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The pioneering work of Durrer and associates has made available unique data showing activation isochrones in human hearts. To be certain that the complex experimental procedures do not seriously affect the activation sequence and also to validate accepted basic premises concerning the genesis of the electrocardiogram (ECG), it appears to be essential to show a reasonable correspondence between the subject's ECG before death and ECG's reconstructed from the activation data and heart-lead models. This paper reports the results of such a study. The comparison is evaluated in quantitative terms using several types of correlation coefficient. The significance of these is further evaluated through comparisons of similar coefficients from a random sample of normal records. The correlation coefficient considered to have the most general applicability gives a value of .80; only one subject from the random group showed a higher correspondence. A particular set of leads chosen to minimize the effects of inhomogeneities not accounted for in the modelling process, clearly selected the subject's records from all others with a correlation coefficient of .91 compared to .87, the highest from the random set. Considering the practical limitations on the accuracy of the models underlying these tests, the results are considered, with certain exceptions, to be supportive of the accuracy of the activation experiments and the assumption of a uniform double layer as the ECG source.

Magnetocardiograms (MCGs) of six subjects with representative cardiac abnormalities and of one well-studied normal subject are compared with the 12-lead ECGs and VCGs of these subjects. The MCGs are recordings of the component of the magnetic vector which is normal to the skin, measured across the chest on a 5 cm X 5 am grid; an example is also presented of a sequence of instantaneous MCG maps. The heart abnormalities include myocardial infarction, angina pectoris, intraventricular conduction disturbances, and ventricular hypertrophy. The various MCG maps of the normal subject show MCG changes as a result of changes in body morphology (loss of weight), changes in the subject's position during recording, and changes as a result of exercise. They are presented as a basis for understanding some of the variability of MCG maps.

The pattern of arrhythmias following capacitor discharges of increasing amplitude, which have been observed by the authors in cultured myocardial cells from chick embryos, was compared to the arrhythmia patterns caused by similar discharges in experimental animals and humans, as reported in the literature. While the absolute voltages and currents causing each type of arrhythmia showed great variation, the scatter decreased considerably when the stimulus level was recalculated on the basis of peak current density in myocardial tissue, and was reduced further when the peak potential gradient at the cell level was used as the common basis of comparison. The similarity in the arrhythmia patterns and in the voltage gradients at which they occur indicates that the mechanism of these arrhythmias may be similar in cultured cells and intact animals and humans.

The direct-current magnetocardiogram, which shows the T-Q (baseline) shift, is used to clarify the cause of S-T depression induced by stress testing in the human heart. Measurements are made of the amount of baseline shift associated with the S-T depression. Results are presented of a well-documented patient, with typical coronary artery disease, undergoing a two-step exercise test. Before exercise, there was no S-T or baseline shift. During exercise, the S-T segment became depressed and the baseline segment was simultaneously elevated, at about 70% of the S-T amplitude. After termination of exercise, the baseline elevation disappeared somewhat more rapidly than the S-T depression. These results were consistent in repeated tests of this patient. Because the baseline shift is a reflection of an injury current, these results confirm the belief that exercise-induced S-T depression is mostly due to an injury current which is interrupted during the S-T interval. The baseline shift seen here is the first non-invasive measurement of an injury current in the human heart, and its presence and time-course generally agree with measurements in the animal heart. This work also confirms that the direct-current magnetocardiogram, although not practical for clinical purposes, is useful as a research tool.

The direct-current magnetocardiogram not only shows the features usually seen on the electrocardiogram, but also shows the T-Q (baseline) shift due to cardiac injury current. The first direct-current magnetocardiogram measurements of the human heart are presented here. The hypothesis tested is that there is no injury current associated with the S-T shift seen in two electrocardiogram abnormalities: early repolarization, and left bundle branch block. The data from three typical early repolarization subjects and one typical left bundle branch block patient are presented. It is found, in each case, that although there is appreciable S-T shift, there is essentially no baseline shift on the direct-current magnetocardiogram. The absence of baseline shift proves that the S-T shifts in these cases are not "apparent" shifts, caused by a dc injury current which is interrupted during the S-T interval; instead, these are "true" S-T shifts caused by a current flowing only during systole, presumably due to an altered repolarization of the ventricles. It is also found that the direct-current magnetocardiogram does not have routine clinical application because of a practical problem. This is the presence of false baseline shifts due to noncardiac currents, mostly in the gastrointestinal tract, which could be suppressed in only about one-third of the subjects. However, the direct-current magnetocardiogram may be useful as a research tool, for clarifying the cause of the S-T shift in selected subjects.

Myocardial cells isolated from 8-day chick embryos were grown in monolayer culture under conditions that produce "standard embryonic" and "adult-type" cells. These cells were subjected to electric field stimulation that had a waveshape and intensities similar to those used in clinical electric countershock procedures. Photocell mechanograms obtained before, during, and after stimulation were correlated with simultaneously measured transmembrane potentials to determine the relationship between membrane polarization and arrhythmia production that occured after the stimulus. The results of these experiments demonstrate that a predictable sequence of mechanical responses occurs after stimuli ranging in intensity from 6 to 200 V/cm. This sequence, which closely resembles that observed in vivo after similar stimulation intensities, consists of a single response (activation), tachyarrhythmia, relaxed arrest followed by transient tachyarrhythmia, arrest with contracture, and cellular fibrillation. This diverse pattern of arrhythmias is associated with a prolonged depolarization of the cell membrane which increases with the intensity of the applied stimulus. It is probable that this depolarization is caused by a transient electromechanical deformation of the cell membrane during the shock. These findings contribute to a better understanding of the causes of the arrhythmias that appear after clinical and experimental electric countershock procedures.

Atrial activity can influence the ability of a failing artificial pacemaker to excite the heart. An appropriately timed atrial beat may cause failure in excitation by pacemaker stimuli which are usually successful in ventricular capture. Conversely, stimuli which usually fail in excitation may be made to succeed by an appropriately timed atrial beat. Two case reports and a review of the literature are presented. Alternative mechanisms for this influence of atrial activity are electrotonic effects (Wedensky facilitation or inhibition) and mechanical effects (motion of the pacing catheter or ventricular myocardium). The authors consider the latter mechanism preferable.