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Based on a 3-D emulational body torso model, the influence of changes of heart position caused by deep inspiration etc. on body surface potential maps(BSPMs) was studied in forward electrocardiography. In this report, BSPMs and ECGs during QRS were provided while the heart was in the normal position, or rotated clockwise to the vertical or counterclockwise to the transverse.
The utility of body surface potential mapping to improve interpretation of electrocardiographic information lies in the presentation of thoracic surface distributions to characterize underlying electrophysiology less ambiguously than that afforded by conventional electrocardiography. Localized cardiac disease or abnormal electrophysiology presents itself electrocardiographically on the body surface in a manner in which pattern plays an important role for identifying or characterizing these abnormalities. Thus, in myocardial infarction, transient myocardial ischemia, Wolff-Parkinson-White syndrome, or ventricular ectopy, observation of electrocardiographic potential patterns, their extrema, and their magnitudes permits localization and quantization of the abnormal activity. Conventional electrocardiography assesses pattern information incompletely and does not use information of distribution extrema locations or magnitudes. Thus, increases or decreases in the magnitudes of electrocardiographic features (ST-segment potential displacement, amplitude, or morphology of Q, R, S, or T waves) associated with changes in cardiac sources (ischemia, infarction, conduction abnormalities, etc.) as measured from fixed leads have a high likelihood of being misinterpreted if the distribution itself is changing. In this study, the authors demonstrate the utility of estimating distributions from small numbers of optimally selected leads, including conventional leads, to reduce uncertainty in the interpretation of electrocardiographic information. This issue is highly relevant when thresholds are used to detect significance of potential levels (exercise testing, detection of myocardial infarction, and continuous monitoring to assess ST-segment changes). Significance of this work lies in improved detection and characterization of abnormal electrophysiology using conventional or enhanced leadsets and methods to estimate thoracic potential distributions.
OBJECTIVES: To investigate a noninvasive technique to localize the atrial insertion site of concealed accessory pathways based on the analysis of body surface potential maps (BSPMs) of retrograde P waves in dogs with simulated retrograde pathways. ANIMALS AND METHODS: Orthodromic tachycardias were simulated by atrial stimulations at eight different sites around the atrioventricular ring with long (250 ms and 300 ms) and short (100 ms and 130 ms) coupling times in 14 anesthetized dogs to have P waves well separated from the T wave or occurring during the T wave, respectively. The distance between pacing sites was 15 to 40 mm in group 1 (eight dogs) and 2 mm (in the right atrial free wall region) in group 2 (six dogs). Beats were signal-averaged during 30 s and BSPMs were constructed from 63 unipolar leads. RESULTS: The P wave BSPM pattern for any specific stimulation site was stable and reproducible (correlation coefficient greater than 0.98), and similar in different dogs at long coupling interval stimulations. The thoracic distribution of negative potentials and position of the potential minimum clearly identified the stimulation site when long coupling time stimulations were used. The spatial resolution of the technique as determined by comparison of correlation coefficients in group 2 was 6 mm (P<0.05). When short coupling time stimulations were used (fast tachycardia simulation), the T wave masked the P wave potential distribution in four of eight dogs, but the retrograde P wave map could still be accurately extracted by subtracting a straight line joining the onset and offset of the P wave in 24 of 28 (86%) of the tachycardia simulation sites in these four dogs. CONCLUSIONS: The BSPM patterns of simulated retrograde P waves are specifically related to the site of atrial stimulation. Although the T wave altered these BSPM patterns, a subtraction technique recovered the pattern of the retrograde P wave in 93% of all simulated orthodromic tachycardias. The spatial resolution of the retrograde P wave BSPM method was 6 mm.
A numerical simulation for body surface potential mapping was investigated using Boundary Element Method (B.E.M.). After forward simulation, we investigated the accuracy and stability of ECG inverse solution from the viewpoint of Minimum Description Length Principle (MDL). It became obvious that the solution containing up to 16th expansion components is optimal for ECG inverse problem.
