Effect of anisotropy on ventricular vulnerability to unidirectional block and reentry by single premature stimulation during normal sinus rhythm in rat heart.

Single high-intensity premature stimuli when applied to the ventricles during ventricular drive of an ectopic site, as in Winfree's "pinwheel experiment," usually induce reentry arrhythmias in the normal heart, while single low-intensity stimuli barely do. Yet ventricular arrhythmia vulnerability during normal sinus rhythm remains largely unexplored. With a view to define the role of anisotropy on ventricular vulnerability to unidirectional conduction block and reentry, we revisited the pinwheel experiment with reduced constraints in the in situ rat heart. New features included single premature stimulation during normal sinus rhythm, stimulation and unipolar potential mapping from the same high-resolution epicardial electrode array, and progressive increase in stimulation strength and prematurity from diastolic threshold until arrhythmia induction. Measurements were performed with 1-ms cathodal stimuli at multiple test sites (n = 26) in seven rats. Stimulus-induced virtual electrode polarization during sinus beat recovery phase influenced premature ventricular responses. Specifically, gradual increase in stimulus strength and prematurity progressively induced make, break, and graded-response stimulation mechanisms. Hence unidirectional conduction block occurred as follows: 1) along fiber direction, on right and left ventricular free walls (n = 23), initiating figure-eight reentry (n = 17) and tachycardia (n = 12), and 2) across fiber direction, on lower interventricular septum (n = 3), initiating spiral wave reentry (n = 2) and tachycardia (n = 1). Critical time window (55.1 ± 4.7 ms, 68.2 ± 6.0 ms) and stimulus strength lower limit (4.9 ± 0.6 mA) defined vulnerability to reentry. A novel finding of this study was that ventricular tachycardia evolves and is maintained by episodes of scroll-like wave and focal activation couplets. We also found that single low-intensity premature stimuli can induce repetitive ventricular response (n = 13) characterized by focal activations.NEW & NOTEWORTHY We performed ventricular cathodal point stimulation during sinus rhythm by progressively increasing stimulus strength and prematurity. Virtual electrode polarization and recovery gradient progressively induced make, break, and graded-response stimulation mechanisms. Unidirectional conduction block occurred along or across fiber direction, initiating figure-eight or spiral wave reentry, respectively, and tachycardia sustained by scroll wave and focal activations.

T-wave alternans in LQTS: repolarization-rate dynamics from digital 12-lead Holter data.

T-wave alternans (TWA) is a harbinger of ventricular vulnerability and an important prognostic indicator for torsade de pointes and likely sudden death in patients with LQTS. We analyzed the occurrence of TWA in 18 patients with LQTS (7 males, 11 females, ages ranging from 6 months to 32 years--median 8.4 years). Analysis was performed with software to investigate dynamics of cycle length mediated repolarization changes. Digital Holter ECG analysis revealed macroscopic, true TWA in 3 of 18 patients. TWA showed a variable morphological expression. One patient had continuous changes of T wave polarity, but not on a periodic beat-to-beat basis. Onsets of macroscopic TWA were preceded by long/short cycle length sequences and tachycardic rates above 130 to 140 bpm. Impact of ventricular premature beats on TWA onset was insignificant. Two of the identified patients with TWA had sudden cardiac death during follow-up (one refused PM therapy). At present, TWA cannot be detected automatically from Holter ECGs and therefore may be missed, despite the potential danger for the individuals. The observation that predominantly high beat rates and not beat rate changes, per se, triggered episodes of TWA renders difficult general therapeutic recommendations for the identified patients at risk.

Electrocardiographic measures of repolarization revisited: why? what? how?

