R. Chris Hand

Surface recording of electrical activity from the region of the bundle of His.

Abstract In 16 dogs, by appropriate filtering and digital averaging on a PDP-9 computer, we were able to enhance the detection of electrical activity of interest in the P-R segment of the electrocardiogram. In instances (1) when such activity in the surface record coincided temporally with the internal recording from the bundle of His area, (2) when, with atrioventricular nodal block, the electrical activity of interest continued to be associated with the internally recorded His bundle deflection and not with atrial activity, and (3) when, with production of transmission delay between the bundle of His and the ventricle, the surface signal of interest continued to be associated with the internal His bundle deflection, a common signal source was considered likely. In certain instances the surface signal of interest in the P-R segment occurred well after the internally recorded His bundle deflection but about 15 msec before the earliest evidence of ventricular activity. In these instances, when the tests cited were applied and the blip of interest was associated with ventricular activity, the origin of the blip was thought to be in the region of the bundle branches. In the 16 animals studied, one or more pieces of the evidence described were present to localize the origin of the signal. In seven animals, the signal was thought to originate from the bundle of His, in six from the region of the bundle branches and in three from both the bundle of His and bundle branches.

The influence of electrode placement in the reconstruction and analysis of body surface potential maps from limited thoracic arrays

Despite their capacity to indicate abnormality outside the scope of routine electrocardiography, body surface maps remain extensive, time-consuming research procedures. By contrast, a 35-electrode grid which sums precordial ST segment deviations has received wide attention as a clinical monitor of acute myocardial infarction. First, this study examined the feasibility of recovering essential data from a small electrode array to construct maps equal to those obtained from a much larger array. Such a small-array technique would offer economy, easy application, plus the comprehensiveness and clinical correlation of the large system. Second, the relationships between map, small-array and a 35-component equivalent multipolar generator were explored for a transformation system which both expands the small-array data to map displays and reduces such data to non-redundant waveforms. Comparisons were made between direct maps and those derived from two 35-electrode sets on normal subjects and patients with myocardial infarction or cardiomyopathy. Electrode placement did not conform to the conventional rectangular grid; for one, the electrodes encircled the thorax symmetrically; in the other they were statistically selected for signal information content. We found 1) symmetrical electrode placement and analytic reconstruction of maps from multipolar lead components consistently reproduced known maps well (.91 correlation, 120 microvolts error); but 2) empirical electrode placement and statistical prediction of known maps averaged .99 correlation and 20 microvolts error for the normal training population and .97 and 60 microvolts for the abnormal test sample. Worsening occurred when placement and prediction methods were mixed; however, maps reconstructed by the empirical-statistical approach reduced to a reasonable approximation of equivalent generator scalar leads.

Concentrations of Fluoroalkanes Associated With Cardiac Conduction System Toxicity

When respiratory alterations associated with the inhalation of aerosol propellants were eliminated, it was demonstrated that a ten-minute exposure to trichloromonofluoromethane (Freon 11) at concentrations below 15% never caused death. Rarely, at a concentration of exactly 15% minimal sinus slowing occurred (change less than 10% the base line rate). At concentrations between 15% and 17%, nine animals survived while seven succumbed. Ranges between 17.5% and 21% resulted in seven survivors of 19 animals, while no animal survived a ten-minute exposure to a concentration in excess of 21%. The mode of death was most commonly and ultimate asystole. Concentrations of dichlorodifluoromethane (Freon 12) greater than 95% were necessary to produce death in ten minutes, and severe oxygen deficit was evident.

Use of body surface maps to identify vessel site of coronary occlusion

Body surface mapping is more sensitive than conventional electrocardiography for various cardiac regions. In this pilot study, the authors used isoarea maps of early (the first 40 msec), late (the next 40 msec), and total (early and late, or 80 msec) QRS complex to determine the site of coronary occlusion in patients with known coronary artery disease. In the absence of conduction abnormalities or axis deviation in the 12-lead electrocardiogram, isoarea body surface map data of single-vessel disease were unremarkable; however, isoarea departure maps (ie, the average isoarea map of normal population extracted from the study group) were characteristic. Early departure isoarea maps were revealing in all three coronary artery disease groups, with a large negative potential noted over the anterior thorax, midline for the right coronary artery, left anterior in the left anterior descending artery, and further laterally for the left circumflex artery groups. The late isoarea departure map was distinct in the left circumflex artery group with positive potentials leftward, anterolaterally. Discriminant function analysis revealed a high predictive accuracy for the left anterior descending artery group. Thus, isoarea departure maps hold promise for predicting the site of coronary occlusion in this training set of patients.

