[Clinical application of the analysis of cardiac dipole estimated from the body surface potential mapping-normal cases].
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Results for “Body Surface Potential Mapping”
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Anterior infarctional changes occurring during mid and late ventricular activation detectable by surface mapping techniques.
This is a comparative body surface potential map study of 26 patients with a recent acute anterior myocardial infarction. The mean plus or minus two standard deviations (+/- 2 SD) for the voltage distribution was established at 5 msec intervals throughout the cardiac cycle in 30 normal subjects at each of 142 recording sites. Instances in which a patient's potential distribution fell outside the normal range were analyzed as to location, duration and intensity against the expected time course of ventricular activation. Only four patients had departures from the normal distribution confined to the Q time zone. Twenty patients had not only Q time zone abnormalities, but had areas of both positivity and negativity exceeding +/- 2 SD, which occurred well after 30 msec. Two patients with clearly documented diagnostic Q waves during the first few days of hospitalization had lost these findings by the date of body surface mapping. They did retain, however, departure map findings demonstrating significant abnormalities occurring between 30 and 60 msec after onset of ventricular activation. These changes occurring in the mid and late time zones of the activation sequence are not detectable by conventional electrocardiography or vectorcardiography, yet present a strikingly apparent finding by this technique of analysis and display.
Action Potentials↗
Body surface area of ST elevation and the presence of late potentials correlate to the inducibility of ventricular tachyarrhythmias in Brugada syndrome.
INTRODUCTION: The value of noninvasive markers reflecting repolarization and/or conduction abnormalities in identifying patients with abnormal ECG showing a pattern of atypical right bundle branch block and ST elevation syndrome (Brugada syndrome) at risk for life-threatening arrhythmias is controversial. Because right precordial ST elevation reflects inhomogeneous repolarization, we hypothesized that a correlation between the area of ST elevation, that is, the area of inhomogeneous repolarization, and the inducibility of ventricular tachyarrhythmias (VT) exists. Therefore, the body surface area of ST elevation and the presence of late potentials were compared to the inducibility of VT in patients with the characteristic ECG of Brugada syndrome. METHODS AND RESULTS: A 120-channel body surface potential map was recorded at rest and after administration of a Class I agent (ajmaline, 1 mg/kg) to measure the body surface area of ST elevation (> or = 0.2 mV) in 23 individuals (16 patients had been resuscitated from near sudden cardiac death or had suffered syncope) with an ECG compatible with the diagnosis of Brugada syndrome as well as in 15 healthy controls and in 15 patients with arrhythmogenic right ventricular cardiomyopathy. Late potentials were assessed in 20 of the Brugada patients using signal-averaged ECG. Programmed ventricular stimulation was performed at two ventricular sites with up to three extrastimuli. Mean body surface area of ST elevation (> or = 0.2 mV) of all Brugada syndrome patients was 154 +/- 139 cm2 (control 9 +/- 9 cm2; P < 0.001). In the group of patients with arrhythmogenic right ventricular cardiomyopathy, only one patient was found to have an area of ST elevation (165 cm2). In the presence of ajmaline, area size increased to 330 +/- 223 cm2 in Brugada syndrome patients (P < 0.05). In patients with inducible sustained (n = 15) and nonsustained VT (n = 3), a mean area of 183 +/- 139 cm2 was found, whereas the area was only 52 +/- 58 cm2 in those with no VT induction (P < 0.05). For an area > or = 50 cm2, there were positive and negative predictive values of 92% and 60%, respectively. Positive late potentials were found in 60% of patients and correlated to the inducibility during programmed ventricular stimulation (positive predictive value 100%, negative predictive value 75%; P < 0.001). CONCLUSION: In patients with Brugada syndrome, the body surface area of ST elevation and the presence of late potentials correlate to the inducibility of VT during programmed ventricular stimulation and may be of value as a new noninvasive marker for risk stratification in these patients.
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Value of magnetocardiographic QRST integral maps in the identification of patients at risk of ventricular arrhythmias.
