The 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.
Epicardial 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.
ECGI 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.
Epicardial potentials reveal the strong effects of fiber anisotropy, rotation, imbrication, and coupling on propagation in the intact heart. From the patterns of the surface potentials, we can obtain ...information about the local fiber orientation, anisotropy, the transmural fiber rotation, and which direction the wave front is traveling through the wall. In this study, lessons learned from epicardial potential mapping of large hearts were applied to studies conducted in genetically altered mouse hearts.
An inducible model of the overexpression of a gain-of-function
α5 integrin (cytoplasmic domain truncation) was created in mouse. After 3 days of administration of doxycycline, the animals exhibited an altered electrical phenotype of markedly reduced amplitude of the QRS complex on the surface electrocardiogram. Epicardial potentials were recorded from Langendorff-perfused mouse hearts with
α5 integrin gain-of-function mutations and from wild-type (WT) control hearts. A cylindrical electrode array consisting of 184 sites with 1-mm uniform interelectrode spacing was placed around the heart, and unipolar electrograms were recorded during atrial and ventricular stimulation at different basic cycle lengths.
The total ventricular activation time for the transgenic animals was greater than that of the WT hearts for atrial and ventricular pacing locations. The isopotential maps from the mutated hearts showed a loss of anisotropy, as revealed by the more rounded and less elliptically shaped wave fronts seen immediately after epicardial point stimulation when compared with WT hearts. The weaker potential maxima in the mutated hearts did not exhibit the normal expansion and rotation associated with an advancing wave front in a normal heart, suggesting abnormalities in myocyte coupling in these hearts. Isopotential maps provided additional information about fiber architecture from the electric field that was not obtained from optical recordings alone. These findings provided a phenotypic characterization and specific insights into the mechanisms of the electrical abnormalities associated with altered integrin signaling in cardiac myocytes.
There are no published data showing the three-dimensional sequence of repolarization and the associated potential fields in the ventricles. Knowledge of the sequence of repolarization has medical ...relevance because high spatial dispersion of recovery times and action potential durations favors cardiac arrhythmias. In this study we describe measured and simulated 3-D excitation and recovery sequences and activation-recovery intervals (ARIs) (measured) or action potential durations (APDs) (simulated) in the ventricular walls.
We recorded from 600 to 1400 unipolar electrograms from canine ventricular walls during atrial and ventricular pacing at 350-450 ms cycle length. Measured excitation and recovery times and ARIs were displayed as 2-D maps in transmural planes or 3-D maps in the volume explored, using specially developed software. Excitation and recovery sequences and APD distributions were also simulated in parallelepipedal slabs using anisotropic monodomain or bidomain models based on the Lou-Rudy version 1 model with homogeneous membrane properties.
Simulations showed that in the presence of homogeneous membrane properties, the sequence of repolarization was similar but not identical to the excitation sequence. In a transmural plane perpendicular to epicardial fiber direction, both activation and recovery pathways starting from an epicardial pacing site returned toward the epicardium at a few cm distance from the pacing site. However, APDs were not constant, but had a dispersion of ∼14 ms in the simulated domain. The maximum APD value was near the pacing site and two minima appeared along a line perpendicular to fiber directions, passing through the pacing site. Electrical measurements in dog ventricles showed that, for short cycle lengths, both excitation and recovery pathways, starting from an epicardial pacing site, returned toward the epicardium. For slower pacing rates, pathways of recovery departed from the pathway of excitation. Highest ARI values were observed near the pacing site in part of the experiments. In addition, maps of activation-recovery intervals showed mid-myocardial clusters with activation-recovery intervals that were slightly longer than ARIs closer to the epi- or endocardium, suggesting the presence of M cells in those areas. Transmural dispersion of measured ARIs was on the order of 20-25 ms. Potential distributions during recovery were less affected by myocardial anisotropy than were excitation potentials.
