The effect of nontransmural necroses on epicardial potential maps during paced activation: a simulation study.

A number of studies have indicated that epicardial potentials provide detailed spatiotemporal information about the spread of electrical activation within the ventricular wall. Here, we used a computer model to simulate activation sequences and corresponding epicardial potential maps in the ventricles damaged by localized necroses. Our findings agreed with those of experimental studies performed for epicardial pacing locus in a complete transient loss of one of the positive areas when the necrosis was located subepicardially, and in a transient gap in the expanding positive areas when the necrosis was located intramurally and subendocardially. This study--by systematically comparing simulated epicardial potential maps with those recorded on the exposed canine hearts--constitutes an important step in validation of our model.

Value and limitations of an inverse solution for two equivalent dipoles in localising dual accessory pathways.

Investigations were carried out into whether an equivalent generator consisting of two dipoles could be used to detect dual sites of ventricular activity. A computer model of the human ventricular myocardium was used to simulate activation sequences initiated at eight different pairs of sites positioned on the epicardial surface of the atrio-ventricular ring. From these sequences, 117-lead body surface potentials (covering the anterior and posterior torso), 64-lead magnetic field maps (above the anterior chest) and 128-lead magnetic field maps (above the anterior and posterior chest) were simulated and were then used to localise dual accessory pathways employing pairs of equivalent dipoles. Average localisation errors were 12 mm, 12 mm and 9 mm, respectively, when body surface potentials, 64-lead and 128-lead magnetic fields were used. The results of the study suggest that solving the inverse problem for two dipoles could provide additional information on dual accessory pathways prior to electrophysiological study.

ECG body surface isointegral and isoarea maps (BSM) in 30 and 60-years-old healthy humans.

ECG body surface isointegral and isoarea maps (BSM) are the sensitive indications of local electrical depolarization and repolarization changes both in controls and in coronary artery disease. In the present work the absolute values of maximum and minimum (extremum) in BSM have been compared in 24 healthy persons (20-36 years) with 18 older ones (54-70) of both sexes, non-smokers and without cardiovascular diseases in their medical history. Twenty-nine parameters of the heart electric field were registered by 96 unipolar electrodes placed regularly on the thorax and analyzed by the system Cardiag. A lower heart rate and a longer QT interval were found in older persons. The maximum (extremum) of isointegral and isoarea maps was less positive and the minimum was less negative in the older than in the younger subjects (p < 0.01). The maximum Q-wave amplitude on surface thorax was significantly lowers in older than in younger persons. The results confirmed the age-dependent decrease of QRS and T wave potentials.

Optimal electrocardiographic leads for detecting acute myocardial ischemia.