Ventricular repolarization continues to be an enigma to clinical cardiologists and cardiac electrophysiologists. On the one hand, a century of experience has documented an association between abnormal T-wave morphology, QT prolongation and dispersion, T-wave alternans, and nonspecific ST-T waves with arrhythmia risk or negative prognostic outcome. On the other hand, recent advances in molecular electrophysiology have definitively implicated abnormal function and structure of cardiac ion channels associated with repolarization as primary arrhythmogenic mechanisms in long QT syndrome, Brugada's Syndrome, and idiopathic ventricular fibrillation and ventricular tachycardia. In spite of this extensive clinical experience and newly established mechanistic knowledge, robust measurements of repolarization and sensitive algorithms for reliable assessment of risk and prediction of arrhythmia occurrence have remained elusive. New insights into electrocardiographic waveform that reflect and capture the underlying spatial and dynamic characteristics of repolarization offer opportunity to devise clinical indices of repolarization that might be more predictive of risk or outcome than those currently used. Experimental and model data show evidence that the location and size of repolarization lesions may be deduced from T waveform. The changes of repolarization induced by altered activation sequence, and cycle length mediated alterations to repolarization offer additional means to assess the magnitude and significance of such lesions that are linked to increased arrhythmogenic risk. This article explores indices of repolarization that are sensitive to repolarization and its change and that provide opportunity to better characterize and assess repolarization for risk stratification.

Mechanisms in T-wave alternans caused by intraventricular block.

It is recognized that 2:1 intraventricular (IV) block can result in T-wave alternans but is usually assumed that it would also affect QRS waveform. Block in a local region is not, however, varied activation sequence of the same muscle mass because the blocked region is not activated and is not part of the mass that is activated in cycles without block. Also, the block region may have electrocardiogram (ECG) effects when its state differs from other regions. In view of those considerations, the ECG effects of IV block were evaluated by using a computer model of excitation and recovery. ECGs were calculated from differences between the excited state and various degrees of recovery. Results provided evidence that boundaries associated with regions of block rather than regions having varied activation sequence were the major factors in T-wave alternans caused by IV block. Effects of the boundaries included cancellation of the effects of IV block on QRS complexes. Findings suggest that IV block cannot be excluded as a mechanism of T-wave alternans in the absence of QRS alternans.

Estimates of repolarization dispersion from electrocardiographic measurements.

BACKGROUND: Repolarization dispersion (Rd) is frequently mentioned as a predictor of cardiac abnormalities. We present a new measure of Rd based on the root-mean-square (RMS) curve of an ECG lead set and compare its performance with that of the commonly used QT dispersion (QTd) measure with the use of recovery times measured from directly recorded canine electrograms. METHODS AND RESULTS: Using isolated, perfused canine hearts suspended in a torso-shaped electrolytic tank, we simultaneously recorded electrograms from 64 epicardial sites and ECGs from 192 "body surface" sites. RMS curves were derived from 4 lead sets: epicardial, body surface, precordial, and a 6-lead optimal set. Repolarization was altered by changing cycle length, temperature, and activation sequence. Rd, calculated directly from recovery times of the 64 epicardial potentials, was then compared with the width of the T wave of the RMS curve and with QTd for each of these 4 lead sets. The correlation between T-wave width and Rd for each lead set, respectively, was epicardium, 0.91; body surface, 0.84; precordial, 0.72; and optimal leads, 0.81. The correlation between QTd and Rd for each lead set was epicardium, 0.46; body surface, 0.47; precordial, 0.17; and optimal leads, 0.11. CONCLUSIONS: RMS curve analysis provides an accurate method of estimating Rd from the body surface. In contrast, QTd analysis provides a poor estimate of Rd.

Estimates of repolarization and its dispersion from electrocardiographic measurements: direct epicardial assessment in the canine heart.

This study investigates a technique to estimate dispersion based on the root mean square (RMS) signal of multiple electrocardiographic leads. Activation and recovery times were measured from 64 sites on the epicardium of canine hearts using acute in situ or Langendorff perfused isolated heart preparations. Repolarization and its dispersion were altered by varying cycle length, myocardial temperature, or ventricular pacing site. Mean and dispersion of activation and recovery times, and activation-recovery interval (ARI) were calculated for each beat. The waveform was then calculated from all leads. Estimates of mean and dispersion of activation and recovery times and mean ARI were derived using only inflection points from the RMS waveform. QT intervals were also measured and QT dispersion was determined. Estimates determined from the RMS waveform provided accurate estimates of repolarization and were, in particular, a better measure of repolarization dispersion than QT dispersion.

