Bruno Taccardi

Noninvasive Electrocardiographic Imaging Reconstruction of Epicardial Potentials, Electrograms, and Isochrones and Localization of Single and Multiple Electrocardiac Events

BACKGROUND The goal of noninvasive electrocardiographic imaging (ECGI) is to determine electric activity of the heart by reconstructing maps of epicardial potentials, excitation times (isochrones), and electrograms from data measured on the body surface. METHODS AND RESULTS Local electrocardiac events were initiated by pacing a dog heart in a human torso-shaped tank. Body surface potential measurements (384 electrodes) were used to compute epicardial potentials noninvasively. The accuracy of reconstructed epicardial potentials was evaluated by direct comparison to measured ones (134 electrodes). Protocols included pacing from single sites and simultaneously from two sites with various intersite distances. Body surface potentials showed a single minimum for both single- and double-site pacing (intersite distances of 52, 35, and 17 mm). Noninvasively reconstructed epicardial electrograms, potentials, and isochrones closely approximated the measured ones. Single pacing sites were reconstructed to within < or = 10 mm of their measured positions. Dual sites were located accurately and resolved for the above intersite distances. Regions of sparse and crowded isochrones, indicating spatial nonuniformities of epicardial activation spread, were also reconstructed. CONCLUSIONS The study demonstrates that ECGI can reconstruct epicardial potentials, electrograms, and isochrones over the entire epicardial surface during the cardiac cycle. It can provide detailed information on local activation of the heart noninvasively. Its uses could include localization of cardiac electric events (eg, ectopic foci), characterization of nonuniformities of conduction, characterization of repolarization properties (eg, dispersion), and mapping of dynamically changing arrhythmias (eg, polymorphic VT) on a beat-by-beat basis.

Effect of myocardial fiber direction on epicardial potentials.

BackgroundUnderstanding the relations between the architecture of myocardial fibers, the spread of excitation, and the associated ECG signals is necessary for addressing the forward problem of electrocardiography, that is, predicting intracardiac and extracardiac ECGs from known intracardiac activity. So far, these relations have been studied experimentally only in small myocardial areas. In this study, we tested the hypothesis that potential distributions measured over extensive epicardial regions during paced beats reflect the direction of superficial and intramural fibers through which excitation is spreading in both the initial and later stages of ventricular excitation. We also tried to establish whether the features of the epicardial potential distribution that correlate with fiber direction vary as a function of pacing site, intramural pacing depth, and time elapsed after the stimulus. An additional purpose was to compare measured epicardial potentials with recently published numerical simulations depicting the three-dimensional spread of excitation in the heart muscle and the associated potential fields. Methods and ResultsThe hearts of 18 mongrel dogs were exposed and 182 to 744 unipolar electrograms were recorded from epicardial electrode arrays (2.3 × 3.0 to 6.5 × 6.5 cm). Hearts were paced at various intramural depths through an intramural needle. The overall number of pacing sites in 18 dogs was 241. Epicardial potential distributions, electrographic waveforms, and excitation time maps were displayed, and fiber directions in the ventricular wall underlying the electrodes were determined histologically. During the early stages of ventricular excitation, the position of the epicardial maxima and minima revealed the orientation of myocardial fibers near the pacing site in all cases of epicardial and intramural pacing and in 60% of cases of endocardial or subendocardial pacing. During later stages of propagation, the rotation and expansion of the positive areas correlated with the helical spread of excitation through intramurally rotating fibers. Marked asymmetry of potential patterns probably reflected epicardial-endocardial obliqueness of intramural fibers. Multiple maxima appeared in the expanding positive areas. ConclusionsFor 93% of pacing sites, results verified our hypothesis that epicardial potential patterns elicited by ventricular pacing reflect the direction of fibers through which excitation is spreading during both the initial and later stages of propagation. Epicardial potential distributions provided information on the site of origin and subsequent helical spread of excitation in an epicardial-endocardial, endocardial-epicardial, or double direction. Results were in agreement with previously published numerical simulations except for the asymmetry and fragmentation of the positive areas.

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.

Potential fields on the ventricular surface of the exposed dog heart during normal excitation.

