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Modifying Ventricular Fibrillation by Targeted Rotor Substrate Ablation: Proof‐of‐Concept from Experimental Studies to Clinical VF
Author(s) -
KRUMMEN DAVID E.,
HAYASE JUSTIN,
VAMPOLA STEPHEN P.,
HO GORDON,
SCHRICKER AMIR A.,
LALANI GAUTAM G.,
BAYKANER TINA,
COE TAYLOR M.,
CLOPTON PAUL,
RAPPEL WOUTERJAN,
OMENS JEFFREY H.,
NARAYAN SANJIV M.
Publication year - 2015
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/jce.12753
Subject(s) - medicine , cardiology , ablation , proof of concept , ventricular fibrillation , catheter ablation , atrial fibrillation , fibrillation , computer science , operating system
Rotor Substrate Ablation Suppresses VF Introduction Recent work has suggested a role for organized sources in sustaining ventricular fibrillation (VF). We assessed whether ablation of rotor substrate could modulate VF inducibility in canines, and used this proof‐of‐concept as a foundation to suppress antiarrhythmic drug‐refractory clinical VF in a patient with structural heart disease. Methods and Results In 9 dogs, we introduced 64‐electrode basket catheters into one or both ventricles, used rapid pacing at a recorded induction threshold to initiate VF, and then defibrillated after 18±8 seconds. Endocardial rotor sites were identified from basket recordings using phase mapping, and ablation was performed at nonrotor (sham) locations (7 ± 2 minutes) and then at rotor sites (8 ± 2 minutes, P = 0.10 vs. sham); the induction threshold was remeasured after each. Sham ablation did not alter canine VF induction threshold (preablation 150 ± 16 milliseconds, postablation 144 ± 16 milliseconds, P = 0.54). However, rotor site ablation rendered VF noninducible in 6/9 animals (P = 0.041), and increased VF induction threshold in the remaining 3. Clinical proof‐of‐concept was performed in a patient with repetitive ICD shocks due to VF refractory to antiarrhythmic drugs. Following biventricular basket insertion, VF was induced and then defibrillated. Mapping identified 4 rotors localized at borderzone tissue, and rotor site ablation (6.3 ± 1.5 minutes/site) rendered VF noninducible. The VF burden fell from 7 ICD shocks in 8 months preablation to zero ICD therapies at 1 year, without antiarrhythmic medications. Conclusions Targeted rotor substrate ablation suppressed VF in an experimental model and a patient with refractory VF. Further studies are warranted on the efficacy of VF source modulation.

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