In patients without significant collaterals, percutaneous transluminal coronary angioplasty (PTCA) produces acute transient ischemia that is detectable in both standard electrocardiograms (ECG) and body surface potential maps (BSPMs). Control recordings made before or between inflations provide personalized baselines, which isolate the effects of ischemia from interpatient differences, such as torso shape and electrode location. In this study, two methods of evaluating PTCA-induced ischemia from BSPM recordings are presented. In the first method, an ECG inverse solution that estimates epicardial potentials from body surface signals using a realistic model of torso geometry is applied. The strength of this method lies in its potential ability to localize areas of cardiac ischemia on the epicardial surface. In the second approach, wavelet transforms were used to perform a multiresolution decomposition of the BSPM data into different frequency bands. The basis functions of the wavelet transform are time-limited and narrow band and hence can be expected to be sensitive to features of the BSPM that originate in discrete electrophysiologic events, such as intrusion of the activation front onto regions of ischemia or arrhythmias due to local conduction abnormalities. The method also offers a means of temporal and frequency localization of cardiac events related to the initiation of injury currents and abnormal conduction due to PTCA-induced ischemia. The inverse solution and the wavelet transform each offer new views of the spatial and temporal courses of acute ischemia potentially leading to new diagnostic insights in ECG patient examination.
BACKGROUND: Left ventricular hypertrophy (LVH) is accompanied by specific changes in ventricular electrophysiology, which are potentially arrhythmogenic. Nevertheless, the electrocardiographic diagnostic signs for LVH have a relatively low predictive power for arrhythmic events and sudden death. We thought that other parameters derived from the surface ECG, not apparent at visual inspection, might be detected by specific analysis of electrocardiographic digital recordings. The purpose of our work was to analyze the surface distribution of repolarization potentials and search for subtle alterations not revealed by the usual electrocardiographic processing, which are likely to reflect ventricular repolarization heterogeneity. METHODS: Body surface potential maps were recorded from 62 chest leads in 16 patients with LVH due to aortic stenosis and in 35 normal subjects. By applying a principal component analysis of the ST-T waves, we computed the similarity index. The value of the similarity index is inversely proportional to the variability of T wave morphology and a low value is considered a marker of repolarization heterogeneity. RESULTS: The similarity index was significantly lower in LVH patients than in normals both in 62 leads (0.73 +/- 0.067 vs 0.77 +/- 0.044, p = 0.03) and in 12 unipolar leads (V1- V8, V3R, VR, VL, VF) extracted from the map (0.77 +/- 0.075 vs 0.81 +/- 0.045, p = 0.03). Moreover, we computed the "late repolarization deviation index", which quantifies the instantaneous variations of surface potential distribution from peak to end of the T wave. This index was significantly higher in LVH patients than in controls (in 62 leads 0.07 +/- 0.05 vs 0.028 +/- 0.016, p = 0.005; in 12 leads 0.064 +/- 0.052 vs 0.024 +/- 0.020, p = 0.008). CONCLUSIONS: The values of similarity index and of late repolarization deviation index found in LVH patients suggest a higher than normal degree of repolarization heterogeneity, not detected by the usual electrocardiographic analysis. Since both indices maintained statistical significance when calculated on the 12 leads derived from our map lead system, they could be reliably computed from digital recordings of the 12 conventional leads.
In the study, a new myocardial infarction (MI) estimation method was developed for estimating MI in the three-dimensional myocardium by means of a heart-model-based inverse approach. The site and size of MI are estimated from body surface electrocardiograms by minimising multiple objective functions of the measured body surface potential maps (BSPMs) and the heart-model-generated BSPMs. Computer simulations were conducted to evaluate the performance of the developed method, using a single-site MI and dual-site MI protocols. The simulation results show that, for the single-site MI, the averaged spatial distance (SD) between the weighting centres of the 'true' and estimated MIs, and the averaged relative error (RE) between the numbers of the 'true' and estimated infarcted units are 3.0 +/- 0.6/3.6 +/- 0.6 mm and 0.11 +/- 0.02/0.14 +/- 0.02, respectively, when 5 microV/10 microV Gaussian white noise was added to the body surface potentials. For the dual-site MI, the averaged SD between the weighting centres of the 'true' and estimated MIs, and the averaged RE between the numbers of the 'true' and estimated infarcted units are 3.8 +/- 0.7/3.9 +/- 0.7mm and 0.12 +/- 0.02/0.14 +/- 0.03, respectively, when 5 microV/10 microV Gaussian white noise was added to the body surface potentials. The simulation results suggest the feasibility of applying the heart-model-based imaging approach to the estimation of myocardial infarction from body surface potentials.