This study identifies the most sensitive electrocardiographic leads for monitoring ST-segment changes caused by acute coronary ischemia. The data set consisted of 120-lead electrocardiograms (ECGs) digitally recorded during balloon-inflation angioplasty in 3 groups of patients with single-vessel disease (left anterior descending [LAD], 32; right coronary artery [RCA], 36; left circumflex [LCx], 23). The ST deviation was measured in all recorded leads during baseline and ischemic states, and its difference between these 2 states (DeltaST) was calculated at 352 sites and plotted as DeltaST maps. The patients in each group were divided, by means of DeltaST criteria, into subgroups of "responders" and "nonresponders." Mean DeltaSTs for each group/subgroup were calculated and standardized by the corresponding standard deviation (SD); these values were plotted as mean DeltaST and t maps. Sites where extrema of DeltaST occurred most frequently were sought in bootstrap trials, performed in each group/subgroup. The results suggest that the optimal sites for the ischemia-sensitive leads are: V(3) (+) and just below V(8) (-) for LAD-related ischemia; the left iliac crest (+) and above V(3) at the third intercostal space (-) for RCA-related ischemia; and just below V(8) (+) and above V(2) at the third intercostal space (-) for LCx-related ischemia. Three "optimal" bipolar leads using these sites registered, in the responders from the LAD, RCA, and LCx groups, mean DeltaST (+/-SD) of 232 +/- 59, 245 +/- 96 and 158 +/- 91 microV, respectively; the corresponding t values were 15.14, 9.90, and 6.75. In the 12-lead ECG, only lead V(3) approached optimal DeltaST and t values for the LAD responders (187 +/- 61 microV; t = 11.75) and lead III for the RCA responders (191 +/- 76 microV; t = 9.73), but even these values were significantly suboptimal (P = 0.0011 and P = 0.0120, respectively). We found that the "optimal" bipolar leads can be derived, to an excellent approximation, from the 12 standard leads or from 3 EASI leads (with 3 electrodes at Frank's transverse level and 1 on the manubrium), by using precalculated regression coefficients. By means of bootstrap trials, we estimated the mean sensitivity (SE) and the mean positive predictive value (PPV) with which 3 "optimal" vessel-specific leads could identify ischemia related to the LAD, RCA, and LCx arteries, in the test set, as (SE/PPV) 94.7/92.8%, 78.7/80.9%, and 81.5/80.9%. A similar diagnostic performance can be achieved by vessel-specific leads derived from the 12-lead ECG (93.0/93.4%, 76.6/82.0%, and 82.7/77.1%) and, interestingly, from the EASI lead system (97.8/88.4%, 78.0/80.2%, and 76.8/83.2%). Thus, although the "optimal" bipolar leads for detecting ischemia related to each of the 3 coronary arteries were found to require sampling outside the 12-lead ECG, these leads can be derived from the full set of 12 standard leads or--for clinical monitoring applications--from the EASI lead system by using fewer electrodes at convenient locations.

Diagnostic accuracy of derived versus standard 12-lead electrocardiograms.

To compare the diagnostic yield of electrocardiograms (ECGs) recorded by 12 standard leads with that of 12-lead ECGs derived from 3 bipolar EASI leads, we analyzed pertinent ECG data for 290 normal subjects and 497 patients who had had a prior myocardial infarction (MI); the latter group comprised 36 patients with a non-Q MI, 282 patients with a Q-wave MI, and 179 patients with a history of ventricular tachycardia (VT). We first estimated statistically an optimal set of coefficients for deriving the 12 standard leads from EASI leads and assessed this transformation in terms of goodness of fit. To gauge the diagnostic information content of the recorded vs. derived 12-lead ECGs, we performed successively two-group diagnostic classification--based on the Cardiac Infarction Injury Score (CIIS)--separating each of the patient subgroups from the normal group; the classification was repeated for 200 sets of patients selected randomly (with replacement), and the results were plotted as mean receiver operating characteristics. We found that derived 12-lead ECGs correlated well with the recorded ones, and reproduced faithfully the diagnostic features needed for the CIIS. When the CIIS was determined from features of the recorded standard 12 leads, its mean diagnostic performance (assessed in terms of area under the receiver operating characteristics curve) was 0.9004 for detecting non-Q MIs, 0.9546 for Q-wave MIs, and 0.9919 for MIs complicated by a history of VT. When, instead, features of derived 12 leads were used to determine the CIIS, diagnostic performance remained virtually unchanged (at 0.8905, 0.9531, and 0.9906, respectively). We conclude that, in our population, EASI-derived 12-lead ECGs contain nearly the same diagnostic information as standard 12-lead ECGs.

Low-frequency component of body surface potential maps identifies patients at risk for ventricular tachycardia.

