Most episodes of sudden cardiac death are due to ventricular tachycardia/fibrillation. Advances in clinical electrophysiology through the use of programmed stimulation and activation mapping have allowed for the development of effective pharmacologic therapy and identification of the area of origin of ventricular tachycardia (VT). Despite these advances, a significant number of VT do not respond to drugs and must be treated surgically. We have developed the method of subendocardial resection guided by activation mapping to treat VT. However, limitations of this and other procedures need resolution. We therefore propose to use programmed stimulation and intraoperative mapping techniques and analysis of tissue from patients with and without VT to more adequately define the electrophysiologic-anatomic derangements responsible for VT and develop surgical procedures to localize and treat these arrhythmias without the procedures themselves being arrhythmogenic.
The specific aims of these proposed studies are: 1) To evaluate the significance of multicomponent electrograms in identifying the assumed reentrant pathways operative during VT. The role of cryothermal mapping in evaluating the significance of these multicomponent electrograms can be established. 2) To assess the potential of intraoperative endocardial and intramural mapping during sinus rhythm to localize sites of early activation during VT which can be used to guide surgery without the requirement of initiation and mapping of each morphologic form of tachycardia. 3) To assess the role of pace-mapping as a guide to surgical intervention of VT when direct mapping of the arrhythmia is not possible. 4) To assess the electrophysiologic substrate arrhythmogenic potential and pathology of ventricular aneurysms in patients without arrhythmias, and compare these findings to those in patients with arrhythmias to determine whether a specific electrophysiologic-anatomic substrate is required for the presence of VT. 5) To develop methods to ascertain the success of surgical interventions by either programmed stimulation or noninvasive techniques. 6) To assess the effects of chronic ischemia and its reversal by coronary artery bypass surgery on temporal dispersion of activation and refractoriness.
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