Termination of Sustained Ventricular Fibrillation During Radiofrequency Catheter Ablation

After a ST-segment elevation inferior myocardial infarction, a patient developed multiple drug-refractory ventricular fibrillation (VF), triggered by a stereotypic premature ventricular complex. During an episode of sustained VF, catheter ablation of the moderator band terminated VF, with transition into monomorphic ventricular tachycardia. To the best of our knowledge, this is the first-in-human report of termination of VF during delivery of radiofrequency energy, which suggests that the focal area on moderator band of Purkinje system had an active role in the perpetuation of VF. (Level of Difficulty: Advanced.)

which suggests that the focal area on moderator band of Purkinje system had an active role in the perpetuation of VF.

HISTORY OF PRESENTATION
A 50-year-old man with a history of hypertension and diabetes presented to an outside hospital with an inferior ST-segment elevation myocardial infarction and underwent percutaneous coronary intervention to the right coronary artery. By report, he developed stuttering chest pain 1 month before presentation.
Despite delayed revascularization with incomplete reperfusion, he developed polymorphic ventricular tachycardia (PMVT) and ventricular fibrillation (VF) requiring 3 separate episodes of resuscitation. Due to cardiogenic shock and right ventricular (RV) infarction, he was placed on mechanical circulatory support (MCS) and transferred to our institution.
Shortly after arrival, he developed VF storm, which worsened his respiratory failure and biventricular heart failure. He was taken to the operating room, and MCS was upgraded to right-sided veno-venous extracorporeal membrane oxygenation (Protek Duo, LivaNova) and a higher-flow Impella 5.5 (Abiomed).
He continued to have episodes of VF, which became incessant and refractory to intravenous amiodarone, lidocaine, and procainamide-despite over 10 defibrillation attempts within a 48-hour period.
On physical examination, the patient was in VF, was intubated, and mean arterial pressure was 50 to

LEARNING OBJECTIVES
To be able to manage electrical storm after myocardial infarction. To understand that catheter ablation may have an important therapeutic role in drug refractory VF. To understand the purported mechanism of VF after myocardial infarction and examine the possibility of underlying Purkinje activity involved in both the initiation and maintenance of VF.

DISCUSSION
To the best of our knowledge, this is the first reported observation of direct termination of sustained VF during delivery of RF energy. VF can be subdivided into VF associated with structural heart disease and VF in the setting of no apparent cardiomyopathy,

FIGURE 3 Local Electrogram Recorded at Successful Moderator Band Site
Intracardiac electrocardiogram recorded from the tip of the ablation catheter (Abl d) during sustained ventricular fibrillation at 100 mm/s sweep speed. Before radiofrequency delivery, intermittent high-frequency electrogram components, which may be consistent with Purkinje potentials, were recorded (red asterisks). is highly active in these cells, and its inhibition may be the mechanism by which quinidine has a therapeutic effect in these patients. 1 In the present case, quinidine was initiated and led to longer periods of sinus rhythm between defibrillation but without cessation of VF episodes.
In cases of refractory electrical storm, catheter ablation of VF after MI should be considered. Ablation of idiopathic VF has been well-described and performed by targeting early coupled PVC triggers that usually arise from the Purkinje network. 2 More recently, catheter ablation of VF storm after MI has been described with a similar approach of targeting PVCs arising from the fascicles at the border region of scar. 3,4 In this context, 2 reported cases observations have shown mechanically supported VF that selfterminated in the EP laboratory after RF catheter ablation to sites of Purkinje activation. 5,6 However, the present case may be the first in which VF directly and promptly terminated to monomorphic VT during

CONCLUSIONS
As previous studies have reported, catheter ablation of refractory VF storm can be highly effective in selected refractory cases. However, the literature to date have described ablation of PVC triggers during sinus rhythm as the strategy for preventing recurrent VF. This novel report of direct termination of sustained VF during a single application of radiofrequency energy into MMVT demonstrates that interruption of VF is a mechanistic possibility with ablation. A second radiofrequency application promptly terminated VT to sinus rhythm without the requirement for defibrillation. Anatomic structures that have been established as triggers for VF, such as the moderator band, may also play a mechanistic role in the perpetuation and maintenance of sustained VF.

FUNDING SUPPORT AND AUTHOR DISCLOSURES
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.