Simulated torsade de pointes--the role of conduction defects and mechanism of QRS rotation.

A possible mechanism of torsade de pointes consisting of moving sites of reentry in the presence of disparate recovery of excitability has been previously proposed. This study evaluates the role of conduction defects in that mechanism. A computer model that simulated propagation, cycle length dependent recovery of excitability, and slow propagation during incomplete recovery and in conduction defects was used. Localized conduction defects consisting of slow propagation were shown to allow reentry at changing locations in the presence of uniform recovery properties. Later activation within defects resulted in later recovery, which permitted independent antegrade propagation adjacent to the defects. Retrograde propagation in the defects then resulted in reentry. The location of serial reentry changed because retrograde propagation and antegrade recovery had opposing directions and met distal to the origin of antegrade excitation. This mechanism was similar to that produced by disparate recovery and the combination of conduction defects and disparate recovery permitted the mechanism to occur with less marked disparity than otherwise required. The study also showed bidirectional serial reentry around a localized conduction defect or region of disparate recovery, which resulted in rotation of QRS peaks around the isoelectric line. The study provided evidence that either conduction defects or disparate recovery of excitability may be a substrate for torsade de pointes. It also indicated that combination of these factors might permit torsade de pointes when neither alone does so. This provides a possible explanation for the special propensity of quinidine and other drugs that slow conduction as well as prolong recovery to result in torsade de pointes. Findings also suggested a more explicit mechanism for rotation of QRS peaks about the electrocardiogram baseline than was previously available.

Thoracic location of the lead with maximal ST-segment deviation during posterior and right ventricular ischemia: comparison of 18-lead ECG with 192 estimated body surface leads.

By using our database of continuous 18-lead electrocardiographic (ECG) recordings (standard + V3-5R + V7-9) during coronary angioplasty, we selected 68 patients with left circumflex balloon occlusions (posterior ischemia model) or proximal right coronary artery balloon occlusions (right ventricular IRV] ischemia model). ST-segment amplitudes (J + 60 ms) at preangioplasty baseline were subtracted from maximal ST amplitudes during balloon inflation to create a positive or negative change score (deltaST) for each of the 18 leads. DeltaST elevation was used to describe a change in the ST level in the positive direction from baseline, whether or not actual ST elevation from the isoelectric line was present. DeltaST depression was used to describe a change in the ST level in the negative direction from baseline, whether or not actual ST depression from the isoelectric line was present. ST amplitudes from 8 of the 12 standard leads were then used to estimate ST amplitudes at 192 body surface sites spanning the entire anterior and posterior thorax using the transformation technique of Lux. Thoracic distributions of the DeltaST values were displayed on a torso figure, including locations of the 18 lead locations and points of maximal ST elevation and depression. The 192 estimated body surface unipolar leads were compared with 18-lead ECGs (bipolar and unipolar). During 53 left circumflex occlusions, the maximal deltaST elevation was always located in the 18-lead ECG, with the most frequent locations at leads III, II (41%), V7-8 (34%), and V5-6 (25%). The maximal deltaST depression was located outside the 18-lead ECG (89%), with the most frequent locations above standard lead V2 (67%) and V3 (14%). During 16 proximal right coronary artery occlusions, the maximal deltaST elevation was always located in the 18-lead ECG, with the most frequent locations at leads III (81%) and V2-3R (13%). The maximal deltaST depression was located outside the 18-lead ECG (93%), with the most frequent locations above standard lead V2 (50%), V3 (14%), and V4 (14%). We conclude that maximal deltaST elevation is always located in the 18-lead ECG and maximal deltaST depression is frequently located outside of 18-lead ECG during left circumflex and proximal right coronary artery occlusions. Future studies are required to determine the bipolar leads for the 192 estimated body surface potential mapping leads.

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.

Uncertainty of the electrocardiogram: old and new ideas for assessment and interpretation.

