[A body surface potential mapping system equipped with a microprocessor for the dynamic observation of potential pattern].
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The aim of our study was to assess if repolarization BSPM were able to evaluate the site, size and severity of chronic ischaemic damages and if BSPM were in any way related to the regional attenuation of myocardial contractility or to the site of coronary artery occlusion. The BSPM were obtained from 69 patients suffering from coronary artery disease confirmed by coronarography, with at least 75% occlusion of at least one coronary artery. According to the site of single occlusion, or a combination of the sites of multiple occlusions, the patients were divided into 6 subgroups. According to the region of attenuated kinetics the same group of 69 patients was also divided into other 6 subgroups. As in the polarity distribution there was only a limited accordance in BSPM with coronarographic and echocardiographic findings, in the localization of extreme values there were very important specific changes in patients with normal kinetics as determined by both contrast ventriculography and two-dimensional echocardiography. The repolarization maps can distinguish patients with coronary artery disease and normal echocardiography from healthy persons with a sensitivity of 85% and a specificity of 65% in the case of the isoareal map from the ST segment (RIAM) and 90% and 85%, respectively, in the case of the isointegral map from the whole ST-T segments (RIIM).
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Body surface potential maps (BSPMs) recorded during pace mapping provide an important non-invasive means for identifying local cardiac events; recent clinical studies demonstrated that endocardial pacing sites can be resolved within less than 10 mm. We sought to determine whether similar spatial resolution could be achieved during epicardial pacing. Four patients who were undergoing either heart valve replacement (one), aortocoronary bypass graft (one), or both (two) were studied. In each patient, a pair of epicardial electrodes was placed intraoperatively at the middle aspect of the right ventricular free wall. The distance between the neighbouring electrodes was 10 mm. Five days after the surgery, ECGs were acquired from 35 leads during pacing from each epicardial electrode. We determined the distributions of QRS integrals (the net area under the ECG signal) and compared integrals corresponding to pacing from each of the adjacent electrodes using statistical indices. Student's t-test was applied to these indices and in all the patients revealed that differences in distributions of QRS integral maps were statistically significant (p < 0.01). Results of our study indicate that the non-invasive acquisition of body surface ECGs could resolve epicardial breakthrough sites within 10 mm, which may be useful in facilitating therapeutic ablations in patients with ventricular tachycardias.
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.
Body surface potential maps were recorded from 140 chest leads in 25 patients affected by the idiopathic long QT syndrome (LQTS) and in 25 healthy control subjects matched for age and sex. Potential time integrals of the QRST and ST-T intervals were calculated at each lead point and displayed as isointegral (ISOI) maps. The main abnormalities noted on the QRST and ST-T ISOI maps were one area of negative values larger than normal in the right anterior and inferior thorax and a complex multipeak distribution of the integral values. At least one abnormality was present in 19 (76%) of the patients with LQTS and four (16%) of the control subjects (p less than .001). Each ISOI map was also represented as a weighted sum of nine fundamental components (eigenvectors) to detect and quantitate the nondipolar content. The percent contribution of the nondipolar eigenvectors (all eigenvectors beyond the third) was significantly higher in the LQTS group than in the control group (p less than .005). Specifically, an abnormally high nondipolar content on the QRST ISOI maps was observed much more frequently for patients with LQTS than for control subjects (nine or 36% vs one or 4%), and this was also true on the ST-T ISOI maps (14 or 56% vs one or 4%). No correlation was found between the major abnormalities on body surface maps and syncopal episodes. However, the high prevalence (76%) of these alterations among the patients with LQTS and their infrequent occurrence in the control population strongly suggests that they may be useful markers for the diagnosis of atypical cases. The prominent electronegative area on the anterior thorax can be related to delayed repolarization of a portion of the anterior wall of the heart. This finding is in agreement with the hypothesis that lower than normal right cardiac sympathetic activity is the main pathogenetic mechanism of LQTS. Multipeak distribution and high nondipolar content suggest regional electrical disparities in the ventricular recovery process. This may in part account for the high susceptibility of patients with LQTS to malignant arrhythmias.
Useful Lessons from Body Surface Mapping. Body surface potential maps (BSMs) depict the time varying distribution of cardiac potentials on the entire surface of the torso. Hundreds of studies have shown that BSMs contain more diagnostic and prognostic information than can be elicited from the 12-lead ECG. Despite these advantages, body surface mapping has not become a routinely used clinical method. One reason is that visual examination and sophisticated analysis of BSMs do not permit inferring the sequence of excitation and repolarization in the heart with a sufficient degree of certainty and detail. These limitations can be partially overcome by implementing inverse procedures that reconstruct epicardial potentials, isochrones, and ECGs from body surface measurements. Furthermore, ongoing experimental work and simulation studies show that a great deal of information about intramural events can be elicited from measured or reconstructed epicardial potential distributions. Interpreting epicardial data in terms of deep activity requires extensive knowledge of the architecture of myocardial fibers, their anisotropic properties, and the role of rotational anisotropy in affecting propagation and the associated potential fields.