It has been shown that regional ventricular repolarization properties can be reflected in body surface distributions of electrocardiographic QRST deflection areas (integrals). We hypothesize that these properties can be reflected also in the magnetocardiographic QRST areas and that this may be useful for predicting vulnerability to ventricular tachyarrhythmias. Magnetic field maps were obtained during sinus rhythm from 49 leads above the anterior chest in 22 healthy (asymptomatic) control subjects (group A) and in 29 patients with ventricular arrhythmias (group B). In each subject, the QRST deflection area was calculated for each lead and displayed as an integral map. The mean value of maximum was significantly larger in the control group A than in the patient group B (1,626+/-694 pTms vs. 582+/-547 pTms, P<0.0001). To quantitatively assess intragroup variability in the control group A and intergroup variability of the control and patient groups, we used the correlation coefficient r and covariance sigma. These indices showed significantly less intragroup than intergroup variation (e.g., in terms of sigma, 28.0x10(-6)+/-12.3x10(-6) vs. 3.4x10(-6)+/-12.5x10(-6), P<0.0001). Each QRST integral map was also represented as a weighted sum of 24 basis functions (eigenvectors) by means of Karhunen-Loeve transformation to calculate the contribution of the nondipolar eigenvectors (all eigenvectors beyond the third). This percentage nondipolar content of magnetocardiographic QRST integral maps was significantly higher in the patient group B than in the control group A (13.0%+/-9.1 % vs. 2.6%+/-2.0%, P<0.0001). Discriminations between control subjects and patients with ventricular arrhythmias based on magnitude of the maximum, covariance sigma, and nondipolar content were 90.2%, 90.2%, and 86.3% accurate, with a sensitivity of 89.7%, 93.1%, and 75.9%, and a specificity of 90.9%, 86.4%, and 100%. We have shown that magnitude of the maximum and indices of variability and nondipolarity of the magnetocardiographic QRST integral maps may predict arrhythmia vulnerability. This finding is in agreement with earlier studies that used body surface potential mapping and suggests that magneticfield mapping may also be a useful diagnostic tool for risk analysis.
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Magnetocardiographic and electrocardiographic exercise mapping in healthy subjects.
In 12-lead electrocardiography (ECG), detection of myocardial ischemia is based on ST-segment changes in exercise testing. Magnetocardiography (MCG) is a complementary method to the ECG for a noninvasive study of the electric activity of the heart. In the MCG, ST-segment changes due to stress have also been found in healthy subjects. To further study the normal response to exercise, we performed MCG mappings in 12 healthy volunteers during supine bicycle ergometry. We also recorded body surface potential mapping (BSPM) with 123 channels using the same protocol. In this paper we compare, for the first time, multichannel MCG recorded in bicycle exercise testing with BSPM over the whole thorax in middle-aged healthy subjects. We quantified changes induced by the exercise in the MCG and BSPM with parameters based on signal amplitude, and correlation between signal distributions at rest and after exercise. At the ST-segment and T-wave apex, the exercise induced a magnetic field component outward the precordium and the minimum value of the MCG signal over the mapped area was found to be amplified. The response to exercise was smaller in the BSPM than in the MCG. A negative component in the MCG signal at the repolarization period of the cardiac cycle should be considered as a normal response to exercise. Therefore, maximum ST-segment depression over the mapped area in the MCG may not be an eligible parameter when evaluating the presence of ischemia.
Biomedical Engineering↗
A field-compatible method for interpolating biopotentials.
Mapping of bioelectric potentials over a given surface (e.g., the torso surface, the scalp) often requires interpolation of potentials into regions of missing data. Existing interpolation methods introduce significant errors when interpolating into large regions of high potential gradients, due mostly to their incompatibility with the properties of the three-dimensional (3D) potential field. In this paper, an interpolation method, inverse-forward (IF) interpolation, was developed to be consistent with Laplace's equation that governs the 3D field in the volume conductor bounded by the mapped surface. This method is evaluated in an experimental heart-torso preparation in the context of electrocardiographic body surface potential mapping. Results demonstrate that IF interpolation is able to recreate major potential features such as a potential minimum and high potential gradients within a large region of missing data. Other commonly used interpolation methods failed to reconstruct major potential features or preserve high potential gradients. An example of IF interpolation with patient data is provided to illustrate its applicability in the actual clinical setting. Application of IF interpolation in the context of noninvasive reconstruction of epicardial potentials (the "inverse problem") is also examined.
Action Potentials↗
[Patterns of body surface isointegral maps for anteroseptal and inferior myocardial infarction].