The electrocardiogram (ECG) is a highly complex, dynamic and stochastic phenomenon. Although it provides a valuable, noninvasive and rapid means of assessing cardiac state and its change, uncertainties in its measurement and variation in the underlying electrophysiology that generates the ECG make difficult further improvement in its reliability for detecting and monitoring cardiac pathologies and conditions. This article reviews the sources of variability and uncertainty in ECG measurement and interpretation, revisits some old ideas for dealing with them, and proposes some novel directions for improving accuracy of ECG assessment and interpretation. We shall explore relative information content of lead systems, representation of ECG signals and patterns, and estimation of ECG distributions from limited lead systems. In addition, we will compare strategies for measuring ECG information and suggest new paradigms for feature extraction that reduce the sensitivity of assessment accuracy to intrinsic and extrinsic measurement errors. Finally, we review the importance of including dynamic information in ECG assessment, both for interpreting current cardiac state as well as for monitoring its change and significance.

Three-dimensional activation mapping in ventricular muscle: interpolation and approximation of activation times.

Interpolation plays an important role in analyzing or visualizing any scalar field because it provides a means to estimate field values between measured sites. A specific example is the measurement of the electrical activity of the heart, either on its surface or within the muscle, a technique known as cardiac mapping, which is widely used in research. While three-dimensional measurement of cardiac fields by means of multielectrode needles is relatively common, the interpolation methods used to analyze these measurements have rarely been studied systematically. The present study addressed this need by applying three trivariate techniques to cardiac mapping and evaluating their accuracy in estimating activation times at unmeasured locations. The techniques were tetrahedron-based linear interpolation, Hardy's interpolation, and least-square quadratic approximation. The test conditions included activation times from both high-resolution simulations and measurements from canine experiments. All three techniques performed satisfactorily at measurement spacing < or = 2 mm. At the larger interelectrode spacings typical in cardiac mapping (1 cm), Hardy's interpolation proved superior both in terms of statistical measures and qualitative reconstruction of field details. This paper provides extensive comparisons among the methods and descriptions of expected errors for each method at a variety of sampling intervals and conditions.

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.

Estimation of epicardial activation maps from intravascular recordings.

Multielectrode catheters provide a percutaneous means of recording activation near the epicardium but only for a relatively small number of sites that are restricted to the major coronary vessels. We have applied a statistical signal processing technique to estimate the value of activation time over the entire epicardium (490 sites) from leadsets consisting of 4 to 40 sites aligned with major branches of the coronary veins. We tested this method using data from high-resolution epicardial mapping from six dog hearts and 153 activation sequences. A study including data from both normal and infarcted dog hearts yielded estimates of activation time, with mean correlation coefficients ranging from 0.97 to 0.84 and achieved localization of earliest site of activation to within 3 to 15 mm, depending on training parameters and leadset. These results suggest that with 10 to 15 catheter-mounted electrodes, it may be possible to reconstruct epicardial activation maps from percutaneous recordings.

Paradoxical QRST integral changes with ventricular repolarization dispersion.

Body surface QRST integral (QRSTI) maps have been shown theoretically to reflect disparity of intrinsic repolarization properties and have been experimentally linked to increased arrhythmia susceptibility. Paradoxically, a lower magnitude of QRSTI in patients with heart disease and at risk for arrhythmias has been reported. We hypothesized that this paradoxical reduction in QRST magnitude is a consequence of increased heterogeneity of repolarization gradients in normal hearts. We generated QRSTI using a previously published heart model to compare QRSTI for aligned and random repolarization gradients. The heart model consisted of 50,000 cubic units in an anatomically correct arrangement that included parameters to simulate anisotropic conduction and inhomogeneous distribution of refractoriness. Body surface potential maps (BSPMs) were generated on a torso surface assuming a homogeneous torso and using the boundary element method for normal alignment of repolarization gradients and spatially reassigned repolarization values that randomized repolarization directions. QT duration was measured by the subtraction of Q onset time from T offset time on the BSPM. T offset was defined as the last potential to be detected at intervals of 3 ms that was above the threshold of 0.1 mV during recovery. The time of T offset showed a consistent tendency to shift to the left posterior and to split. When slow conduction velocities were assigned, BSPMs showed delayed propagation and multiple extrema. QRSTI showed systematic magnitude decrease with increasing randomness of repolarization gradient direction. Ventricular fibrillation (VF) could be induced by successive extrastimuli under the conditions of over 70% deviation and slow conduction of 0.5 m/s for the longitudinal direction. In conclusion, a possible explanation for the paradoxical reduction in QRSTI in the presence of constant repolarization disparity is the change in alignment of repolarization gradients.

