Reconstruction of endocardial potentials and activation sequences from intracavitary probe measurements. Localization of pacing sites and effects of myocardial structure.

BACKGROUND: Mapping of endocardial activation is an important procedure for diagnosing cardiac arrhythmias and locating the arrhythmogenic site before treatment. The objective of the present study was to develop and test a mathematical method to reconstruct the endocardial potentials and activation sequences (isochrones) from potential data measured with a noncontact, intracavitary multielectrode probe (the "inverse problem"). METHODS AND
RESULTS: A boundary element based mathematical method, combined with a numeric regularization technique, was developed for computing the inverse solution. Endocardial potentials were computed from intracavitary potentials measured with a multielectrode probe placed in the cavity of an isolated, perfused canine left ventricle. Data were acquired during rhythms induced by electrical stimuli applied at different locations and varying depths within the myocardium. Endocardial potentials were measured using intramural needles to evaluate the accuracy of the inverse solutions by direct comparison. Inversely computed endocardial potentials, from measured probe potentials, reconstruct with good accuracy the major features (potential maxima and minima, regions of negative and positive potentials) compared with the measured endocardial potentials. During early activation, the computed endocardial potentials exhibit a potential minimum in close proximity to the pacing site, determining the location of the stimulus with good accuracy (within 10-mm error). Multiple stimuli, as close as 10 to 20 mm to each other, can be distinguished and localized to their sites of origin by the inverse reconstruction. Similar to the measured endocardial potentials, the spatial distribution of the computed endocardial potentials reflects the underlying cardiac fiber direction, and dynamic changes of the computed endocardial potentials reflect the rotation of fibers with intramural depth. Maps of isochrones show good correspondence between the isochrones determined from the computed endocardial potentials and those determined directly from the measured endocardial potentials.
CONCLUSIONS: Compared with actual, measured endocardial potentials and activation sequences, endocardial potential patterns and activation sequences can be reconstructed on a beat-by-beat basis from cavitary potentials measured with a multielectrode, noncontact probe. The approach presented here is shown to reconstruct, with 10-mm accuracy and resolution of 10 to 20 mm, local events of cardiac excitation (eg, pacing sites). In addition, the reconstructed endocardial potentials correctly reflect the underlying fibrous structure of the myocardium. These results demonstrate the feasibility of the approach. In the experiments, the probe position and endocardial geometry were determined invasively. To be clinically applicable, the reconstruction method should be combined with a noninvasive method for determining the probe-cavity geometry in the catheterization laboratory. It could then be developed into a catheter-based technique for locating arrhythmogenic sites and for studying and diagnosing conduction abnormalities, reentrant activity, and the effects of drugs and other interventions on cardiac activation and arrhythmias.