Key result
DC shock ablation in dogs triggers transient VT resolving within 1 week due to fibrosis.
Why the study?
What is the electrophysiologic and histologic mechanism of ventricular tachycardia after in vivo DC shock ablation in dogs?
Population
15 closed-chest dogs
Design
Preclinical
Follow-up
up to 1 week
Authors
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Hypothesis-generating for post-ablation VT mechanisms in this model; leaves open translation to clinical catheter ablation.
What is the electrophysiologic and histologic mechanism of ventricular tachycardia after in vivo DC shock ablation in dogs?
Ventricular tachycardia following DC shock ablation in dogs is caused by abnormal automaticity in the subendocardial border zone, which resolves as the tissue becomes fibrotic over 1 week.
Hauer et al. (1991) studied Ventricular tachycardia (n=15). DC shock catheter ablation was evaluated on Electrophysiologic and histologic characteristics of the ablation border zone and occurrence of VT. DC shock ablation in dogs induced ventricular tachycardia originating from cells with abnormal automaticity in the subendocardial border zone, which disappeared within 1 week as the zone became fibrotic.
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