Effect of various regimens of chronic and acute nicotine exposure on myocardial infarct size in the dog

Smoking is a risk factor for atherosclerotic coronary heart disease, and the risk increases with increasing numbers of cigarettes smoked. The effect of cigarette smoking on the size of acute myocardial infarction (AMI) has not been evaluated. This study describes the effect of 1 component of tobacco smoke, nicotine, on the size of experimentally induced AMI in closed-chest dogs. Daily exposure to nicotine before AMI increased the volume of infarcted tissue (p less than 0.0001). Acute exposure to nicotine (with prior chronic exposure) resulted in a larger volume of infarcted tissue (p less than 0.0001). Thus, chronic, acute and post-AMI exposure to nicotine has an adverse effect on the volume of subsequent infarcted tissue, and continued exposure after AMI further enlarges infarct size.

On the Possibility of Directly Relating the Pattern of Ventricular Surface Activation to the Pattern of Body Surface Potential Distribution

A system of three 320-element spheres was employed to represent the endocardial and epicardial surfaces of the left ventricle and the body surface. The two inner (heart) spheres were considered electrogenic, and each active subunit was given an onset time and a monophasic action potential; these subunits were treated as source dipoles for successive instants in time. The potential distribution at any instant resulting on the outer (torso) surface was calculated from adding together the corresponding proportionate effects of all active subunits, each treated as dipolar sources. This result was compared to multipolar reduction of simultaneous endocardial and epicardial action potential patterns which, when combined, gave a net multipolar generator content enabling outer pattern approximation. The identity between the patterns of torso surface potential, systematically calculated from multiple dipoles, and those produced from the multipolar reduction provided three insights: 1) the whole surface treatment of the multipolar method is faster, 2) both show an offset term related to the monophasic nature of the sources and similar to that found in live data, and 3) such a model may provide a vehicle for experimentally testing the contribution of intramural sources to body surface potential maps.

The determination of the human ventricular gradient from body surface potential map data

We have analyzed the Wilson ventricular gradient in terms of body surface potential maps and of the reduction of such surface patterns to equivalent dipoles or vectors. While the ventricular gradient traditionally was treated as first a scalar, then a vector concept, we found that the three entities (QRS area, T area, QRST area) did not reduce to vectors with a common location. However, conventional vector addition (QRST area = QRS area + T area) did precisely apply. Further we found considerable more-than-vector or extra-dipolar information remaining for all three entities after removal of the dipole effect. This suggests that maps of these entities should be considered the boundaries of complex electrical fields rather than simple surface effects of vectors.

A Reappraisal of the Mitral B‐Bump (B‐Inflection): Its Relationship to Left Ventricular Dysfunction

A prolonged AC interval, decreased PR ‐ AC interval, and a B‐inflection (“bump” or “notch”) on the mitral AC slope, have been widely regarded as evidence of abnormally high LVEDP for the last 16 years. However, several groups have questioned the reliability of these signs as predictors of high LVEDP. In 50 patients subjected to LV catheterization, we found no correlation between LVEDP and the AC interval or PR ‐ AC interval. A better correlation was obtained between the presence of a B‐inflection and diminished LV ejection fraction on angiocardiography. In our series, the B‐inflection was noted in 1/19 patients with LVEDP < 15 mmHg as well as LV ejection fraction > 55%, but it was present in 7/10 patients with LVEDP over 15 mmHg, as well as LV ejection fraction < 55%. When properly recorded, the presence of a B‐inflection is a useful sign of significant LV dysfunction.

Variation in the precordial QRS transition zone in normal subjects

From body surface potential map data for 51 normal young men (with QRS axis between 0 and 90 degrees) both the spatial QRS area vector and the isoarea map of the QRS were obtained. Acting on Grants assumption that the transition zone defined a plane perpendicular to the spatial QRS vector, we determined the angular shift in altitude and azimuth required to move the spatial vector of each individual to the position of the group mean. We then shifted the precordial map of the transition zone of each individual with the same angular correction. These resulting transition zone boundaries clustered much closer to each other, but did not move into absolute coincidence. We interpreted the nearness-to-fit to be an estimate of the degree to which the precordial QRS configurations conformed to a common simple vector or dipolar pattern.