AIMS: To investigate the ability of spectral features of signal-averaged body-surface potential maps in identifying post-infarction patients who are at risk of developing ventricular tachycardia. METHODS AND RESULTS: We recorded 120 lead body surface potential maps during sinus rhythm in 135 subjects (45 patients with healed myocardial infarction but no history of ventricular tachycardia, 45 patients with both healed myocardial infarction and at least one episode of sustained ventricular tachycardia, and 45 normal subjects) and analysed spectral features of body surface potential maps selected on the basis of isoharmonic maps for given bands of the frequency spectrum. We found that in the low-frequency band (1-11 Hertz), the group-mean power spectra of leads located at isoharmonic map maxima were significantly different (P<0.0001) between the two groups of myocardial infarction patients. We estimated that this single feature alone can prospectively identify myocardial infarction patients at risk for ventricular tachycardia with a predictive accuracy of 74+/-6%. CONCLUSION: Our results suggest that the bulk of diagnostic information associated with arrhythmogenicity resides in the low-frequency band of the power spectrum. This finding is at variance with the established notion that only the high-frequency component of signal-averaged electrocardiograms carries such information.

Simulated epicardial potential maps during paced activation reflect myocardial fibrous structure.

Using a three-dimensional propagation model of the human ventricular myocardium, we studied the role of fibrous structure in generating epicardial potential maps. This model represents the myocardium as an anisotropic bidomain with an equal anisotropy ratio, and it incorporates a realistic representation of anatomical features, including epi-endocardial fiber rotation in the compact portion of the wall (compacta) and a distinct fiber arrangement of the trabeculated portion (trabeculata). Activation sequences were elicited at various intramural depths, and maps were calculated throughout a 60 ms sequence. The simulated maps closely resembled those measured by others in the canine heart. During the early stages of activation, a typical map featuring a central minimum flanked by two maxima emerged, with the axis joining these extrema approximately parallel to the fibers near the pacing site, and the axis joining the maxima rotated in the same direction as the fibers for different pacing depths; for endocardial and subendocardial pacing this map changed into one with an oblong positive area. During the later stages of activation, the positive areas of the maps expanded and rotated with the transmural fiber rotation. In concurrence with experiments, we saw a fragmentation and asymmetry of expanding and rotating positive areas. The latter features-apparently caused by the interface between the compacta and trabeculata, variable local thickness of the wall, or local undulations of the vetricular surface-could not be reproduced by more idealized, slab models.

Antidepressant drugs and heart electrical field.

Some antidepressant drugs, especially tricyclic ones--(TCA), have cardiovascular side effects. To compare the effects of antidepressant drugs, the electrocardiogram (ECG), vectorcardiogram (VCG), and body surface maps (BSM) were recorded in psychiatric patients without cardiovascular diseases treated by a) TCA amitriptyline or dosulepin (daily dose 50-200 mg, 22 patients), b) lithium (serum level 0.66 +/- 0.08 meq/l, 21 patients), c) selective serotonine reuptake inhibitor citalopram (daily doses 20-60 mg, 30 patients), and in 23 control patients. In the TCA-treated patients, the heart rate was increased, QT and RR intervals shortened (p < 0.01, antimuscarinic effect). This was not observed in lithium- and citalopram-treated patients. All antidepressants decreased the absolute maximum values of depolarization isointegral maps, lithium and TCA reduced the initial and citalopram the later phase of depolarization. Citalopram slightly diminished the amplitude of the R wave. The results confirm the antimuscarinic effects of TCA in therapeutic doses and specify the intraventricular effects of antidepressants.

Accuracy of single-dipole inverse solution when localising ventricular pre-excitation sites: simulation study.

Different factors are investigated that may affect the accuracy of an inverse solution that uses a single-dipole equivalent generator, in a standardised inhomogeneous torso model, when localising the pre-excitation sites. An anatomical model of the human ventricular myocardium is used to simulate body surface potential maps (BSPMs) and magnetic field maps (MFMs) for 35 pre-excitation sites positioned on the epicardial surface along the atrioventricular ring. The sites of pre-excitation activity are estimated by the single-dipole method, and the measure for the accuracy of the localisation is the localisation error, defined as the distance between the location of the best-fitting single dipole and the actual site of pre-excitation in the ventricular model. The findings indicate that, when the electrical properties of the volume conductor and lead positions are precisely known and the 'measurement' noise is added to the simulated BSPMs and MFMs, the single-dipole method optimally localises the pre-excitation activity 20 ms after the onset of pre-excitation, within 0.71 +/- 0.28 cm and 0.65 +/- 0.30 cm using BSPMs and MFMs, respectively. When the standard torso model is used to localise the sites of onset of the pre-excitation sequence initiated in four individualised torso models, the maximum errors are as high as 2.6-3.0 cm (even though the average error, for both the BSPM and MFM localisations, remains within the 1.0-1.5 cm range). In spite of these shortcomings, it is thought that single-dipole localisations can be useful for non-invasive pre-interventional planning.