A goal of the present paper was to determine the patterns of the QRS isointegral maps for the two location of myocardial infarction: anteroseptal (aMI) and inferior (iMI), using a method of body surface potential mapping (BSPM) with a 87-electrode Fukuda Denshi system. The maps were recorded in the two groups of the patients with previous (6-12 month earlier), clinically documented, Q-wave myocardial infarction. The examined group comprised 36 patients with aMI and 32 patients with iMI. The analysis concerned the isointegral maps of the assigned seven time intervals within the QRS complex (the A-G maps), rendering the patterns of positive and negative potential distribution, likewise the group-mean values of minima and maxima for each of the analyzed maps. The increased area of negative potential, as compared with the corresponding control maps, was observed in the maps of the A, B and D intervals in the aMI group. Contrary, in the iMI group a pathological negative potential was found only in the E maps (the second half of the QRS complex). The comparative analysis of the potential extremes revealed in the aMI group the significantly more negative minima in the A, B, D and E maps and lower maxima in the A and B maps. However, in the iMI group the only statistically significant difference were the lower minima for the E maps. The investigations resulted in creating the patterns of the pathological distribution of the negative potential and the minimum values in the isointegral QRS maps, which are specific for the anteroseptal and inferior myocardial infarction.
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Derivation of an optimal lead set for measuring ectopic atrial activation from the pulmonary veins by using body surface mapping.
Atrial fibrillation is often initiated by atrial premature beats originating in the pulmonary veins. Non-invasive localization of these ectopic beats would be of significant value in guiding therapy. Body surface potential mapping was performed in nine patients undergoing invasive electrophysiologic study. Signals were recorded from 62 electrodes during pace mapping from each of the pulmonary veins. Optimal electrodes for localizing pulmonary vein activation were sequentially chosen. Seven optimal electrodes (6 anterior, 1 posterior) for recording ectopic atrial activation originating in the pulmonary veins were selected. The seven optimal electrode set performed better than the standard 9 electrode ECG at estimating the full body surface map (correlation 97 vs. 95.7%; p < 0.05). Seven optimally selected electrodes can estimate the body surface potential distribution during ectopic atrial activation orignating from the pulmonary veins. The ability of this electrode configuration to discriminate the site of origin of ectopic atrial beats requires prospective evaluation.
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Correlation between body surface isopotential maps and left ventriculograms in patients with old anterior myocardial infarction.
In 30 patients with old anterior myocardial infarction, body surface isopotential maps were correlatively studied with left ventriculographic findings. In 25 patients with ventricular asynergy restricted to the anterior segments, surface potential abnormalities due to infarction were observed during specific phases of QRS and in specific portions of the chest surface depending on the location and extent of severe ventricular asynergy (akinesis and dyskinesis). However, the remaining 5 patients with co-existing severe asynergy in the inferoposterior segment, showed body surface potential maps quite different from those of the above 25 patients. It was suggested that body surface isopotential maps were useful in detecting the location and extent of ventricular severe asynergy in patients with old anterior myocardial infarction.
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Electrocardiographic imaging: I. Effect of torso inhomogeneities on body surface electrocardiographic potentials.
INTRODUCTION: Body surface potential maps (BSPMs) and conventional ECG reflect electrical sources generated by cardiac excitation and repolarization and noninvasively provide important diagnostic information about the electrical state of the heart. Because the heart is located within the torso volume conductor, body surface potentials also reflect the effects of torso inhomogeneities, which include blood, lungs, bone, muscle, fat, and fluid. It is necessary to characterize and understand these effects in order to interpret BSPM and ECG in terms of cardiac activity without "contamination" from the inhomogeneous volume conductor. METHODS AND RESULTS: Actual measured epicardial and body surface potentials were obtained during normal sinus rhythm and for different pacing protocols from a Langendorff-perfused dog heart suspended in a human-shaped torso tank. Accurate geometry of the torso inhomogeneities was digitized from the Visual Human Project and appropriately introduced into a computer model of the tank setup. The geometry and electrical properties of the volume conductor could be varied. Both homogeneous and inhomogeneous torsos have major smoothing effects on BSPM, which is of very low resolution compared with its corresponding epicardial potential pattern. Relative to a homogeneous torso, the inhomogeneities have only a minor effect on BSPM patterns. They augment potential magnitudes depending on the pattern of epicardial activation. Variations of geometry and electrical properties within the normal physiologic range have minimal effects. CONCLUSION: Effects of torso inhomogeneities on 12-lead ECGs are minimal, and the associated ECG changes fall within the range of normal interindividual variations.
Algorithms↗
MCG to ECG source differences: measurements and a two-dimensional computer model study.