Useful Lessons from Body Surface Mapping TACCARDI, BRUNO; PUNSKE, BONNIE B.; LUX, ROBERT L. ...
Journal of cardiovascular electrophysiology,
July 1998, Letnik:
9, Številka:
7
Journal Article
Recenzirano
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 he 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 he 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.
1 Nora Eccles Harrison Cardiovascular Research and Training Institute, 2 Department of Bioengineering; and 3 Scientific Computing Institute, University of Utah, Salt Lake City, Utah; and 4 ...Dipartimento di Biologia Evolutiva e Funzionale, Universita di Parma, Parma, Italy
Submitted 14 December 2007
; accepted in final form 4 February 2008
Published studies show that ventricular pacing in canine hearts produces three distinct patterns of epicardial excitation: elliptical isochrones near an epicardial pacing site, with asymmetric bulges; areas with high propagation velocity, up to 2 or 3 m/s and numerous breakthrough sites; and lower velocity areas (<1 m/s), where excitation moves across the epicardial projection of the septum. With increasing pacing depth, the magnitude of epicardial potential maxima becomes asymmetric. The electrophysiological mechanisms that generate the distinct patterns have not been fully elucidated. In this study, we investigated those mechanisms experimentally. Under pentobarbital anesthesia, epicardial and intramural excitation isochrone and potential maps have been recorded from 22 exposed or isolated dog hearts, by means of epicardial electrode arrays and transmural plunge electrodes. In five experiments, a ventricular cavity was perfused with diluted Lugol solution. The epicardial bulges result from electrotonic attraction from the helically shaped subepicardial portions of the wave front. The high-velocity patterns and the associated multiple breakthroughs are due to involvement of the Purkinje network. The low velocity at the septum crossing is due to the missing Purkinje involvement in that area. The asymmetric magnitude of the epicardial potential maxima and the shift of the breakthrough sites provoked by deep stimulation are a consequence of the epi-endocardial obliqueness of the intramural fibers. These results improve our understanding of intramural and epicardial propagation during premature ventricular contractions and paced beats. This can be useful for interpreting epicardial maps recorded at surgery or inversely computed from body surface ECGs.
propagation patterns; excitation mapping
Address for reprint requests and other correspondence: B. B. Punske, Univ. of Utah, Nora Eccles Harrison CVRTI, 95 South 2000 East, Salt Lake City, Utah 84112-5000 (e-mail: punske{at}cvrti.utah.edu )
The goal of this study was to experimentally evaluate a novel noninvasive electrocardiographic imaging modality during intramural reentrant ventricular tachycardia (VT).
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.
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.
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.
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.
Spatial Distribution of the QT Interval. 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.
Despite the widespread use of electrocardiogram (ECG), changes in cardiac activity resulting from ischemia or altered recovery characteristics sometimes remain electrocardiographically “silent” or ...are first detectable by techniques that measure ventricular contractility, such as ultrasound or blood pressure. Especially
local changes in repolarization can go undetected when ECG electrodes do not lie close to the area of the heart affected. Experiments were performed on an isolated, perfused canine heart suspended in a realistically shaped, instrumented, electrolytic torso tank with the goal of determining some mechanisms for these ambiguities. By recording simultaneously both epicardial and torso tank surface potentials, complete descriptions were obtained of the electrical response to interventions such as coronary occlusions and alterations in pacing site and frequency. One hypothesis was that some interventions produce highly variable ECG responses primarily because of differences in their location within the heart. To test this, the effect was measured of repeating the same intervention as the heart's location and orientation in the tank were varied. A numerical forward solution was also used to investigate variation of torso tank potentials with heart location. The resulting changes in tank surface potentials illustrate how, for example, precordial ST-segment shifts following occlusion change from elevation to depression to become almost undetectable as the heart rotates in the tank. The results suggest that some events are electrocardiographically silent because of the complex geometric relationship of the heart, torso, and site of the lesion, as well as the spatial sampling and analysis techniques used in detection.
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