Spatial resolution of body surface potential maps and magnetic field maps: a simulation study applied to the identification of ventricular pre-excitation sites.

The spatial resolution of body surface potential maps (BSPMs) and magnetic field maps (MFMs) is investigated by means of an anatomically accurate computer model of the human ventricular myocardium. BSPMs and MFMs are calculated for the simulated activation sequences initiated at 35 pre-excitation sites located along the atrioventricular (AV) ring of the epicardium. Changes in the BSPMs and MFMs corresponding to different pre-excitation sites are quantified in terms of the correlation coefficient r. The spatial resolution (selectivity) for a given pre-excitation site is defined as the half-distance between those neighbouring locations at which morphological features of maps, in terms of r, become distinct (r < 0.95). It is found that, at 28 ms after the onset of pre-excitation and with no noise added, this distance +/- SD, for all sites along the AV ring for the 117-lead BSPMs, is 0.83 +/- 0.32 cm, and for the 64-lead and 128-lead MFMs it is 1.54 +/- 0.84 cm and 1.15 +/- 0.43 cm, respectively. The findings suggest that, when features of non-invasively recorded electrocardiographic and magnetocardiographic map patterns are used for identifying accessory pathways in patients suffering from WPW syndrome, BSPMs are likely to provide more detailed information for guiding the ablative treatment than MFMs. For some sites MFMs provide more information. Both modalities may provide additional assistance to the cardiologist in locating the site of the accessory pathway.

Value of simulated body surface potential maps as templates in localizing sites of ectopic activation for radiofrequency ablation.

Body surface potential maps recorded during catheter pace mapping can facilitate the localization of the site of origin of ventricular tachycardia. In this study, we investigated the value of a realistic computer model of the human ventricular myocardium in generating body surface potential maps as templates for identifying sites of ectopic activation. Our model features an anatomically accurate geometry and an anisotropy due to transmural fibre rotation, that were reconstructed with a spatial resolution of 0.5 mm. It simulates the electrotonic interactions of cardiac cells by solving a nonlinear parabolic partial differential equation, but it behaves as a cellular automaton when the transmembrane potential exceeds the threshold value. We successfully validated our model by comparing the simulated activation sequences--described by isochronal maps, epicardial potential maps and body surface potential maps--with the measured sequences of epicardial and body surface maps reported in the literature. By systematically pacing the left ventricular and right ventricular endocardial surfaces in our ventricular model, we generated a database of 155 QRS-integral maps, which provides a high-resolution reference frame for localizing distinct endocardial pacing sites. This database promises to be a useful tool in improving the performance of catheter pace mapping used in combination with body surface potential mapping. Overall, the results demonstrate that our computer model of the human ventricular myocardium is well suited for complementing a database of QRS-integral maps obtained during clinical pace mapping and can help enhance the efficacy of the ablative treatment of ventricular arrhythmias.

The inverse problem of electrocardiography: a solution in terms of single- and double-layer sources of the epicardial surface.

