refractory periods (FRPs) were measured at epicardial, intramural, and septal sites in pentobarbital anesthetized dogs. The sinus node was crushed and the atria were driven at a fixed rate. Activation times at the test sites were measured from electrograms recorded from closely spaced bipolar electrodes. The test stimuli were cathodal “make” stimuli delivered to one pole of the pairs of electrodes. FRPs at the base of the free wall of the left ventricle and of the septum were shorter than FRPs at the apex. FRPs on the epicardium were shorter than those on the endocardium, and FRPs on the right side of the septum were shorter than those on the left side of the septum. The findings indicate that normal ventricular recovery properties are systematically distributed and inversely related to activation sequence. Areas of the ventricle activated early have the longest FRPs, and areas activated late have the shortest FRPs. This distribution of recovery properties tends to make all portions of the ventricles complete recovery at about the same time, and may play a protective role in the prevention of reentrant arrhythmias. This distribution of recovery properties is also applicable to an explanation of the configuration of normal T waves.

Clinically practical lead systems for improved electrocardiography: comparison with precordial grids and conventional lead systems.

The use of limited leads for estimating total body surface potential distributions was investigated as a practical solution to the problem associated with extensive electrocardiographic sampling used in surface potential mapping. Two practical, limited lead sets of 32 leads each were derived and contrasted to a set of 30 precordial leads similar to those used in ST-segment and QRS mapping for estimating infarct size, and to a set of nine leads simulating those used in conventional 12-lead examinations. The two arrays, one of which excluded posterior sites for use in recumbent patients, showed little difference in ability to estimate 192 lead measured maps (average rms voltage error of 35,V and average correlation coefficient of 0.97). The 30- and 9-lead arrays consistently showed twice the voltage (72,uV) and poorer pattern estimation (average correlation coefficient of 0.91) than either of the 32 lead arrays. These findings indicate the need for 20-35 properly located electrodes for accurate total body surface potential estimation. They also show that there is no difference in the abilities of a 30-lead precordial array and conventional leads to estimate maps

The electrocardiogram and the central nervous system

Abstract Abnormalities of ECG wave form occur in some patients with central nervous system lesions. Distinctive electrocardiographic abnormalities associated with central nervous system lesions are prolonged QT intervals, large upright or deeply inverted T waves, bradycardia, and prominent U waves. In some instances deeply inverted T waves occur, similar to those due to acute myocardial infarction. Less striking abnormalities of the ST segments and T waves occur in some cases, and may be misinterpreted as due to ischemic heart disease, drugs, or electrolyte disorders. It is likely that the ECG changes are mediated by abnormalities of sympathetic tone to the heart. A functional change in action potential form as the cause of the ECG findings is supported by the findings of normal hearts at autopsy and by the experimental data showing almost immediate ECG changes during sympathetic stimulation and ablation. Anatomic cardiac lesions, however, have been reported in some patients dying with central nervous system disease and in experimental animals with central nervous system stimulation or induced lesions.

Nonuniform epicardial activation and repolarization properties of in vivo canine pulmonary conus.

The relation between nonuniform epicardial activation and ventricular repolarization properties was studied in 14 pentobarbital anesthetized dogs and with a computer model. In 11 dogs, isochrone maps of epicardial activation sequence were constructed from electrograms recorded from the pulmcnary conus with 64 electrodes on an 8 × 8 grid with 2-mm electrode separation. The heart was paced from multiple sites on the periphery of the array. Uniformity of epicardial activation was estimated from activation times at test sites and their eight neighboring sites. Acceleration shortened and deceleration prolonged refractory periods. The locations of acceleration and deceleration sites of activation differed during drives from various sites, and differences in uniformity of activation during pairs of drives were correlated to differences fa refractory periods (r =0.76, range 0.59–0.93). In three additional experiments, transmural activation sequence maps were constructed from electrograms recorded from needle-mounted electrodes placed upstream and downstream to epicardial activation delays. Activation proceeded from epicardium to endocardium upstream to the delays and from endocardium to epicardium downstream to the delays. A computer simulation of two-dimensional action potential propagation based on the Beeler-Reuter myocardial membrane model provided insights to the mechanism for the results of the animal experiments. The two-dimensional sheet modeled the transmural anisotropic histology of the canine pulmonary conus and corresponded to previous reports and histology of specimens from five experiments. Simulated activation patterns were similar to those found in the experimental animals. In addition, action potentials were electronically prolonged at sites of deceleration and shortened at sites of acceleration, results comparable to the animal experiments. Our findings demonstrate that the location of areas of nonuniform epicardial activation is dependent on drive site and that nonuniform activation electronically modulates repolarization properties. Therefore it seems likely that the site of origin of ectopic ventricular complexes, especially in ischemic myocardium where activation is nonuniform, could be an important determinant of whether ectopic activity initiates sustained tachyarrhythmias.

Diagnosis of old inferior myocardial infarction by body surface isopotential mapping

Body surface isopotential maps obtained from 28 patients with old inferior wall myocardial infarction were compared with maps from 120 normal subjects. The 12 lead electrocardiogram of 8 of the 28 patients (29 percent) with inferior wall infarction was normal or showed only nondiagnostic ST-T wave abnormalities at the time the isopotential maps were obtained. In all patients with inferior wall infarction the isopotential map showed a minimum (area of negative potentials) on the inferior or right thoracic surface during the early portions of the QRS complex. This finding was observed in patients with normal or nonspecific abnormalities in the 12 lead electrocardiogram as well as those with QRS abnormalities. By contrast, the minimum during the early QRS complex in normal subjects was located on the right upper back and shoulder region...