We studied the normal spread of excitation on the anterior and posterior ventricular surface of open-chest dogs by recording unipolar electrograms from an array of 1124 electrodes spaced 2 mm apart. The array had the shape of the ventricular surface of the heart. The electrograms were processed by a computer and displayed as epicardial equipotential maps at 1-msec intervals. Isochrone maps also were drawn. Several new features of epicardial potential fields were identified: (1) a high number of breakthrough points; (2) the topography, apparent widths, velocities of the wavefronts and the related potential drop; (3) the topography of positive potential peaks in relation to the wavefronts. Fifteen to 24 breakthrough points were located on the anterior, and 10 to 13 on the posterior ventricular surface. Some were in previously described locations and many others in new locations. Specifically, 3 to 5 breakthrough points appeared close to the atrioventricular groove on the anterior right ventricle and 2 to 4 on the posterior heart aspect; these basal breakthrough points appeared when a large portion of ventricular surface was still unexcited. Due to the presence of numerous breakthrough points on the anterior and posterior aspect of the heart which had not previously been described, the spread of excitation on the ventricular surface was “mosaic-like,” with activation wavefronts spreading in all directions, rather than radially from the two breakthrough points, as traditionally described. The positive potential peaks which lay ahead of the expanding wavefronts moved along preferential directions which were probably related to the myocardial fiber direction.

A Noninvasive Imaging Modality for Cardiac Arrhythmias

BackgroundThe last decade witnessed an explosion of information regarding the genetic, molecular, and mechanistic basis of heart disease. Translating this information into clinical practice requires the development of novel functional imaging modalities for diagnosis, localization, and guided intervention. A noninvasive modality for imaging cardiac arrhythmias is not yet available. Present electrocardiographic methods cannot precisely localize a ventricular tachycardia (VT) or its key reentrant circuit components. Recently, we developed a noninvasive electrocardiographic imaging modality (ECGI) that can reconstruct epicardial electrophysiological information from body surface potentials. Here, we extend its application to image reentrant arrhythmias. Methods and ResultsEpicardial potentials were recorded during VT with a 490 electrode sock during an open chest procedure in 2 dogs with 4-day-old myocardial infarctions. Body surface potentials were generated from these epicardial potentials in a human torso model. Realistic geometry errors and measurement noise were added to the torso data, which were then used to noninvasively reconstruct epicardial isochrones, electrograms, and potentials with excellent accuracy. ECGI reconstructed the reentry pathway and its key components, including (1) the central common pathway, (2) the VT exit site, (3) lines of block, and (4) regions of slow and fast conduction. This allowed for detailed characterization of the reentrant circuit morphology. ConclusionsECGI can noninvasively image arrhythmic activation on the epicardium during VT to identify and localize key components of the arrhythmogenic pathway that can be effective targets for antiarrhythmic intervention.

Potential fields generated by oblique dipole layers modeling excitation wavefronts in the anisotropic myocardium. Comparison with potential fields elicited by paced dog hearts in a volume conductor.

The potential distribution in a homogeneous, cylindrical volume conductor surrounding an isolated paced dog heart was first measured and then calculated by using a mathematical model that simulates an anisotropic excitation wavefront spreading through the heart muscle. The study was performed with a view to establish to what extent the anisotropy of cardiac generators affects the potential field in the extra-cardiac conducting media at a great distance from the heart. The model considers an oblique dipole layer on the wavefront which, assuming axial symmetry of the electrical properties of the fibers, can be viewed as the superposition of an axial and a transverse dipole layer. These layers are, respectively, parallel and perpendicular to the local fiber direction. A notable feature of the model is that, in the case of axial symmetry, the potential field due to such an oblique distribution is also equivalent to the sum of the potentials generated, respectively, by a normal and an axial dipole layer. In this form, the model generalizes the classical, uniform double layer model, upon which the solid angle theory is based, by adding to it an axial component. The features of the measured potential fields, which could not be interpreted on the basis of the solid angle theory, were satisfactorily reproduced by the model, at least on a qualitative basis. The results clearly showed the dominant role played by the axial component of the potential field even at a considerable distance from the heart.

Body-surface maps of heart potentials: tentative localization of pre-excited areas in forty-two Wolff-Parkinson-White patients.

SUMMARY Heart potentials were recorded from the entire chest surface in 42 patients suffering from Wolff-Parkinson-White syndrome. We were able to identify six types of surface maps, according to the location of the potential maximum and minimum during the delta wave. For each of these types we suggested the most likely location of the pre-excited region around the A-V rings (types 1 to 5) or in the interventricular septum (type 6). In 13 patients belonging to Types 1, 2, 3, 5 and 6 our hypotheses were in agreement with intracardiac recordings, epicardial maps or surgical results obtained by others. Isopotential surface maps provide more information on the location of the pre-excited area than conventional ECGs, particularly when these exhibit intermediate features between Types A and B.