We propose a new method for imaging activation time within three-dimensional (3D) myocardium by means of a heart-excitation model. The activation time is estimated from body surface electrocardiograms by minimizing multiple objective functions of the measured body surface potential maps (BSPMs) and the heart-model-generated BSPMs. Computer simulation studies have been conducted to evaluate the proposed 3D myocardial activation time imaging approach. Single-site pacing at 24 sites throughout the ventricles, as well as dual-site pacing at 12 pairs of sites in the vicinity of atrioventricular ring, was performed. The present simulation results show that the average correlation coefficient (CC) and relative error (RE) for single-site pacing were 0.9992+/-0.0008/0.9989+/-0.0008 and 0.05+/-0.02/0.07+/-0.03, respectively, when 5 microV/10 microV Gaussian white noise (GWN) was added to the body surface potentials. The average CC and RE for dual-site pacing were 0.9975+/-0.0037 and 0.08+/-0.04, respectively, when 10 microV GWN was added to the body surface potentials. The present simulation results suggest the feasibility of noninvasive estimation of activation time throughout the ventricles from body surface potential measurement, and suggest that the proposed method may become an important alternative in imaging cardiac electrical activity noninvasively.
The diagnostic information contained in the standard 12-lead electrocardiogram was assessed by comparing the classification results produced by the standard leads for various clinical settings, such as normal versus myocardial infarction or versus left ventricular hypertrophy to those achieved by 120-lead data or body surface potential maps (BSPMs). Separately, optimal signal leads were extracted from the BSPM by ranking all leads in function of their capability of reconstructing the BSPM. Ranking was achieved by deriving eigenvalues from the covariance matrix calculated from all leads and corresponding measurements. Thus, while comparing the results from the standard leads (diagnostic leads) to those from the original raw map data, a comparison was also performed with respect to the best signal leads, namely the four best and the eight best. From the results observed for all bi- and multigroup classifications, it appeared that the diagnostic yield of the 12 standard leads matched those obtained with a number of signal leads lying between 4 and 8. This indicated that a large overlap still existed between the leads composing the 12-lead ECG (in fact, only 8 independent leads). Another interesting observation resulted from this investigation: although classifiers (discriminating variables) used for classification were identical, whether they originated from the raw standard leads (derived from the raw maps) or from standard leads reconstructed with four or eight signal leads, reconstructed measurements performed better than original measurements. This paradox can be explained by looking at the respective F values. Indeed, since increased F values result from higher ratios between the difference of group means and the composite variance from the pooled groups, higher differences and/or smaller variances produce larger ratios and hence, better group separations.
Body surface Laplacian maps (BSLMs) have been previously reported to provide enhanced capability in localizing and resolving multiple spatially separate myocardial events. However, only a few studies have been reported on the clinical applications of BSLM. To test the clinical utility of BSLMs, BSLMs and body surface potential maps (BSPMs) during ventricular depolarization for complete right or left ventricular bundle branch block (CRBBB or CLBBB) were studied in ten patients in each group. As a control group, ten healthy subjects were also studied using the same procedure. One hundred and twenty-eight electrodes were placed uniformly over the entire chest and back of the subjects. BSLMs were computed from recorded potentials, using a numerical algorithm. The BSLMs showed multiple and more localized positive and negative activities compared with the BSPMs. In healthy subjects, the BSLMs showed multiple areas of positive activity overlying the RV, LV, and the RV outflow, and negative activity corresponding to RV free-wall breakthrough and LV anterolateral breakthrough sites, whereas the BSPMs could not separate RV and LV activities. In the patients with CRBBB, the BSLMs showed more localized areas of activity corresponding to the LV apex breakthrough and LV lateral breakthrough, and separated LV lateral and posterior activation. In the patients with CLBBB, the BSLMs showed multiple RV activation, and propagating activation of LV from lateral to posterior. The BSLMs appear to provide enhanced capability in detecting multiple ventricular electrical events associated with normal and abnormal conduction and a more detailed activation sequence of both ventricles in healthy subjects and in the patients with CRBBB and CLBBB. BSLM may provide an important alternative to other imaging modalities in localizing cardiac electrical activity noninvasively.
A comparison was made to determine the ability of optimal sets of 2-6 unipolar leads and a normal Holter lead set to estimate ST potential distributions changes induced by balloon inflation during angioplasty. The performance of these lead sets was compared to measurements observed in recorded 32-lead body surface maps. Unipolar lead potentials were estimated using a linear, least mean squared error estimator of the total body surface map. The correlation between maximum ST potential change in the body surface map and that predicted by the unipolar lead sets ranged from 0.84-0.93. The correlation between maximum ST segment change measured from the body surface map and measured from the Holter leads was 0.29. Therefore, shifts in ST segment potentials can accurately be estimated from a small number of unipolar leads. In contrast, current bipolar ambulatory recording techniques may introduce significant bias to such estimates.