An approach to the inverse problem of electrocardiography that involves an estimation of the electric potentials (double-layer equivalent sources) on the heart's epicardial surface from the electrocardiographic potentials that are measurable on the body surface has received considerable attention. This report deals with a heretofore unexplored extension of this approach, one that yields, in addition to the electric potentials on the epicardial surface, the normal components of their gradients (single-layer equivalent sources). We show that this formulation has at least three advantages over the formulation in term of epicardial potentials alone: (1) single-layer equivalent sources, which reflect the flow of current across the epicardial surface, are well suited for the imaging of regional ischemia and infarction; (2) the transfer matrix linking the epicardial and body-surface potentials for this formulation is less ill conditioned than that for the formulation in terms of potentials alone; (3) the input vector for inverse calculations consists of spatially filtered (rather that directly measured and therefore noise) body-surface potentials. To establish the feasibility of this new formulation of the inverse problem and to compare it with the formulation in terms of potentials alone, we used a realistically shaped boundary-element model of human torso. By calculating singular values less ill conditioned. We then directly calculated epicardial and body-surface potentials for a single dipole located centrally and for three simultaneously active dipoles located eccentrically in the torso's heart region and used these results to test three methods that are prerequisites of a successful inverse solution: Tikhonov regularization, linearly constrained least squares, and an L-curve method. The feasibility of the new formulation was demonstrated by the fact that the method based on the linearly constrained least squares improved on overregularized Tikhonov solutions over a wide range of regularization parameters, and it yielded solutions that were more accurate than the best-possible Tikhonov solutions. Moreover, the L-curve solution procedure, which requires no a priori information about the solution, yielded slightly underregularized, but accurate, estimates for the optimal regularization parameter and the corresponding best-possible Tikhonov solution. Our results also showed that replacing--in the interest computational economy--quadrature formulas for the planar triangles with various approximate formulas for the nodes of the model reduces the accuracy of the inverse solution.

Spatial features in body-surface potential maps can identify patients with a history of sustained ventricular tachycardia.

BACKGROUND: Regional disparities of ventricular primary-repolarization properties contribute to an electrophysiological substrate for arrhythmias. Such disparities can be assessed from body-surface distributions of ECG QRST areas. Our objective was to isolate and test those features of QRST-area distributions that would be suitable for identifying patients at risk for life-threatening ventricular arrhythmias. METHODS AND RESULTS: We recorded ECGs simultaneously from 120 leads during sinus rhythm for 204 patients taking no antiarrhythmic drugs: half had had sustained ventricular tachycardia (VT); the other half, a myocardial infarction but no history of VT. For each patient, we calculated the QRST area in each lead and, using Karhunen-Loeve (K-L) expansion, reduced these data to 16 coefficients (each relating to one spatial feature, an eigenvector, derived from the total set of 204 QRST-area maps). Using stepwise discriminant analysis, we selected feature subsets that best discriminated between the two groups, and we estimated by a bootstrap procedure using 1000 trials how these subsets would perform on a prospective patient population. The mean diagnostic performance of the classifier for 1000 randomly selected training sets (n = 102 in each, with both groups equally represented) increased monotonically with the number of features used for classification. The initial trend for the corresponding test sets (n = 102 in each) was the same but reversed when the number of features exceeded eight. For an optimal set of eight spatial features, the sensitivity and specificity of the classifier for detecting patients with VT in 1000 test sets were (mean +/- SD) 90.3 +/- 4.3% and 78.0 +/- 6.1%, and its positive and negative predictive accuracies were 80.7 +/- 4.2% and 89.2 +/- 4.2%, respectively. Use of QRS duration as a supplementary feature to eight K-L coefficients can, in the test sets, increase specificity to 80.9 +/- 5.4% and positive predictive accuracy to 82.8 +/- 3.9% compared with the results for the optimal number of eight K-L features alone. CONCLUSIONS: Multiple body-surface ECGs contain valuable spatial features that can identify the presence of an arrhythmogenic substrate in the myocardium of patients at risk for ventricular arrhythmias. Our results compare very favorably with those achieved by any other known test, invasive or noninvasive, for arrhythmogenicity.

Application of an electrocardiographic inverse solution to localize ischemia during coronary angioplasty.

