title: Prediction of the location and time of spontaneous termination of reentrant ventricular tachycardia for radiofrequency catheter ablation therapy.
abstract: Ventricular tachycardia caused by reentrant excitation can lead to cardiac arrest and sudden death. Drug treatment and surgical procedures have been used with limited effectiveness. Catheter ablation methods are more promising because they are less invasive than surgery. Although ablation has come to be highly effective in the treatment of supraventricular tachycardias, the overall success rate remains low for ventricular tachycardias, which may be due in part to an inaccurate localization of the reentrant pathway. The authors hypothesize that a site in the myocardium exists that is critical for the maintenance or reentry and that when ablated, will result in permanent cessation of the tachycardia. The authors also hypothesize that this is the same site where the reentrant impulse blocks during spontaneous termination of tachycardia. A series of experiments has been designed to determine if there are specific properties of extracellular electrograms recorded from reentrant circuits that would enable the circuits to be identified without activation maps and, more specifically, allow the site of block causing spontaneous termination to be localized. For quantitative analysis of electrograms, a paradigm is developed to characterize electrogram morphology using a canine infarct model. Changes in morphology (shape, size, and location of signal deflections) can be considered (1) motions of a coordinate system and/or (2) conformational changes of shape. To a first approximation, stationarity over short time segments is assumed so that the motions and conformations can be parameterized. These parameters were extracted for 50 cardiac cycles during an episode of nonsustained ventricular tachycardia, in which 196-bipolar electrode pairs were positioned in an array format across the epicardial surface of the heart. The results of these studies of changes in electrogram morphology suggest that during cycles 5 to 49 of ventricular tachycardia, in many electrograms near the circuit, the cycle length increases linearly, the amplitude increases, and the duration of activation decreases. During cycles 50 to 54, the cycle length increases much more markedly, the amplitude decreases, and the duration of activation increases. These observations suggest that cycle lengthening may be an important property of some spontaneous terminations, and moreover that other morphologic characteristics are affected differently at different stages of cycle lengthening. Further, all motion parameters tended to oscillate from cycle to cycle in either an alternans pattern or longer oscillation. The variations in morphology were typically only a few percent from cycle to cycle. Such variability would not be evident using only ruler-and-caliper measurements made by hand because of the lack of precision and the sheer volume of data. It is expected that this approach for characterization of electrogram morphology will be extremely useful clinically to (1) increase speed and accuracy of ablation site selection and (2) reduce multichannel electrogram recording complexity during ablation site selection.
authors.affiliation: Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.
authors.forename: E J
authors.initials: EJ
authors.lastname: Ciaccio
authors.forename: A L
authors.initials: AL
authors.lastname: Wit
authors.forename: M M
authors.initials: MM
authors.lastname: Scheinman
authors.forename: S M
authors.initials: SM
authors.lastname: Dunn
authors.forename: M
authors.initials: M
authors.lastname: Akay
authors.forename: J
authors.initials: J
authors.lastname: Coromilas
mesh_terms: D000465:Algorithms; D000818:Animals; D018780:Body Surface Potential Mapping; D017115:Catheter Ablation; D004285:Dogs; D004562:Electrocardiography / Q000379:methods; D004594:Electrophysiology; D005544:Forecasting; D006329:Heart Conduction System / Q000473:pathology / Q000503:physiopathology; D006339:Heart Rate; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D010496:Pericardium / Q000473:pathology / Q000503:physiopathology; D017180:Tachycardia, Ventricular / Q000473:pathology / Q000503:physiopathology / Q000601:surgery*; D013997:Time Factors; D016276:Ventricular Function