Using computer simulations, we systematically investigated the limitations of an inverse solution that employs the potential distribution on the epicardial surface as an equivalent source model in localizing pre-excitation sites in Wolff-Parkinson-White syndrome. A model of the human ventricular myocardium that features an anatomically accurate geometry, an intramural rotating anisotropy and a computational implementation of the excitation process based on electrotonic interactions among cells, was used to simulate body surface potential maps (BSPMs) for 35 pre-excitation sites positioned along the atrioventricular ring. Two individualized torso models were used to account for variations in torso boundaries. Epicardial potential maps (EPMs) were computed using the L-curve inverse solution. The measure for accuracy of the localization was the distance between a position of the minimum in the inverse EPMs and the actual site of pre-excitation in the ventricular model. When the volume conductor properties and lead positions of the torso were precisely known and the measurement noise was added to the simulated BSPMs, the minimum in the inverse EPMs was at 12 ms after the onset on average within 0.65 +/- 0.26 cm of the pre-excitation site. When the standard torso model was used to localize the sites of onset of the pre-excitation sequence initiated in individualized male and female torso models, the mean distance between the minimum and the pre-excitation site was 0.67 +/- 0.31 cm for the male torso and 0.82 +/- 0.53 cm for the female torso. The findings of our study indicate that a location of the minimum in EPMs computed using the inverse solution can offer non-invasive means for pre-interventional planning of the ablative treatment.
BACKGROUND: QT interval dispersion (QTd) is conventionally interpreted as a result of repolarization heterogeneity in ventricular myocardium. However, another concept of QTd origin has been discussed recently, suggesting that different projections of the repolarization vector into individual ECG leads could be responsible for the differences in QT interval duration. Moreover, the reproducibility could be influenced by factors both electrocardiographic (T wave amplitude, U wave) and extracardiac (noise, ECG measures). In the presented study we have followed the QTd in two groups of patients with proved changes of an electric heart field. METHODS AND RESULTS: Studied groups: 1. Control group, 2. Healthy pregnant women, 3. Patients treated with dosulepine. QT interval was measured from 80 unipolar chest leads used for body surface potential mapping. The QTd was significantly higher in both experimental groups in comparison with the control group (p < 0.001). Significant correlation was found between the QTd and dosulepine plasma level (p < 0.001). Also amplitude of the T wave loop was in both groups decreased and its width increased (both p < 0.001). CONCLUSIONS: If appropriate procedure of measurement is used, the QTd is significantly increased in many physiological and pathological states. Clinical relevancy of borderline increased values has to be interpreted very carefully.
Imaging the myocardial activation sequence is critical for improved diagnosis and treatment of life-threatening cardiac arrhythmias. It is desirable to reveal the underlying cardiac electrical activity throughout the three-dimensional (3-D) myocardium (rather than just the endocardial or epicardial surface) from noninvasive body surface potential measurements. A new 3-D electrocardiographic imaging technique (3-DEIT) based on the boundary element method (BEM) and multiobjective nonlinear optimization has been applied to reconstruct the cardiac activation sequences from body surface potential maps. Ultrafast computerized tomography scanning was performed for subsequent construction of the torso and heart models. Experimental studies were then conducted, during left and right ventricular pacing, in which noninvasive assessment of ventricular activation sequence by means of 3-DEIT was performed simultaneously with 3-D intracardiac mapping (up to 200 intramural sites) using specially designed plunge-needle electrodes in closed-chest rabbits. Estimated activation sequences from 3-DEIT were in good agreement with those constructed from simultaneously recorded intracardiac electrograms in the same animals. Averaged over 100 paced beats (from a total of 10 pacing sites), total activation times were comparable (53.3 +/- 8.1 vs. 49.8 +/- 5.2 ms), the localization error of site of initiation of activation was 5.73 +/- 1.77 mm, and the relative error between the estimated and measured activation sequences was 0.32 +/- 0.06. The present experimental results demonstrate that the 3-D paced ventricular activation sequence can be reconstructed by using noninvasive multisite body surface electrocardiographic measurements and imaging of heart-torso geometry. This new 3-D electrocardiographic imaging modality has the potential to guide catheter-based ablative interventions for the treatment of life-threatening cardiac arrhythmias.