The unidentified information content of the electrocardiogram.

DEVELOPMENT of practical recording methods for the human electrocardiogram was rapidly followed by important medical applications. Electrocardiography was established as the major means of classifying disturbances of cardiac rhythm and an important aid in the recognition of myocardial disease including infarction. Applications have been sufficiently significant to result in widespread use of the method and there have been continuing technological improvements and extensions of the methods utility. At the present time and as presently used, electrocardiography is one of the major medical diagnostic methods. Despite considerable utility, it is unlikely that the full medical significance of electrocardiographic examination has been achieved. A variety of theoretic considerations together with supporting experimental and clinical observations suggest that the record may contain information of equal or even greater medical significance than that now obtained. This communication will review some of these considerations and observations. Material will be presented under the headings of regional cardiac examination, prognostic utility, and extended diagnostic applications. None of these represent totally new objectives for electrocardiographic examination but each offers substantial possibilities for improved use of the technique. The material reviewed does not include all areas in which improvements of electrocardiography are likely and should be viewed only as selected examples. Much of the material is necessarily speculative although some theoretic and/or clinical and experimental support for the speculations in each area will be furnished.

Experimental evidence for regional cardiac influence in body surface isopotential maps of dogs.

Isopotential maps based on 192–200 body surface electrocardiograms were obtained for 20 dogs during multiple patterns of ventricular activation. The purposes of the study were to determine whether the cardiac location of events responsible for surface potentials had a recognizable influence on surface potential patterns and to examine the influence of electrical events occurring simultaneously in multiple cardiac regions. Substantially different effects of electrical activity in various cardiac regions on body surface potentials were evidenced by the body surface location of potential maxima and minima and by patterns of isopotential lines during early portions of ventricular excitation initiated at different ventricular sites. Simultaneous stimulation at some sites gave surface potential distributions with multiple extrema. These were demonstrated to be due to effects of the different cardiac regions, because addition of potentials due to stimulation of the individual sites duplicated those associated with simultaneous stimulation of the same sites. It was also shown that body surface locations of maxima and minima are not related in the same manner to the cardiac location of the responsible events when these events are present in single and multiple regions. Slopes of potentials due to events in single cardiac regions were shown to combine with slopes produced by events in other regions to yield maxima or minima at new body surface locations. Results of the study support the possibility of regional cardiac examination by electrocardiograph) but suggest that this will require quantitative descriptions of the details of potential patterns in addition to the location of potential peaks.

Computer simulations of three-dimensional propagation in ventricular myocardium. Effects of intramural fiber rotation and inhomogeneous conductivity on epicardial activation.

Three-dimensional membrane-based simulations of action potential propagation in ventricular myocardium were performed. Specifically, the effects of the intramural rotation of the fiber axes and inhomogeneous conductivity on the timing and pattern of epicardial activation were examined. Models were built, with approximately 400,000 microscopic elements arranged in rectangular parallelepipeds in each model. Simulations used the nonlinear Ebihara and Johnson membrane equations for the fast sodium current. Constructed models had histological features of ventricular myocardium. All models were anisotropic. In a subset of the models, an abrupt intramural rotation of the fiber axes was included. This feature was also combined with randomly distributed inhomogeneous conductivity and regions of high transverse resistance to represent nonuniform anisotropy in a further subset of the models. Epicardial stimuli were applied for each simulation. Three-dimensional activation patterns and epicardial isochron maps were constructed from the simulations. We noted that the rotation of fiber axes accelerated epicardial activation distant from the stimulus site. The inhomogeneous conductivity caused regional acceleration and deceleration of activation spread. We also noted features of epicardial activation that resulted from the fiber rotation, and the inhomogeneous conductivity corresponded to that observed in maps from experimental animals.

The relation of localized myocardial warming to changes in cardiac surface electrograms in dogs.

We studied the relationship of the size and severity of alteration of recovery properties in localized areas to changes in cardiac surface electrograms in experiments on six open-chest dogs. Alterations in recovery properties were induced thermally because size and severity of the affected area could be controlled on the basis of physical principles which were modeled. We recorded unipolar electrograms from 75 cardiac surface sites simultaneously during stimulation of atria and pulmonary conus in control periods and in the presence of warmed areas of varying sizes and intensities. Size of the areas was controlled by the diameter of an aperture through which a light source was directed. Intensity was controlled by the light source excitation voltage. Myocardial temperature was monitored with a thermistor. The QRS, STT, and QRST deflection areas were determined by computer processing and displayed as isoarea maps. Difference maps also were determined by subtracting control QRST isoarea maps from those obtained in the presence of warmed areas. QRST area difference maps were related closely to the size and severity of the thermally induced changes in recovery properties. With areas of the same size and increasing myocardial temperatures, the magnitude of the change in QRST area increased, and the gradient of contour lines between the affected and unaffected areas increased. When myocardial temperature at the center of the warmed area was kept constant and the size of the warmed area was increased, the affected cardiac surface area increased, but the number of isoarea contours remained approximately the same. These findings suggest that the change in QRST isoarea maps may be a useful indicator of lesion size when combined with an index of lesion severity such as the QRST area change in the electrogram with the maximum change. QRST areas during both activation orders were similar, suggesting that the QRST area is independent of changes in activation sequence.