J.A. Abildskov

Limited Lead Selection for Estimation of Body Surface Potential Maps in Electrocardiography

Body surface potential mapping has shown promise as a technique to improve the resolution and accuracy of diagnostic electrocardiography, but the cost and effort required to obtain maps have made wide spread use impractical. As a step toward a practical system, the problems of redundancy and uniqueness of electrocardiographic signal information contained in large numbers of leads were investigated. An algorithm for optimal selection of a limited number of leads was developed. Data obtained from 132 human subjects including some with normal electrocardiograms (ECG) as well as some with abnormal ECGs, were used in the study. Estimation of body surface potentials from limited leads was evaluated using three criteria, including rms error, mean correlation coefficient between limited lead and total lead maps, and error to signal power ratio. Using 30 leads the average rms error was 32 ¿V, average correlation coefficient was .983 and noise to signal power was 3.5% in the presence of 20 ¿V rms noise. Another finding was that optimal sites are not unique, i.e., different sets of optimal sites may be found which perform equally well. This result has practical implications for the design of lead systems for estimating maps on the critically ill and on patients undergoing stress tests.

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.

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.

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 Mechanism of Simulated Torsade de Pointes in a Computer Model of Propagated Excitation

Mechanism of Torsade de Pointes. A computer model that simulated propagation, nonuniform cycle length dependent recovery of excitability, and slow propagation during incomplete recovery in cardiac muscle has been shown to exhibit behavior similar to torsade de pointes. The conditions required in the model resembled those in long QT syndromes with regionally prolonged ventricular repolarization. In the model, premature excitation of a path with relatively short refractory periods resulted in sequential reentry of that path from a region with longer refractory periods. Sites of reentry become progressively more distal to the site of initiation. The episodes terminated spontaneously when reentrant excitation reached the end of unclosed paths or collided in closed paths. Each reentry site moved away from its initial position in the short recovery path because the distance traversed by propagation in that path exceeded the distance at which reentry occurred via the longer recovery region. The migrating sites of reentry resulted in changing QRS waveform in calculated electrocardiograms including changing QRS polarity when calculated from appropriate sites. Variations of the basic behavior occurred with nonuniform distribution of refractory periods within relatively short and long refractory period regions and included unidirectional progression of reentry sites and multiple circuits of reentry in closed paths. Termination of serial reentry at times other than those when activation reached the end of unclosed paths or collided in closed paths also occurred with nonuniform distribution of refractory periods. Findings provide a plausible explanation for the changing QRS waveform, spontaneous termination, and association of torsade de pointes with long QT syndromes but do not elucidate the mechanism of initiation of the tachyarrhythmia.

Time course of vulnerability to fibrillation after experimental coronary occlusion

Abstract The early time course of vulnerability of the ventricles to fibrillation after coronary artery occlusion was measured in 6 dogs. The duration of a train of 60 Hz stimuli with currents of 2 to 3 times the diastolic threshold was used as the measure of vulnerability to fibrillation. Within 2 minutes of coronary occlusion the duration of the train of 60 Hz stimuli inducing fibrillation fell by an average of 25 percent of control values. Five minutes after coronary occlusion the duration of the train was an average of 34 percent shorter than control values. In all animals, the duration of the train required to produce fibrillation began to increase 30 minutes after coronary occlusion and approached control values. The relation of these findings to the time course of arrhythmias in experimental infarction and the early high mortality rate in cases of infarction in man is discussed.

Relation of cardiac surface QRST distributions to ventricular fibrillation threshold in dogs.

The relation between ventricular fibrillation threshold (VFT) and cardiac surface QRST area distributions was studied in eight pentobarbital-anesthetized dogs. Unipolar epicardial electrograms were recorded from 64 sites evenly distributed on the right and left ventricles. Localized areas of short repolarization properties were produced by directing five intensities of light onto the surface of the anterior right ventricle through apertures of three sizes. VFT, measured at the center of the lesion, decreased during warming and had a high negative correlation to the change (warming-control) in QRST area (delta QRST1) in the electrogram recorded from the center of the lesion. This correlation was independent of lesion size. For the six experiments, the correlation coefficients for 400-, 800-, and 1,600-mm2 lesions averaged -0.95, -0.94, and -0.96, respectively. The correlation between VFT and delta QRST1 without regard to lesion size averaged -0.88. VFT also had a negative correlation to root mean square (RMS)delta QRST because of warming. RMS delta QRST was calculated from the change in QRST areas (warming-control) in all 64 electrograms. The correlation between VFT and RMS delta QRST was dependent on lesion size. For all experiments, the correlation between VFT and RMS delta QRST averaged -0.97, -0.93, and -0.93 for 400-, 800-, and 1,600-mm2 lesions, respectively. The correlation between VFT and RMS delta QRST without regard to lesion size, however, was considerably lower, -0.59. The results of this study provide the first direct evidence that VFT is correlated with cardiac surface QRST area distributions.

Mechanisms in simulated torsade de pointes

Torsade de Pointes. A mechanism of torsade de pointes consisting of moving sites of reentrant excitation has been proposed on the basis of findings with a computer model. Substantialadditions to that mechanism are now proposed based on further studies with the same model.The model simulated propagation, cycle length‐dependent recovery of excitability, and slowpropagation during incomplete recovery. Regions of relatively short and long recovery wereassigned because of evidence of regional prolongation of recovery in long QT syndromes inwhich torsade dc pointes is frequent. As previously reported, premature excitation in the shortrecovery region initially propagated independently, then entered the long recovery region andreentered the short recovery region distal to the site of origin. Reentrant excitation initiated asimilar series of events, and serial reentry at systematically changing locations resulted inchanging patterns of excitation compatible with the changing QRS waveform in torsade depointes. Episodes terminated when reentrant excitation reached the end of unclosed shortrecovery paths, collided in closed paths, or encountered refractoriness in the presence ofnonuniform short recovery. In this study, it was shown that excitation preceding reentry hadimportant effects on the mechanism. These included reversal of the direction of serial reentry, bidirectional serial reentry, reentry at multiple sites from the same parent conditions, andoccurrence of reentry without the requirement of slow propagation. Evidence for a Dopplershift of cycle lengths in regions from which serial reentry was receding or approaching wasobtained. Sustained serial reentry was also demonstrated and is a possible mechanism for polymorphic ventricular tachycardia. Findings further define a possible mechanism of torsade depointes.

Attempted surgical division of the preexcitation pathway in the Wolff-Parkinson-White syndrome

Abstract In a patient with type B Wolff-Parkinson-White syndrome, epicardial activation sequence mapping was carried out at the time of surgery for concurrent mitral stenosis. The patients preoperative course had been characterized by cardiac failure and repeated episodes of atrial tachyarrhythmia (fibrillation and flutter) which were difficult to control by conventional medical therapy. The mapping procedure revealed a broad area of preexcitation in the atrioventricular groove at the lateral right margin of the heart. Preexcitation was not present at the moment of incision, and attempted surgical interruption of the preexcitation pathway was unsuccessful. After surgery, there was a reduced incidence of tachyarrhythmia, but electrocardiographic evidence of preexcitation existed. Possible reasons for failure to sever the preexcitation pathway are considered.