To reduce the effect of electrode position variations on the diagnostic interpretation of an ECG, ECG and VCG interpretations were combined. The reduction was assessed by generating ECGs with displaced electrodes for a group of subjects using Body Surface Potential Maps (BSPMs). VCGs were reconstructed from the ECGs. The group consisted of normals, cases with myocardial infarction (MI), and with left ventricular hypertrophy (LVH). The effects of four types of electrode position changes were assessed for the diagnostic categories MI and LVH. The combined interpretation proved to be less sensitive to large changes than either the ECG or the VCG interpretation alone. The number of small changes increased for the combined interpretation. The combined interpretation showed higher agreement with a human expert than the ECG interpretation alone.
Tricyclic antidepressant drugs dosulepine (TCA), serotonin selective reuptake inhibitor (SSRI) and prophylactic agent with antidepressant effect lithium carbonicum (Li) have different cardiovascular side-effects. We compared them in the prophylactic therapy of periodic affective disorder in remission with TCA, SSRI and Li. Our previous papers confirmed the most prominent effects of heart electric field parameters in TCA patients (Slavícek et al., 1998). In the present work we studied for the first time the dose-dependent changes of ECG, body surface potential maps (BSPM - parameter DIAM 30, 40) in 43 TCA dosulepine, 40 SSRI citalopram and 30 Li outpatients (Hamilton scale: HAMDŁ10; age 40+/-5 years; treated for depressive disorders or bipolar disorders). The daily doses of dosulepine were 50-250 mg, citalopram 20-80 mg, Li plasma levels 0.66+/-0.08 meq/l. The electrocardiogram (ECG), vectorcardiogram (VCG), and BSPM were measured and calculated by the Cardiag 112.1 diagnostic system. The results have shown a relation between the dose of dosulepine and extremum (maximum and minimum) of depolarization isoarea map in dosulepine, but not in citalopram patients. The repolarization BSPM changes were most pronounced in SSRI patients. Lithium in long-term prophylaxy (1-22 years) caused only minimal ECG BSPM changes. The present results correspond with our previous observations.
BACKGROUND: The purpose of this report is to describe the body surface potential maps (BSPMs) during idiopathic ventricular tachycardia (VT) and to determine what differences exist between different idiopathic VT morphologies. METHODS AND RESULTS: We performed BSPMs during VT on 12 consecutive patients (3 women and 9 men; mean age, 42 +/- 13 years) presenting symptomatic idiopathic VT referred to our institution for electrophysiological study. Basal ECG, chest radiograph, and echocardiogram were normal in all patients. Clinical tachycardia showed left bundle branch block pattern (LBBB) in 9 patients, with sustained VT in 5 and nonsustained VT in 4, and right bundle branch block pattern (RBBB) in 3 with sustained VT. We found a unique pattern of BSPMs in each of the 9 patients during idiopathic LBBB VT configuration, whether sustained or nonsustained VT. This pattern appeared at the onset of the QRS and remained stable during the whole QRS complex. The area of minimal potential located in the upper anterior part of the torso was compatible with an origin of VT in the right ventricular outflow tract, as confirmed in 5 patients by successful radiofrequency ablation. We found an evolving pattern with two phases in each of the three RBBB VTs. The electrical axis during the initial part of the QRS could correspond to an endocardial-epicardial vector. The second phase, with a high voltage and area of minimal potential located in the inferior and anterior part of the torso, was compatible with a left ventricular apical origin that was confirmed by epicardial and endocardial mapping during cryosurgery in 1 patient. For all the VTs, the QRS isoarea maps showed the same pattern as the second phase of the QRS. CONCLUSIONS: Two different BSPM patterns were found. All LBBB VTs had the same stable pattern corresponding to an infundibular origin. All RBBB VTs had an evolving pattern that stabilized in the second part of the QRS complex corresponding to an apical origin.
OBJECTIVE: We aimed to study the involvement of atrial repolarization in body surface potentials. METHODS: Electrocardiograms of healthy subjects were recorded using a 64-lead system. The data analysis focused on the PQ intervals while devoting special attention to the low-amplitude signals during the PQ segment: the segment from the end of the P wave until onset QRS. The data were analyzed by inspecting body surface potential maps and the XYZ signals of the vectorcardiogram. RESULTS: Standard P-wave features exhibited normal values. The local potential extremes were found at positions not sampled by the standard leads. The PQ segment was found to be not isoelectric, the time course of the potential distribution being very similar to that during the P wave but for a reversed polarity and about 3-fold lower magnitudes. CONCLUSION: The results demonstrate a significant involvement of atrial repolarization during the PQ interval and essentially discordant "atrial T waves," suggesting a small dispersion of atrial action potential durations.