(Circulation. 2000;101:2458.)
© 2000 American Heart Association, Inc.
Brief Rapid Communications |
From the Division of Cardiovascular Disease, Department of Medicine, University of Alabama, Birmingham.
Correspondence to Nipon Chattipakorn, MD, PhD, 1670 University Blvd, Rm B140, Birmingham, AL 35294-0019. E-mail: toon{at}crml.uab.edu
BackgroundAfter shocks with an
50% probability of success for the upper limit of vulnerability
(ULV50) 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
ULV50.
Methods and ResultsTen S1 stimuli were delivered from the right ventricular apex at a 300-ms coupling interval in 5 pigs. Biphasic shocks were delivered from right ventricularsuperior vena cava electrodes after the last S1 stimulus. The ULV50 was determined using an up/down protocol with T-wave scanning. Radiofrequency ablation was performed endocardially at the apical LV. The ULV50 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 ULV50 were significantly decreased after LV apex ablation by 19% and 34%, respectively. However, no difference existed in ULV50 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.
ConclusionsSubendocardial ablation at the apical LV markedly decreases ULV50, 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.
Key Words: ablation fibrillation shock
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