Localization of Ischemia. This study demonstrates the utility of an electrocardiographic inverse solution, coupled with body surface potential mapping (BSPM), in localizing acute ischemia in patients undergoing percutaneous transluminal coronary angioplasty (PTCA). PTCA balloon inflations produce complete occlusion and acute transient ischemia, which can be detected electrocardiographically with BSPM. Comparisons between maps recorded both during and before the inflation of the PTCA balloon allow patient- and artery-specific characterizations of the resulting ischemia. Knowledge of the patient's coronary anatomy and the location of the occlusion site by coronary angiography permit an estimation based on cardiac hemodynamics of the region of myocardium most likely to suffer from PTCA-induced ischemia. Electrocardiographic inverse solutions provide a means of predicting cardiac potentials from body surface maps. In this study, we describe an inverse solution we have developed to localize the transient ischemia produced by PTCA. To validate the procedure, we compared the locations of predicted ischemia in seven patients with a qualitative estimate of the perfusion region based on fluoroscopic examination of each patient's coronary anatomy and PTCA balloon location. In each case, the region of ischemia predicted by the model included the perfusion zone determined fluoroscopically. These results suggest that electrical changes induced by acute ischemia can be localized with an electrocardiographic inverse solution.

The effects of unilateral stellate ganglion blockade on human cardiac function during rest and exercise.

INTRODUCTION: Left-sided stellate ganglion predominance has been proposed as a mechanism responsible for lethal ventricular arrhythmias, due to heterogenous ventricular repolarization. To determine the cardiovascular effects of such asymmetric sympathetic ganglion innervation in man, studies were performed in 15 patients undergoing unilateral stellate ganglion blockade for the management of chronic arm pain. METHODS AND RESULTS: Standard 12-lead ECGs, systemic blood pressure, body surface potential mapping, and radionuclide angiography were performed during rest and graded exercise before and after blockade. Successful unilateral blockade was accomplished in 13 of the patients, 11 of whom had right-sided blockade and two left-sided blockade. No significant changes due to blockade of stellate ganglia, including QT intervals, were detected during rest or graded exercise in standard ECGs. No cardiac rhythm disturbances occurred in these states. Body surface potential maps and arterial blood pressure were similar during resting supine and upright positions, as well as immediately after exercise before and after blockade. Unilateral ganglionic blockade did not modify resting or exercise cardiac ejection fractions. CONCLUSION: Unilateral stellate blockade in man does not induce untoward cardiovascular effects during rest or exercise.

Electrocardiographic body surface mapping in patients with ventricular tachycardia. Assessment of utility in the identification of effective pharmacological therapy.

BACKGROUND: Body surface maps of net QRST deflection areas (isointegrals) reflect regional ventricular repolarization properties. Vulnerability to ventricular tachyarrhythmias is associated with maps that feature multiple islands (extrema) of positive and negative values; such maps reflect regional disparity of ventricular recovery properties. The value of body surface mapping in prediction of the efficacy of antiarrhythmic therapy for ventricular tachyarrhythmias has not been determined. METHODS AND RESULTS: Isointegral ECG body surface mapping was performed in 51 patients with inducible ventricular tachycardia having programmed stimulation studies at baseline and after oral quinidine therapy. The degree of nondipolarity of QRST isointegral distribution was expressed by the number of extrema and by the percentage contribution of nondipolar eigenvectors after Karhunen-Loeve transformation. QRST isointegral nondipolarity was greater in ventricular tachycardia patients than in 51 age- and sex-matched normal subjects expressed as mean number of extrema (4.1 +/- 2.8 versus 2.0 +/- 0.2, respectively), mean eigenvector-determined nondipolar content percentages (12.4 +/- 10.1% versus 4.5 +/- 4.9%), prevalence of abnormal numbers of extrema (63% versus 4%), or prevalence of abnormal nondipolar content percentages (33% versus 4%) (each p less than 0.01). Quinidine prevented ventricular tachycardia induction in 14 patients. Patients for whom quinidine was or was not effective had similar nondipolarity indexes at baseline. However, maps on quinidine differed as a function of antiarrhythmic efficacy. Although effective therapy produced no significant mean changes in nondipolarity, ineffective therapy increased the number of extrema compared with baseline (5.4 +/- 3.4 versus 3.8 +/- 2.5, respectively) (p = 0.002). Individually, 43% of patients on effective therapy had drug-induced decreases in numbers of extrema compared with 14% of those on ineffective therapy (p = 0.02). Furthermore, 29% of patients on effective therapy showed drug-induced increases in numbers of extrema compared with 62% of those on ineffective therapy (p = 0.03). CONCLUSIONS: QRST isointegral body surface mapping shows promise as a noninvasive measure of drug efficacy in patients with ventricular tachycardia.