Noninvasive ECG Imaging of Electrophysiologically Abnormal Substrates in Infarcted Hearts A Model Study

BACKGROUND Myocardial infarction and subsequent remodeling create substrates with altered electrophysiological (EP) properties that are highly arrhythmogenic. Existing ECG methods cannot always detect the existence of such substrates nor provide any detailed information about their EP characteristics. A noninvasive method with such capabilities is greatly needed for identifying patients at risk of arrhythmias and for guidance and evaluation of therapy. Recently, we developed a noninvasive ECG imaging modality that can reconstruct epicardial EP information from body surface potentials. We extended its application to hearts with structural disease and examined its ability to detect and characterize abnormal EP substrates. METHODS AND RESULTS Epicardial potentials were recorded with a 490-electrode sock from an open-chest dog. Recordings were obtained from a normal heart and from the same heart 2 hours after left anterior descending coronary artery occlusion and ethanol injection to create an infarct. Body surface potentials were generated from these epicardial potentials in a human torso model. Realistic geometry errors and measurement noise were added to the torso data, which were then used to noninvasively reconstruct epicardial potentials and electrograms (EGMs), with excellent accuracy. EP characteristics associated with the infarct substrate were reconstructed, including (1) a negative region over the infarct, (2) EGMs with large predominant negative deflections (eg, Q-wave EGMs), (3) Q-wave EGMs with superimposed RS deflections reflecting local activation of surviving myocardium within the infarct border zone, (4) reduced magnitudes of EGM negative derivatives, and (5) negative QRS integrals of EGMs over the infarct. CONCLUSIONS ECG imaging can noninvasively detect and map abnormal EP substrates associated with infarction and structural heart disease.

Noninvasive electrocardiogram imaging of substrate and intramural ventricular tachycardia in infarcted hearts.

OBJECTIVES The goal of this study was to experimentally evaluate a novel noninvasive electrocardiographic imaging modality during intramural reentrant ventricular tachycardia (VT). BACKGROUND Myocardial infarction and subsequent remodeling produce abnormal electrophysiologic substrates capable of initiating and maintaining reentrant arrhythmias. Existing noninvasive electrocardiographic methods cannot characterize abnormal electrophysiologic substrates in the heart or the details of associated arrhythmias. A noninvasive method with such capabilities is needed to identify patients at risk of arrhythmias and to guide and evaluate therapy. METHODS A dog heart with a four-day-old infarction was suspended in a human shaped torso-tank. Measured body surface potentials were used to noninvasively compute epicardial potentials, electrograms and isochrones. Accuracy of reconstruction was evaluated by direct comparison to measured data. Reconstructions were performed during right atrial pacing and nine cycles of VT. RESULTS Noninvasively reconstructed potential maps, electrograms and isochrones identified: 1) the location of electrophysiologically abnormal infarct substrate; 2) the epicardial activation sequences during the VTs; 3) the locations of epicardial breakthrough sites; and 4) electrophysiologic evidence for activation of the Purkinje system and septum during the reentrant beats. CONCLUSIONS Electrocardiographic imaging can noninvasively reconstruct electrophysiologic information on the epicardium during VT with intramural reentry, provide information about the location of the intramural components of reentry and image abnormal electrophysiologic substrates associated with infarction.

QT interval dispersion: dispersion of ventricular repolarization or dispersion of QT interval?

The QT interval (QTI) has long been useful as a clinical index of the duration of ventricular repolarization, particularly as a marker of prolonged repolarization and its well-established association with arrhythmogenic cardiac states. Likewise, inhomogeneity (dispersion) of repolarization has been linked definitively to increased susceptibility to reentrant arrhythmias. Recent studies have reported the use of QTI dispersion as a meaningful clinical index to identify patients at risk, but the interpretation of the measurement has been controversial. A Langendorff-perfused, isolated canine heart suspended in a torso-shaped, electrolytic tank filled with NaCl-sucrose solution was used to investigate the relationship between body surface QTIs and ventricular repolarization measured directly from the cardiac surface by using activation-recovery intervals, which have been documented to reflect the duration of local action potentials as well as local refractory periods. The data showed poor correlation between cardiac surface activation-recovery intervals and QTIs, as well as the insensitivity of QTIs to regional repolarization shortening in the presence of prolonged repolarization elsewhere. Furthermore, the data confirmed that torso tank QTI dispersion does not reflect directly the full range of measured ventricular repolarization inhomogeneity. It is concluded that body surface QTI dispersion is not a reliable index of repolarization dispersion.