Noninvasive indices of repolarization and its dispersion.

In experimental studies using Langendorff perfused, isolated canine hearts immersed in a torso-shaped electrolytic tank we studied repolarization and its dispersion using direct epicardial measurements and newly derived, noninvasive body surface indices. Activation recovery intervals (ARIs) measured from 64 epicardial sites based on differences between activation times (ATs) and recovery times (RTs) provided direct measures of repolarization. The indirect, torso surface indices were derived from inflections of the root-mean-square (RMS) voltage of the torso tank surface electrocardiograms recorded simultaneously with the epicardial data. For cycle lengths ranging from 300 to 900 ms, and electrolyte temperatures ranging from 32 degrees C to 40 degrees C we calculated mean, variance, and range of ATs, RTs, and ARIs from the epicardium. From epicardial and torso surface RMS waveforms, we used times of R and T peaks and their differences to estimate mean ATs, RTs, and ARIs, respectively. The RMS T wave width as determined from the second derivative inflections on either side of the T peak served as an estimate of the dispersion of RTs. In parallel studies, we showed that the direct measures of repolarization and its dispersion were reflected in RMS waveforms generated from the epicardial electrograms themselves. In this study, we confirm that the torso and epicardial RMS waveforms reflect comparable information for estimating repolarization and its dispersion. Furthermore, the derived measures provide a method to assess mean ARIs and dispersion of RTs on a beat-to-beat basis and during abnormal (ectopic ventricular) activation sequences.

Mechanisms of the spatial distribution of QT intervals on the epicardial and body surfaces.

INTRODUCTION: The role of QT dispersion as a predictor of arrhythmia vulnerability has not been consistently confirmed in the literature. Therefore, it is important to identify the electrophysiologic mechanisms that affect QT duration and distribution. We compared the spatial distributions of QT intervals (QTI) with potential distributions on cardiac and body surfaces and with recovery times on the cardiac surface. We hypothesized that the measure of QTI is affected by the presence of the zero potential line in the potential distribution, as well as the sequence of recovery. We also investigated use of the STT area as a possible indicator of recovery times on the cardiac surface. METHODS AND RESULTS: High-resolution spatial distributions of QTI and potentials were determined on the body surface of human subjects and on the surface of a torso-shaped tank containing an isolated canine heart. Additionally, spatial distributions of QTI, recovery times, and STT areas were determined on the surface of exposed canine hearts. Unipolar electrograms were recorded during atrial and ventricular pacing for normal hearts and cases of myocardial infarction. Regions of shortest QTI always coincided with the location of the zero potential line on the cardiac and body surfaces. On the cardiac surface, in regions away from the zero line, similarities were observed between the patterns of QTI and the sequence of recovery. STT areas and recovery times were highly correlated on the cardiac surface. CONCLUSION: QTI is not a robust index of local recovery time on the cardiac surface. QTI distributions were affected by the position of the zero potential line, which is unrelated to local recovery times. However, similarities in the patterns of QTI and recovery times in some regions may help explain the frequently reported predictive value of QT dispersion. Preliminary results indicate STT area may be a better index of recovery time and recovery time dispersion on the epicardium than QTI.

High-density epicardial mapping during current injection and ventricular activation in rat hearts.

