EP News: Case Reports

  • T. Jared Bunch
    Address reprint requests and correspondence: Dr T. Jared Bunch, Department of Internal Medicine, Division of Cardiovascular Medicine, University of Utah School of Medicine, 30 North 1900 East, Room 4A100, Salt Lake City, UT 84132.
    Department of Internal Medicine, Division of Cardiovascular Medicine, University of Utah School of Medicine, Salt Lake City, Utah
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Published:November 04, 2020DOI:
      Ablation for ventricular fibrillation (VF) is founded upon the need to identify, map, and treat triggering premature ventricular contractions (PVCs) that often arise from the Purkinje network in both the absence and presence of structural heart disease. Mapping these PVCs as they relate to triggering and maintenance of VF is limited by hemodynamic instability, even with supportive therapies. Hasegawa et al ( share the case of a 64-year-old man with resuscitated VF and a history of myocardial infarction. During hospitalization, multiple episodes of recurrent VF resulted in the need for venoarterial extracorporeal membrane oxygenation (ECMO) for support. Repeat angiography did not identify an ischemic source or intracoronary thrombus. VF persisted despite ECMO and amiodarone. On day 16 of ECMO support, an ablation was performed, and nearly regular Purkinje activities were identified preceding each local endocardial ventricular activation with a mean cycle length of 330 ms. Ablation at the location impacted the arrhythmia, with transition of VF triggers mediated by Purkinje triggers from discrete sites. After ablation of all identified sites the VF resolved, and the patient maintained in sinus rhythm. However, he subsequently died of persistent brain injury. This study highlights the role of Purkinje-mediated triggers of VF and provides additional insight into their role in the maintenance of arrhythmia and the scope of potential arrhythmogenic substrates in patients with structural heart disease.
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