In this work we combine body surface potential map (BSPM) and magnetocardiogram (MCG) measurements with computer simulations in order to elucidate a recent thesis that claims the orthogonality of the main sources of MCG and ECG. Body surface currents and MCG pseudo currents are calculated from measured BSPM and MCG data, respectively. In contrast to the MCG-ECG source orthogonality thesis, we observe the main orientation of the BSPM currents and MCG pseudo currents to have similar axis during most of the depolarization R wave. In an attempt to explain such measurements we simulate a 2D transmural slice of the left ventricle in contact to a volume conductor. The main magnetic source currents along the wave front are indeed orthogonal to the extracellular electric current. However, fiber orientation inhomogeneity through the ventricular wall, volume conductor interface, wave front shape and extra- and intracellular potential distributions, all distort the symmetry of the current loops that contain the wave front currents. The resulting asymmetry rotates the main axis of the pseudo MCG currents away from the orthogonal axis of the body surface currents. Thus, the simulation results could solve the apparent contradiction between the orthogonal source theory and the observed similar ECG and MCG main current axis.
Body Surface Potential Mapping↗
[Analysis of the foci of ectopic stimuli based on body surface mapping of cardiac potentials during sinus rhythm].
This paper submits results of cardiac potentials mapping recorded from the body surface in a 87-electrodes Fukuda-Denshi system in 10 patients exhibiting documented ventricular cardiac rhythm disturbances. Isopotential and isointegral maps of depolarisation periods of the ventricles were analysed for sinus cycle and additional ventricular activations. The results were then compared to those of a 15-persons reference group of people not displaying any cardiac rhythm disturbances. Occurrence was pointed out of aberration at different cardiac activation time, manifested as additional potential extremes during QRS as well ventricular repolarization. The additional extremes during ventricular repolarization are of a persistent potential character, probably resulting in disturbed activation.
Action Potentials↗
A model study of the sensitivity of body surface potential distribution to variations of electrode placement.
The effect of electrode displacement as one of the sources of reproducibility errors in body surface potential maps was studied using a realistic computer model of the cardiac electric field. A uniform dipole layer model of the cardiac generator and a realistic geometry of the torso, heart, and lungs was adopted for the simulation of surface potentials during ventricular activation. The effect of systematic electrode displacement in terms of longitudinal shifts and variations of longitudinal size (height) of the mapped area was studied. The map reconstruction error of three different limited lead systems and the variability of maps measured on all points of the mapping grid, as well as maps reconstructed from limited lead systems, were investigated and quantified. A mean relative error of map reconstruction of less than 3.5% was found for longitudinal shifts from -4.4 to +1.7 cm, and for longitudinal size changes from 65 to 108% of the initial area. For vertical displacements of electrodes between the limits of +/- 2.0 cm for full grid maps and +/- 1.4 cm if limited lead systems were used, the mean relative error of the maps remained under 5%.
Body Surface Potential Mapping↗
P-wave body surface potential distribution in rats.
The aim of this study was to investigate body surface potential distribution during the P wave in Wistar rats. We performed body surface potential mapping by means of a 64-channel synchronous electrocardiotopography. The positive area covered the caudal part of the thorax, and the negative one covered the cranial part of the thorax. During the P wave, we observed 1 maximum and 1 minimum on the body surface. The dynamics of the P-wave body surface potential distribution in rats was characterized by minor movement of the positive and negative areas, and a counterclockwise shift of the extrema on the ventral body surface. The obtained results are discussed in comparison with those in dogs and humans.
Action Potentials↗
Imaging dispersion of myocardial repolarization, I: comparison of body-surface and epicardial measures.
