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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Introduction: Recent work has shown that rotor characteristics can distinguish sustained versus non-sustained ventricular fibrillation (VF). However, the significance of functional VF substrates on patient outcomes is not studied. Methods: In 26 consecutive patients presenting for ventricular arrhythmia ablation procedures, 64-electrode basket catheters were inserted into both the left and right ventricles and VF was induced and defibrillated at 11±3 seconds. Computational phase analysis was performed and each VF cycle was characterized as rotor, focal, or disorganized activation. Follow-up data were analyzed for arrhythmia recurrence and compared to rotor stability. Forward stepwise regression analysis incorporating age, history of CHF, history of a-fib, history of prior MI, number of VTs induced, and presence of post-procedure inducible VT was performed to determine the strongest predictor of procedural outcome. Results: Of 26 patients, 19 had sustained VF, and 16 underwent attempted ablation (7 VT, 9 PVC). Optimization of the Youden index for the ROC analysis regarding rotor stability and procedural outcome demonstrated that maximum rotor stability of > 14.5 rotations (corresponding to total rotor prevalence of 71%) provided optimal sensitivity of 85% and specificity of 87% for arrhythmia recurrence. Among these, greater rotor stability was significantly associated with ventricular arrhythmia recurrence (86% versus 11%, p = 0.01) (Table 1), and was the strongest predictor of outcomes. Recurrence was independent of presenting arrhythmia. Conclusions: Functional VF/VT metrics were the strongest predictor of ventricular arrhythmia outcomes compared to traditional predictors in this series of patients. This suggests that functional substrate characteristics may provide added insight into recurrence mechanisms. Whether they may identify a target for future interventions requires further study.

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