Quantitative two-dimensional echocardiographic assessment of left ventricular shape in ischemic heart disease.

Since data on systematic noninvasive quantitative assessment of left ventricular (LV) shape in ischemic heart disease are very scanty, we used new size-independent LV shape descriptors to study the correlation between LV shape and LV ejection fraction in 46 men with a 70% or more stenosis of one or more coronary arteries on angiography. Angiocardiographic LV ejection fraction was over 55% [mean: 69 (+/- 6 SD)%] in 20 patients (group I), and under 55% [mean: 43 (+/- 9 SD)%] in 26 patients (group II). Our LV shape descriptors showed statistically significant differences between group I and group II patients, indicating a more spherical LV shape in group II (p values less than 0.005). Within the whole patient group (N = 46), and also within the subgroup of patients with regional LV hypokinesis or akinesis (N = 26), correlation between LV shape alteration (toward the spherical) and LV ejection fraction was not strong; it was better in the subgroup (N = 10) with regional LV wall dyskinesis. There was poor correlation between angiocardiographic LV chamber volume and alteration (toward spherical) in LV shape. Thus, we have documented quantitatively that patients with ischemic heart disease and low LV ejection fraction tend to have a more spherical LV shape than patients with a normal ejection fraction. Quantification of LV shape based on simple, easily made two-dimensional echocardiographic measurements may help in noninvasive identification of patients with deteriorating LV function, especially when a change toward the spherical is detected in serial echocardiograms.

Relation between the ventriculographic silhouette and topography of thoracic potential in coronary artery disease.

The body surface potential map obtained within 30 days of cardiac catheterization was examined in 180 patients with coronary artery disease. Radii to the systolic and diastolic boundaries of the right anterior oblique ventriculogram were measured at 18 degrees intervals; isointegral voltages were tabulated for early and late halves of the QRS complex at 35 definitive electrode sites. Multivariate analysis showed all ray lengths depended on all 70 voltage values. Linear transformation matrices to predict ray length from voltage distribution were calculated for a training set which was successively expanded from 80 to 160 at increments of 20 patients. Training set expansion led to a progressive decrease in the error of reproduction of the ray lengths for patients outside the training set. There is a strong relation between ventriculographic contours in patients with coronary artery disease and body surface potential values during early and late QRS complexes. Even in simplified linear formulation, the relation is detectable throughout a large population despite interindividual variations in anatomic geometry.

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.

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 Grant's 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.

The degree to which myocardial infarct site and size determine the electrocardiographic axis. Analysis of correlative data by computational modeling.

The spatial electrical QRS axis was determined for 428 twelve-lead electrocardiograms from patients subsequently shown by postmortem dissection to have ventricular myocardial fibrosis or necrosis. Four 16-segment ventricular models of the heart were used to "predict" the spatial electrical QRS axis from known ventricular mass and deficit. The raw model I in ideal anatomic position and vectors perpendicularly outward for each muscle segment showed a mean correlation value of -0.494; model II was rotated in the chest to produce best fit with a correlation of 0.638, but the anatomic orientation was not reasonable; model III maintained original position and orientation but the vectors were scaled (correlation 0.780); and model IV, with nonperpendicular vectors, yielded a mean correlation of 0.793. The exceptions to good predictability formed a distinct subset largely composed of electrocardiograms with some form of variant intraventricular conduction (slight QRS widening, fascicular block patterns and "indeterminate frontal-plane axis").

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.

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.

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.

A study of the effects of nicotine in the intact dog and the propensity for arrhythmias.

This is a study of the effects of nicotine exposure in the intact dog on the propensity for arrhythmias. The mean effective and total refractory periods were prolonged after nicotine. The diastolic current threshold was increased after nicotine in every animal, yet the threshold for repetitive firing was decreased in four animals, all of which had individually prolonged relative refractory periods. We conclude that nicotine may increase the propensity for arrhythmias when an appropriately timed premature stimulus, of sufficient strength, encounters a ventricle with sufficient dispersion of refractoriness to allow re-entrant arrhythmias to be sustained.

Surface reflections of cardiac excitation and the assessment of infarct volume in dogs. A comparison of methods.

Ventricular depolarization was analyzed in intact dogs by simultaneously recording body surface potential maps, McFee axial vectorcardiograms, and a 5 X 4 lead precordial grid of QRS complexes. The purpose of this study was to compare the effectiveness of subtraction approaches, using the simultaneously acquired data. The totally closed chest approach avoided the problem of volume conductor alteration by thoracotomy. Infarct volume was calculated morphologically from measurements of serial ventricular sections. The maximal correlation with anatomic infarct size using the precordial QRS grid approach was 0.51, using cumulative difference data between 1 and 38 msec when the postinfarction grid was substracted from the preinfarction grid. A correlation coefficient of 0.80 was achieved using the numerically integrated data between 1 and 31 msec from the vectorcardiogram, and the body surface potential map achieved a correlation coefficient above 0.88 when the electrical difference of msec 16 was used. These data suggest that estimates of infarct size from selected surface reflections of the activation process are feasible if some sort of preinfarction control data are available. Caution must be exercised to avoid inclusion of electrical effects late in the activation process which contain contamination by highly variable alterations in the excitation sequence due to delayed conduction or alteration in conduction pathway in or near the infarct zone.

New evidence for inferoposterior myocardial infarction on surface potential maps.

Extensive body surface potential recording was performed in 22 patients 2 to 4 weeks after an acute inferoposterior myocardial infarction. Serial isometric projection maps were viewed millisecond by millisecond throughout ventricular excitation, and a second series of maps were examined after removal of the expected range of normal potential distribution. Three major findings outside the normal range appeared: (1) In 6 patients, an early zone of abnormal positivity developed in the left anterior chest at xiphoid level between 15 and 30 msec after onset of the QRS complex; (2) in 13 other patients, a large zone of positivity developed high on the left anterior chest (subclavicular region) between 30 and 60 msec after QRS onset; and (3) in 8 patients the long-lasting rim of negativity about the lower chest was strictly abnormal compared with the expected range. Thus, in 19 of 22 patients the potential map expression was outside the normal range, whereas only eight standard electrocardiograms revealed persistent Q waves with a duration greater than 30 msec. We believe the mid and late activation changes are related to ischemically induced alterations in the temporal sequence of ventricular excitation, not easily appreciated by conventional means of recording but obvious with the departure map technique.

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.