The purpose of this study is to report new methods for manufacturing precision electrode arrays for recording high-resolution potential distributions from epicardial surfaces of small-animal hearts. Electrode arrays of 64 leads (8 x 8) and 121 leads (11 x 11) were constructed with a tulle substrate to which insulated, fine silver wires (60-micrometer diameter) were attached by knots at mesh node intervals of 540 x 720 micrometers. Insulation was removed at the tips of the knots. Potential distributions and waveforms were recorded from saline solutions and rat heart epicardium during ventricular paced beats and during passive current injection in the diastolic interval. Electrical responses obtained from rat epicardium compared favorably with those observed in studies of larger-animal hearts, which used arrays having greater electrode spacing, and revealed the effects of myocardial anisotropy. Epicardial potentials measured early after stimulation in the region surrounding the pacing site were interpreted in terms of potentials generated by an equivalent quadrupolar source. We conclude that electrode arrays for epicardial mapping of small hearts can be constructed with sufficient ease and precision to allow detailed study of fiber structure and electrophysiology in these hearts in normal and pathological conditions.

A novel interpolation method for electric potential fields in the heart during excitation.

In mapping the electrical activity of the heart, interpolation of electric potentials plays two important roles. First, it permits the estimation of potentials in regions that could not be sampled or where signal quality was poor, and second, it supports the construction of isopotential lines and surfaces for visualization. The difficulty in developing robust interpolation techniques for cardiac applications lies in the abrupt change in potential in the vicinity of the activation wave front. Despite the resulting nonlinearities in spatial potential distributions, simple linear interpolation methods are the current standard and the resulting errors due to aliasing can be large if electrode spacing does not lie on the order of 0.5-2 mm--the thickness of the activation wave front. We have developed a novel interpolation method that is based on two observations specific to the spread of excitation in the heart: (1) that propagation velocity changes smoothly within a region large enough to contain several measurement electrodes and (2) that electrogram morphology varies very little in the neighborhood of each sample point except for a time shift in the potential wave forms. The resulting interpolation scheme breaks the interpolation of one highly nonlinear variable--extracellular potential--into two separate interpolations of variables with much less drastic spatial variation--activation time and electrogram morphology. We have applied this method to potentials originally recorded at 1.5 mm spacing and then subsampled at a range of densities for testing of the interpolation. The results based both on reconstruction of isopotential contour maps and statistical comparison showed significant improvement of this novel approach over standard linear techniques. The applications of the new method include improved determination of electrophysiological parameters such as spatial gradients of potential and the path of cardiac activation and recovery, estimation of electrograms at desired locations, and visualization of electric potential distributions.

Useful lessons from body surface mapping.

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.

Electrocardiographic imaging: Noninvasive characterization of intramural myocardial activation from inverse-reconstructed epicardial potentials and electrograms.

BACKGROUND: A recent study demonstrated the ability of electrocardiographic imaging (ECGI) to reconstruct, noninvasively, epicardial potentials, electrograms, and activation sequences (isochrones) generated by epicardial activation. The current study expands the earlier work to the three-dimensional myocardium and investigates the ability of ECGI to characterize intramural myocardial activation noninvasively and to relate it to the underlying fiber structure of the myocardium. This objective is motivated by the fact that cardiac excitation and arrhythmogenesis involve the three-dimensional ventricular wall and its anisotropic structure. METHODS AND RESULTS: Intramural activation was initiated by pacing a dog heart in a human torso tank. Body surface potentials (384 electrodes) were used to compute epicardial potentials noninvasively. Accuracy of reconstructed epicardial potentials was evaluated by direct comparison to measured ones (134 electrodes). Protocols included pacing from five intramural depths. Epicardial potentials showed characteristic patterns (1) early in activation, central negative region with two flanking maxima aligned with the orientation of fibers at the depth of pacing; (2) counterclockwise rotation of positive potentials with time for epicardial pacing, clockwise rotation for subendocardial pacing, and dual rotation for midmyocardial pacing; and (3) central positive region for endocardial pacing. Noninvasively reconstructed potentials closely approximated these patterns. Reconstructed epicardial electrograms and epicardial breakthrough times closely resembled measured ones, demonstrating progressively later epicardial activation with deeper pacing. CONCLUSIONS: ECGI can noninvasively estimate the depth of intramyocardial electrophysiological events and provides information on the spread of excitation in the three-dimensional anisotropic myocardium on a beat-by-beat basis.