BACKGROUND: Body-surface ECG measures (QT dispersion [QTd], QRST integrals) have been used as indices of myocardial repolarization abnormalities with the goal of identifying patients at risk of fatal arrhythmias. The clinical utility of these measures has been questioned. We investigate the complex relationship between epicardial and body-surface potentials in the context of regionally abnormal myocardial repolarization. METHODS AND RESULTS: Epicardial potentials were recorded with a 224-electrode sock from an open-chest dog during control, regional epicardial warming, cooling, and adjacent warming and cooling to induce localized alterations in myocardial repolarization and regions of increased repolarization dispersion. Body-surface potentials were generated from these epicardial potentials in a human torso model. Epicardial estimates of repolarization (activation recovery intervals [ARIs] and QRST integrals) were evaluated for their ability to identify regions with increased repolarization dispersion. Body-surface QRST integrals and QTd in 12-lead ECG and 64-lead body-surface potential maps were evaluated for their ability to detect increased dispersion of myocardial repolarization. Epicardial ARI and QRST integral maps successfully located epicardial regions with increased dispersion of repolarization. The increased dispersion was not consistently reflected in the 12-lead or 64-lead ECG QTd or in the body-surface QRST integral maps. CONCLUSIONS: This study demonstrates the inadequacy of body-surface measures that are thought to reflect myocardial dispersion of repolarization. In contrast, measures based on epicardial electrograms (ARI or epicardial QRST integral maps) provide physiologically relevant information about myocardial repolarization and can locate regions of increased dispersion.
Animals↗
A computer heart model incorporating anisotropic propagation. III. Simulation of ectopic beats.
With the advent of catheter ablation procedures, it has become an important goal to predict noninvasively the site of origin of ventricular tachycardia. Site classifications based on the observed body surface potential maps (BSPMs) during ventricular endocardial pacing, as well as on the patterns of the QRS integrals of these maps, have been suggested. The goals of this study were to verify these maps and their QRS integral patterns via simulation using a computer heart model with realistic geometry and to determine whether the model could improve clinical understanding of these ectopic patterns. Simulation was achieved by initiating excitation of the heart model at different endocardial sites and their overlying epicardial counterparts. This excitation propagated in anisotropic fashion in the myocardium. Retrograde excitation of the model's His-Purkinje conduction system was necessary to obtain realistic activation durations. Simulated BSPMs, computed by placing the heart model inside a numerical torso model, and their QRS integrals were close to those observed clinically. Small differences in QRS integral map patterns and in the positions of the QRS integral map extrema were noted for endocardial sites in the left septal and anteroseptal regions. The simulated BSPMs during early QRS for an endocardial site and its epicardial counterpart tended to be mirror images about the zero isopotential contour, exchanging positive and negative map regions. The simulation results attest to the model's ability to reproduce accurately clinically recorded body surface potential distributions obtained following endocardial stimulation. The QRS integral maps from endocardial sites in the left septal and anteroseptal regions were the most labile, owing to considerable cancellation effects. Conventional BSPMs can be useful to help distinguish between endocardial and epicardial ectopic sites.
Anisotropy↗
Potential role of body surface ECG mapping for localization of atrial fibrillation trigger sites.
Catheter ablation has revolutionized the clinical management of atrial fibrillation (AF) by offering a curative treatment option for this highly prevalent arrhythmia. Ablation therapy is aimed at electrical isolation of the pulmonary veins (PVs) as a means to prevent rapidly firing focal activation within the PVs from penetrating into the left atrium (LA) and initiate reentrant wavelet propagation. However, non-PV AF trigger sites may be present and lead to unsuccessful ablation or post-ablation AF recurrences. Infrequent trigger firing and the difficulty or inability to induce focal trigger activity in the electrophysiology laboratory limits invasive catheter-based mapping of non-PV trigger sites. Identification of AF trigger sites using the surface electrocardiogram (ECG) P wave morphology is feasible but conventional 12-lead scalar recordings do not offer the resolving power to provide discrete regional localization to potentially target catheter ablation. The present paper includes a review of preliminary clinical data on the use of a 65-lead ECG mapping system (Resolution Medical, Inc) for the non-invasive localization of AF trigger sites. This method utilizes a unique previously developed reference database of 34 mean paced P wave integral map patterns which are each specific to activation arising from a discrete segment in the LA and right atrium (RA). Trigger site localization is obtained by matching the P wave integral map morphology of a premature atrial contraction (PAC) with the reference database of 34 mean paced P wave integral map patterns.
Algorithms↗
How many ECG leads do we need?
The number of leads needed in clinical electrocardiography depends on the clinical problem to be solved. The standard 12-lead ECG is so well established that alternative lead systems must prove their advantage through well-conducted clinical studies to achieve clinical acceptance. Certain additional leads seem to add valuable information in specific patient groups. The use of a large number of leads (eg, in body surface potential mapping) may add clinically relevant information, but it is cumbersome and its clinical advantage is yet to be proven. Reduced lead sets emulate the 12-lead ECG reasonably well and are especially advantageous in emergency situations.
Body Surface Potential Mapping↗