Body surface potential maps of human His bundle activity have been difficult to product for two reasons: (1) The peak surface potentials are often less than 5 muv, and (2) the simultaneous atrial repolarization potentials frequently exceed 100 muv. We have therefore amplified surface signals 25 times the standard gain of 1000, and then removed by cross-correlation the static pattern of atrial repolarization for serial 1-msec maps of the P-R segment in five normal men. A consistent finding emerged: a positive anterior chest peak appeared 40 msec before QRS onset, and then-within 10 msec-spread out into a long, low transverse mound before disappearing in 5 more msec. The map data were analytically converted to serial electrical sources: the center of electrical activity moved first slightly down, then directly forward, before retracing its path and disappearing. The retrace and accompanying surface spread-out strongly suggests diverging dipolar sources. Thus the data fit a simple heart source which moves anteriorly and then breaks into two (right and left)-as expected from activation of the bundle of His and its bifurcation into left and right bundle branches.
Research on body surface potential mapping concerned predominantly the ventricular excitation process. There is only very limited data available documenting surface potential distribution during atrial electric events. The goal of this study was to establish the pattern and criteria of the atrial potential maps in the healthy population, which is substantial for a prospective usefulness of the noninvasive registrations of surface maps in atrial arrhythmias. A group of 54 subjects in whom there was no clinical evidence of cardiac dysfunction underwent a procedure of body surface potential mapping. The recordings were performed using the HPM-7100 system simultaneously from 87 leads covering the entire thorax. Isopotential maps registered during the P wave were subjected to the statistical analysis by means of the own system "Heart Map" enabling the qualitative and quantitative estimation of the atrial maps. To avoid a problem of variable heart rate, a time standardization, by the division of the P wave into 10 time intervals, was applied. In order to eliminate an interindividual variability of heart location in the thorax, a distribution of the constituent values without subordinating them to the individual electrodes was proposed. In consequence, the group-mean isopotential maps of the wave P for the normal subjects were created. According to the migration of the maximum throughout the thoracic surface during the P wave, three phases of the isopotential atrial maps were determined: phase 1 (P1-P4) comprising initial 40% of the P wave, phase 2 (P5,P6)-next 20% of the P wave and phase 3 (P7-P10)-the terminal 40% of the P wave duration. These phases reflect the successive sequences of atrial excitation. During the whole atrial depolarization the minimum of potential, changing its value, was located around lead D7. Furthermore, in the results of the analysis of the constituent values sequences, for the P wave time intervals the additional quantitive parameters were calculated, i.e. areas designated by positive and negative potential and the ratio of these areas. The presented findings revealed that surface maps give the precious insight into spread of atrial excitation. Establishing of the distribution pattern and the criteria of the atrial potential maps for normals enables to undertake the further research on the use of this technique in a various atrial pathology.
We investigated the spatial distribution of atrial late potentials (ALP) in patients with paroxysmal atrial fibrillation (Paf) by use of body surface signal-averaged ECG. The P wave-triggered signal-averaged ECG was recorded in 20 patients with Paf and 34 control patients from precordial 16 unipolar leads (standard V1-V6 and two intercostal spaces below and above V1, V2, V4-V6). The duration (Ad) and number of fragmented deflection (Nf) of filtered P wave were measured on each lead. % Area was also calculated by dividing the area for the last 20 msec by the total area of filtered P wave. The lead having any of a significantly longer Ad, larger Nf and smaller % Area in patients with Paf than the controls was designated as ALP positive lead. ALPs were observed in all other than two intercostal spaces above V5 and V6. This finding suggests that the electrophysiological disparity in the whole atrial muscle might be involved in patients with Paf.
In the present study, we report body surface Laplacian mapping of atrial depolarization under sinus rhythm in 8 healthy male subjects. For each subject, 95 unipolar disk electrodes with inter-electrode distance of 2 cm were used to record simultaneously potential ECGs over the anterior chest. The Laplacian ECG was then estimated during the P wave using a novel spline Laplacian technique. The body surface potential map (BSPM) and body surface Laplacian map (BSLM) at different time instants or time intervals of the P wave were constructed and compared. The present results showed that the BSPMs during the P wave were characterized by the rotation of a pair of positive/negative potential distribution from right to left around the anterior torso. On the other hand, the corresponding BSLMs revealed more spatial details, including two positive activities (denoted as P1 and P2, appeared in all 8 subjects), and three negative activities (denoted as N1, N2, and N3, appeared in 7, 7, and 4 subjects, respectively). The separation of these activities and their evolving patterns were also compared and confirmed by computer simulation using a realistic geometry heart-torso model. The above findings may be directly related to the underlying activation sequence during atrial depolarization in healthy subjects, suggesting the potential clinical applications of the Laplacian ECG technique.
