Abstract
Ventricular fibrillation (VF) storm is a life-threatening condition that is particularly challenging to manage when resistant to conventional therapies such as antiarrhythmic drugs, deep sedation, overdrive pacing, and hemodynamic support. We report a case of a 55-year-old male with ischemic heart disease and recurrent VF storm unresponsive to initial treatments, requiring percutaneous cardiopulmonary support to stabilize hemodynamics. A left ventricular inferoseptal Purkinje-related premature ventricular contraction (PVC) was identified as the VF trigger, with continuous propagating activity involving Purkinje and myocardial substrates as the driver. Targeted radiofrequency catheter ablation (RFCA) at the earliest activation site of the triggering PVC and continuous propagating activity effectively suppressed VF and maintained stable sinus rhythm. The patient was successfully weaned off support devices and was discharged with an implantable cardioverter-defibrillator. This case highlights the importance of accurately localizing triggers and drivers in refractory VF management and suggests the efficacy of RFCA in managing VF storm associated with structural heart disease.
Learning objective
1. The origin and exit of the Purkinje-related triggering premature ventricular contraction (PVC) differed. 2. During initiation of ventricular fibrillation (VF), the Purkinje and myocardial potentials fused, exhibiting continuous propagating activity in the limited area surrounding the origin and exit of the triggering PVC. 3. Radiofrequency catheter ablation targeting both the triggering PVC and continuous propagating activity demonstrated notable efficacy in the suppression of the VF storms.
Introduction
Ventricular fibrillation (VF) is a major cause of sudden cardiac death in patients with ischemic heart disease. Managing VF storm focuses on excluding myocardial ischemia and combining therapies such as antiarrhythmic drugs, sedation with mechanical ventilatory, overdrive pacing, or hemodynamic support devices. Nonetheless, the management of VF refractory to these extensive therapeutic efforts is challenging. Radiofrequency catheter ablation (RFCA) targeting the focal Purkinje-related triggering premature ventricular contraction (PVC) and the drivers, such as rotor activity or focal activity, has been reported to reduce VF burden after myocardial infarction [ , ]. However, identifying the trigger and driver of VF remains challenging when sinus rhythm fails to persist despite repetitive defibrillation. Here, we present a case of refractory VF, wherein hemodynamic stability was achieved through the insertion of percutaneous cardiopulmonary support (PCPS), thereby facilitating the identification of triggers and drivers of VF, ultimately leading to a subsequent successful ablation.
Case report
A 55-year-old man was hospitalized for severe heart failure, with a left ventricular (LV) ejection fraction of 20 % and severe hypokinesia observed in the anteroseptal and inferior wall regions. On the fourth day of hospitalization, a subsequent manifestation of VF was observed, necessitating immediate electrical defibrillation, sedation, and pharmacological intervention. Despite these interventions, recurrent episodes of VF persisted. Emergency coronary angiography revealed sub-occlusions of the left anterior descending and right coronary arteries, leading to immediate percutaneous coronary angioplasty. However, VF storms occurred, necessitating multiple applications of electrical defibrillation to transiently restore sinus rhythm. Owing to the deteriorating hemodynamic status, an intra-aortic balloon pump (IABP) and PCPS were promptly inserted. Ventricular burst pacing with a temporary pacemaker was performed once sinus rhythm was reestablished following defibrillation. However, VF resumed within a few minutes. The QRS morphology of the VF-triggering PVC was reproducibly identical, characterized by a right bundle branch block configuration with left-axis deviation and a QRS duration of 139 ms ( Fig. 1 ). RFCA was considered to target the monomorphic PVC responsible for triggering the VF.
After obtaining informed consent from his family, RFCA was performed using a three-dimensional mapping system (CARTO 3; Biosense Webster, Irvine, CA, USA). The VF-triggering PVC morphology suggested a LV inferoseptal origin, and a decapolar catheter (DECANAV®, Biosense Webster) was positioned on the LV inferoseptum via the Agilis® steerable sheath (Abbot, Saint Paul, MN, USA) through a transseptal approach. Electrical defibrillation terminated the VF and maintained sinus rhythm for a few minutes. During sinus rhythm, pace mapping at 100 ppm from the DECANAV® catheter was performed, and the QRS morphology was compared with that of the VF-triggering PVC. When VF manifested, repeated electrical defibrillations were performed. The earliest activation site of the VF-triggering PVC was identified, utilizing a self-referential mapping method [ ]. The origin of the VF-triggering PVC was located at the LV mid-inferoseptum, corresponding to the area of the myocardial infarction. Notably, high frequency and small amplitude Purkinje potentials and large amplitude myocardial potentials were separately observed on electrodes MP 3–4 of the DECANAV® catheter. The earliest Purkinje potentials preceding the QRS onset by 140 ms were firstly recorded by electrodes MP 3–4, and then activated towards electrodes MP 5–6. Conversely, the myocardial potentials were firstly recorded on electrodes MP 7–8 and then activated with a chevron pattern ( Fig. 2 ). Moreover, during the initial few minutes following the onset of VF, the fused potentials with Purkinje potentials and myocardial potentials recorded from MP 3–4 to MP 9–10 alternately excited, covering most of the VF cycle length ( Fig. 3 A ). We defined this phenomenon as continuous propagating activity. After the electrical defibrillation, the pace map from electrodes MP 7–8 exhibited the most consistent QRS morphology with that of the VF-triggering PVC ( Fig. 3 B), suggesting the location was the myocardial exit of the triggering PVC. RFCA was performed using a THERMOCOOL SMARTTOUCH® catheter (Biosense Webster) targeting the origin (MP 3–4 region) and the myocardial exit (MP 7–8 region) of the triggering PVC; however, VF still repeatedly occurred. Additional RFCA encompassing the region spanning from MP 3,4 to MP 9–10, where continuous propagating activity was observed, exhibited notable efficacy in the maintenance of sinus rhythm after electrical defibrillation. The patient was successfully weaned from PCPS and IABP and was subsequently discharged after implanting an implantable cardioverter-defibrillator. Four years post-procedure, no VF episodes occurred.
