Catheter or intraoperative activation mapping studies, or both, were performed in 17 patients with coronary artery disease with two to four distinct configurations of ventricular tachycardia, resistant to a mean of 12.1 ± 6.0 antiarrhythmic drug trials per patient. Mapping studies were performed to guide anticipated surgical ablation of arrhythmias. Activation map data were adequate to determine sites of origin of 30 (64%) of 47 observed tachycardia configurations. These 30 ventricular tachycardias (26 observed clinically) were mapped to 22 separate endocardial sites of origin. Sites of origin of distinct tachycardias were identical or closely adjacent (within 3 cm) in six patients and widely separate (≥4 cm) in eight patients (47% of the group). Activation maps were not adequate to determine sites of origin of 17 (36%) of the 47 tachycardias, including all configurations in three patients. Fifteen patients underwent surgery for control of ventricular tachycardia: aggressive, map-guided endocardial resection (mean 26.5 ± 14.2 cm2) in 12 patients with identified sites of tachycardia origin and extensive resection of visible endocardial scar (2 patients) or encircling endocardial ventriculotomy (1 patient) in those in whom the sites of origin of all clinical tachycardias remained undetermined. Two inoperable patients were treated with amiodarone. During postoperative electrophysiologic tests (11 of 13 surgical survivors), ventricular tachyarrhythmias were initially uninducible in only 4 of 11 patients. However, in two patients only nonclinical arrhythmias (ventricular flutter) were induced. Six (21%) of 29 clinical tachycardias whose sites of origin were either not determined or not resected (right septum or papillary muscle) remained inducible in five patients. Using previously ineffective antiarrhythmic drugs, initially inducible arrhythmias became uninducible (two patients), or harder to induce than preoperatively (five patients). As a result of surgical resections alone or in combination with previously ineffective drugs (and amiodarone in two inoperable patients), there were no recurrences of ventricular tachycardia in 14 (93%) of 15 patients discharged during 19.0 ± 14.3 months of follow-up study. Thus, activation mapping may commonly reveal separate apparent sites of origin for clinically observed, morphologically distinct, highly drug-refractory ventricular tachycardias in patients with coronary artery disease with multiple tachycardia configurations. Extensive surgical resection of identified sites of origin may be required to ablate arrhythmias in these patients. Tachycardias whose sites of origin are not identified or resected may remain inducible. However, aggressive surgical excisions may alter regions involved in the genesis or maintenance of these arrhythmias because they become more difficult to induce postoperatively, more amenable to drug therapy and do not recur. © 1985, American College of Cardiology Foundation. All rights reserved.
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