Body surface potential maps provide more detailed regional cardiac electrophysiologic information than the standard electrocardiogram. We performed a large-scale study of a normal population to form a comparison base for evaluation of the clinical utility of this technique. We analyzed body surface maps from 1113 normal subjects from 10 to 80 years old to detail map features as a function of age, sex, and body habitus. Maps were analyzed by visual inspection and by a spatial and temporal data reduction technique that allows statistical comparison of map features. On average, both QRS and ST-T potentials decreased with increasing age. Potential pattern distributions remained constant from 10 to 40 years. Beyond age 40, larger numbers of maps from normal subjects showed depolarization patterns consistent with delayed activation of the left anterior fasicle, despite normal 12-lead electrocardiograms. Only minor QRS potential amplitude and distribution differences were noted when male and female subjects were compared within groups of similar age and body habitus. Male subjects consistently showed greater average T potential amplitudes. Slender body habitus was associated with a more horizontal "zero" potential line. In female subjects over age 40 there were more extensive low-level negative potentials recorded over the precordium during the ST segment than in men. This study defines the range of normal body surface potential maps in a large clinically normal population and provides a basis for qualitative and statistical comparison with map features of patients with disease.
To determine the efficacy of body surface potential mapping to detect and quantify reperfusion in acute infarction, 66 patients were studied by repeated body surface potential mapping before and after administration of the thrombolytic agent. The QRS and ST-segment were analyzed and compared to the arterial patency as assessed by arteriography within 10 days. The infarct-related vessel was patent in 50 patients and occluded in the remaining 16. In 6 of the 15 patients in whom thrombolytic therapy was started within 2 hours of the onset of chest pain the ST-segment changed from that of an acute infarction pattern to that of a normal pattern, and the QRS pattern either remained normal or recovered prior to discharge. In two additional patients the QRS pattern returned to normal prior to discharge from the hospital. In the 51 patients with later thrombolytic therapy (> or = 2 hours) the degree of ST elevation and depression decreased more than either the control infarction group (36 inferior and 73 anterior patients) or the group in whom reperfusion attempts were unsuccessful, but the pattern of the map remained that of an infarction. The QRS maps showed that in the first 48 hours recovery of potential was insufficient to distinguish those with successful thrombolysis. Early reperfusion could be detected by body surface potential mapping and the eventual damage predicted from the degree of change in the QRS map. Later reperfusion could be surmised but not quantified.
OBJECTIVE: To demonstrate cardiac electrophysiological changes in patients where partial left ventriculotomy was performed and multichannel electrocardiographical measurements and body surface potential mapping were used. METHODS: Body surface ECG signals were recorded during sinus rhythm for one minute. Six patients were operated on with partial left ventriculotomy were monitored. All patients had normal coronary angiography data. The data were acquired prior to the partial left ventriculotomy, and on the second, third, fourth, and fifth postoperative day using 32-body surface leads. The recorded data were analysed by determining ST-40 and QRS integral maps. The analysis was done on a set of selected beats during the sinus rhythm and on the averaged beats. RESULTS: Before the operation, ST-40 maps typically showed an area of strong positive potentials (elevation) over the anterior aspect of the torso and a region of strong negative potentials (depression) over the lateral, and posterior aspects of the torso. After the operation, the ST elevation over the anterior, lateral and posterior aspects of the torso was reduced. An area of marked positive potentials remained in the precordial area (overlying the excised area of the heart), even during the postoperative monitoring interval (day two through day five). We also noticed that the amplitude of cardiac signals decreased by approximately 30% after the partial left ventriculotomy. Qualitative map changes were substantiated by statistical parameters. CONCLUSIONS: Results of our study demonstrate that noninvasive acquisition of body-surface electrocardiographs may detect changes in the cardiac activity of patients undergoing partial left ventriculotomy. This finding suggests that body surface mapping may also be useful in assessing the arrhythmia vulnerability.
