N Chattipakorn1, P C Fotuhi, X Zheng, R E Ideker. 1. Division of Cardiovascular Disease, Department of Medicine, University of Alabama, Birmingham, USA. toon@crml.uab.edu
Abstract
BACKGROUND: After shocks with an approximately 50% probability of success for the upper limit of vulnerability (ULV(50)) of strength, the first few activations appear focally on the epicardium at almost the same site at the left ventricular (LV) apex in both successful and failed induction of ventricular fibrillation (VF). We tested the hypothesis that subendocardial ablation at this early site would decrease the shock strength required for the ULV(50). METHODS AND RESULTS: Ten S1 stimuli were delivered from the right ventricular apex at a 300-ms coupling interval in 5 pigs. Biphasic shocks were delivered from right ventricular-superior vena cava electrodes after the last S1 stimulus. The ULV(50) was determined using an up/down protocol with T-wave scanning. Radiofrequency ablation was performed endocardially at the apical LV. The ULV(50) was determined again 30 minutes after ablation. To determine the importance of the ablation region, this protocol was repeated in another 5 pigs with ablation at the LV base. Delivered voltage (401+/-60 versus 323+/-50 V) and energy (11+/-3 versus 7+/-2 J) for the ULV(50) were significantly decreased after LV apex ablation by 19% and 34%, respectively. However, no difference existed in ULV(50) before and after LV base ablation. Lesions at both the LV apex and base were subendocardial and ranged from 0.8 to 1.1 cm in diameter. CONCLUSIONS: Subendocardial ablation at the apical LV markedly decreases ULV(50), which suggests that the activation originating from this postshock early site is responsible for VF initiation and that interventions to electrically silence this site can influence the outcome of VF induction by ULV shocks.
BACKGROUND: After shocks with an approximately 50% probability of success for the upper limit of vulnerability (ULV(50)) of strength, the first few activations appear focally on the epicardium at almost the same site at the left ventricular (LV) apex in both successful and failed induction of ventricular fibrillation (VF). We tested the hypothesis that subendocardial ablation at this early site would decrease the shock strength required for the ULV(50). METHODS AND RESULTS: Ten S1 stimuli were delivered from the right ventricular apex at a 300-ms coupling interval in 5 pigs. Biphasic shocks were delivered from right ventricular-superior vena cava electrodes after the last S1 stimulus. The ULV(50) was determined using an up/down protocol with T-wave scanning. Radiofrequency ablation was performed endocardially at the apical LV. The ULV(50) was determined again 30 minutes after ablation. To determine the importance of the ablation region, this protocol was repeated in another 5 pigs with ablation at the LV base. Delivered voltage (401+/-60 versus 323+/-50 V) and energy (11+/-3 versus 7+/-2 J) for the ULV(50) were significantly decreased after LV apex ablation by 19% and 34%, respectively. However, no difference existed in ULV(50) before and after LV base ablation. Lesions at both the LV apex and base were subendocardial and ranged from 0.8 to 1.1 cm in diameter. CONCLUSIONS: Subendocardial ablation at the apical LV markedly decreases ULV(50), which suggests that the activation originating from this postshock early site is responsible for VF initiation and that interventions to electrically silence this site can influence the outcome of VF induction by ULV shocks.