Magnetocardiographic functional localization using a current dipole in a realistic torso.

We describe a fast and numerically effective biomagnetic inverse solution using a moving dipole in a realistic homogeneous torso. We applied the localization model and high-resolution magnetocardiographic mapping to localize noninvasively the ventricular preexcitation site in ten patients suffering from Wolff-Parkinson-White syndrome. In all cases, the computed localization results were compared to the results obtained by invasive catheter technique. Using a standard-size torso model in all cases, the average 3-D distance between the computed noninvasive locations and the invasively obtained results was 2.8 +/- 1.4 cm. When the torso was rescaled to better match the true shape of the subject in five cases, the 3-D average was improved to 2.2 +/- 1.0 cm. This accuracy is very satisfactory, suggesting that the method would be clinically useful.

Computer model of excitation and recovery in the anisotropic myocardium. I. Rectangular and cubic arrays of excitable elements.

A computer model of propagated excitation and recovery in anisotropic cardiac tissue is presented that consists of a large number of excitable elements whose subthreshold interactions are governed by the anisotropic bidomain theory but whose suprathreshold behavior (action potential) is largely preassigned. The model's performance was first tested in a two-dimensional configuration with uniform anisotropy; this method allowed comparison of simulated isochrones of excitation and extracellular electrograms with the results of experimental in vitro studies of cardiac tissue. Next the model was used to study propagated excitation in a three-dimensional region representing the anisotropic properties of the ventricular wall, with attention to the effects produced by variable fiber direction from "endocardium" to "epicardium."

Computer model of excitation and recovery in the anisotropic myocardium. II. Excitation in the simplified left ventricle.

A computer model of propagated excitation and recovery in anisotropic cardiac tissue was described in the first report of this series. The model consists of a large number of excitable elements whose subthreshold interactions are governed by the anisotropic bidomain theory but whose suprathreshold behavior (action potential) is largely preassigned. As described in the first report, the model's performance was tested in rectangular and cubic arrays of excitable elements. This second report deals with three-dimensional simulations in a simplified left ventricle with anisotropy; specifically, the activation process in the "normal" ventricle is described (exemplified by the activation sequences started from various endocardial, intramural, and epicardial sites). To further substantiate our model's validity, we compare simulated epicardial and body-surface potential distributions with experimental findings in isolated canine hearts and with clinical evidence provided by electrocardiographic body-surface mapping.

Computer model of excitation and recovery in the anisotropic myocardium. III. Arrhythmogenic conditions in the simplified left ventricle.

A computer model of propagated excitation and recovery in anisotropic cardiac tissue has been described in the first two reports of this series. The model consists of a large number of excitable elements whose subthreshold interactions are governed by the anisotropic bidomain theory but whose suprathreshold behavior (action potential) is largely preassigned. As described in the previous two reports, the model's performance was tested in rectangular and cubic arrays of excitable elements and in the "normal" three-dimensional simplified left ventricle with anisotropy. The present report deals with arrhythmogenic conditions in the simplified left ventricle with anisotropy and ventricular-gradient properties; specifically, we studied activation and recovery in the presence of an ischemic region and under various stimulation protocols. The aim of these simulations was to elucidate the role of reentry in the genesis of ventricular tachycardia. Our simulations produced reentrant activation as a result of appropriate endocardial stimulation.