808-1 Focal Mechanisms Underlying Sustained Ventricular Tachycardia in Ischemic Cardiomyopathy

Abstract

To define the mechanism of ventricular tachycardia (VT) induced by programmed electrical stimulation in the setting of congestive heart failure, 3-dimensional cardiac mapping was performed in six dogs with ischemic cardiomyopathy induced by multiple intracoronary embolizations with microspheres. Ejection fraction (EF) progressively decreased from 54 ± 2 to 30 ± 5% (p < 0.005) after an average of 6 weekly embolizations. Four months later (EF = 28 ± 5%), each dog underwent a thoracotomy with insertion of plungeneedle electrodes into the heart under pentobarbital anesthesia. Continuous recording from 232 intramural sites throughout the left and right ventricles and the interventricular septum was performed during spontaneous rhythm and during programmed stimulation in both the absence and presence of isoproterenol (Iso) (0.1 mg/kg/min). Three dogs (1 at baseline, 2 during Iso) developed sustained VT (SuVT) during programmed stimulation with up to 3 extrastimuli. After the last extrastimulus, the first beat of SuVT (T 1 ) initiated in the subendocardium by a focal mechanism, based on the absence of electrical activity from the termination of the last extrastimulus to the initiation of T 1 despite the presence of multiple intermediate electrode sites. Maintenance of SuVT was also due to a focal mechanism arising in the subendocardium, with a total activation time (TAT) of subsequent SuVT beats (99 ± 14 msec, n = 61 that was comparable to that of initiating beats (85 ± 8 msec. n = 6, p = 0.08). There was no evidence of macroreentry. Episodes of SuVT (n = 3) exhibited TATs of the last extrastimulus before SuVT (106 ± 11 msec) and coupling intervals of T1 (196 ± 70 msec) that were comparable to those observed in nonsustained VT (n = 3) (138 ± 26 msec, p = 0.19; 166 ± 26 msec, p = 0.59). Conduction delay during sinus rhythm in dogs with SuVT (TAT 47 ± 5 msec, n = 10) was comparable to that in dogs without SuVT (TAT 47 ± 4 msec, n = 10, p = 0.96) and was unchanged by Iso (TAT 50 ± 4 msec, n = 7, p = 0.40). In the 2 dogs with inducible SuVT on Iso only, TATs of the last extrastimulus (124 ± 22 msec) and of T 1 (110 ± 36 msec) at baseline were unchanged by infusion of Iso (108 ± 13 msec, p = 0.59; 79 ± 1 msec, p = 0.49). Thus, inducible sustained VT in a model of ischemic cardiomyopathy is due to a focal mechanism, as opposed to macroreentry, and this focal mechanism is enhanced by β -adrenergic stimulation.