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?
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.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for post-ablation VT mechanisms in this model; leaves open translation to clinical catheter ablation.
BACKGROUND: DC shock catheter ablation for the treatment of ventricular tachycardia (VT) may induce VT episodes that disappear within days. METHODS AND RESULTS: A 30-J cathodal shock was delivered to the endocardial left ventricular wall in 15 closed-chest dogs. All dogs had VT during the first day after ablation. Eleven of these dogs were studied on the first day. Extensive epicardial and endocardial activation mapping in vivo, in Langendorff-perfused hearts, and in tissue blocks in a tissue bath localized the site of origin of VT to subendocardial Purkinje fibers in a border zone surrounding the central necrotic ablation lesion. Intracellular recording showed that this zone consisted of a subendocardial superficial layer (SSL) of cells with abnormal characteristics, a resting membrane potential (RMP) of -58 +/- 11 mV (mean +/- SD), and an action potential amplitude (APA) of 61 +/- 20 mV. In addition, the steepness of phase 0 of the action potential was markedly reduced. In three dogs abnormal automaticity was found in a very small area. Immediately below the SSL, cells were normal with an RMP of -78 +/- 5 mV and an APA of 107 +/- 8 mV. Histology confirmed a thin SSL with edematous and necrotic cells, hemorrhage, and infiltration. The other four dogs were studied at 1 week after ablation when VT was absent. Microelectrode impalement in the SSL was either impossible or showed nearly normal action potential characteristics. Histological examination showed a markedly thickened fibrotic subendocardial layer at places where impalement was impossible. Normal subendocardium was found in other areas of the border zone. CONCLUSIONS: Our results indicate that VT after DC shock ablation originates from cells with abnormal automaticity in the superficial subendocardial border zone around the central ablation lesion. Within 1 week edematous and necrotic cells in this border zone are replaced by a fibrotic layer, and this transition is associated with the disappearance of VT.
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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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