An algorithm for the early detection of acute myocardial infarction (MI) using body surface electrocardiographic potential mapping has been developed. The mapping system consists of a 64-hydrogel electrode harness applied rapidly to the anterior chest, from which electrocardiographic signals are stored on a memory card and processed by computer. At each of the 64 points, QRS and ST-T isointegrals and 10 other features of the QRST segment are measured. Using these measurements, new variables are derived that express the shape of the three-dimensional geometric surface of the map. The isointegrals, features, and shape variables are used in a variety of techniques to discriminate between MI and control subjects. Maps were recorded from 69 patients at initial presentation of chest pain suggestive of acute MI and from 80 healthy control subjects. Using a multiple logistic regression technique, 14 variables were identified that correctly classified 79 of the 80 control subjects (specificity, 98.8%) and 65 of the 69 MI patients (sensitivity, 94.2%). The algorithm based on these 14 variables was applied prospectively to maps recorded on a further 48 control subjects and 59 patients with acute MI. Of the MI patients, 31 had inferior, 13 inferoposterior, 10 anterior, 2 posterior, 1 lateral, 1 inferior with right bundle branch block, and 1 anterior non Q wave MI. The algorithm correctly classified all 48 control subjects (specificity, 100%) and 57 of the 59 MI patients (sensitivity, 96.6%). Marked differences in the three-dimensional geometric map surfaces between the control subjects and MI patients were demonstrated. Variables derived from these surfaces form the basis of an algorithm with a high sensitivity and specificity for the automated detection of acute MI. The design of adaptive algorithms and their application to patients with chest pain and atypical electrocardiographic changes, particularly ST depression, may lead to the earlier detection of MI and greater numbers of patients receiving thrombolytic therapy.
An electrocardiographic computer simulation was conducted to study the feasibility of predicting accessory pathway locations in Wolff-Parkinson-White (WPW) syndrome with body surface potential Laplacian maps. Three-dimensional, realistically-shaped heart and torso models were used. Ten accessory pathways (APs) around the atrioventricular ring corresponding to Gallagher et al. were set in the heart model, and body surface Lapacian and potential maps of WPW syndrome with single or multiple APs were simulated and compared to each other. In simulations with a single AP in the anterior walls, the maximum-minimum pairs in Laplacian maps appeared to be similar to those in potential maps with respect to their locations and orientations, but the maximum-minimum pairs in Laplacian maps were sharper and more localized than in potential maps. In simulations with a posterior AP or multiple APs, the maximum-minimum pairs in the Laplacian maps showed features correlative to the AP locations, but no such features were found in potential maps. These results suggest the possibility of using Laplacian maps, as a non-invasive method for predicting accessory pathways locations in WPW syndrome.
The inverse problem of evaluating epicardial potentials from a knowledge of heart and torso geometry as well as body surface potentials is here formulated as a problem in control theory. As is well known, such an inverse problem is ill-posed and a regularization technique has been devised to overrun this difficulty. The resulting regularized problem is well-posed and requires the minimization of a cost function including, besides the square distance of any predicted surface potential distribution from the experimental one, a regularization term involving the second derivatives of the identified epicardial potentials. The results here presented were obtained on a model problem for a plane geometry. Surface potentials generated by multipoles and perturbated with a noise level reflecting both instrumentation and electrode placement uncertainties were fitted by the proposed method and 'epicardial potentials' were determined with a maximum sum square relative error of 15%. The results suggest that by introducing suited regularity constraints, the a priori difficulties inherent to the problem of computing epicardial potentials from torso potentials, can be overcome.
Clinical applicability of inferred pericardial potentials is limited because accuracy is significantly affected by noise in surface electrocardiograms (ECGs), errors in electrode location on the torso model, and errors in the geometry and inhomogeneities of the torso model itself. To quantify effects of electrode location and geometric errors in torso-surface models, we measured locations of 190 electrodes used in body-surface mapping of 11 adults, along with over 2,000 sites on each torso surface. Measurements were made to within 2 mm with an Immersion Personal Digitizer. To quantify effects of errors in pericardial-surface models we also estimated heart position, size, and orientation in each subject from ultrasonic images registered to the body-surface coordinates. Known pericardial potentials were taken from epicardial measurements made during QRS with a 90-electrode sock in an adult male undergoing cardiac surgery. Body-surface ECGs were calculated for each individual from the pericardial maps, using standard boundary-element methods. Accuracy of zero-order-Tikhonov inverse solutions was tested in 91-node pericardial and 1,026-node torso models, individualized for each subject. With 10 microv rms noise added to surface potentials, the optimal regularization constant at each instant in QRS gave a relative error of 0.44 +/- 0.03; it was 0.47 +/- 0.03 using the composite residual and smoothing operator (CRESO) technique. When calculated body-surface potentials from the first 10 subjects were placed at corresponding electrode positions on the torso of the eleventh subject, whose heart size and orientation was the mean of the other 10 subjects, relative error increased to 0.87 +/- 0.06 for optimal regularization. CRESO failed in the fixed torso model. Results demonstrate that a fixed model does not provide useful estimates of pericardial potentials, and that individualized models enhance the performance of techniques for the estimation of regularization parameters.