Author + information
- Received April 25, 2017
- Revision received May 22, 2017
- Accepted June 12, 2017
- Published online December 18, 2017.
- Andrew D. Beaser, MD,
- Kelvin Chua, MBBS,
- Michael T. Broman, MD, PhD and
- Roderick Tung, MD∗ ()
- Center for Arrhythmia Care, Heart and Vascular Center, The University of Chicago Medicine, Pritzker School of Medicine, Chicago, Illinois
- ↵∗Address for correspondence:
Dr. Roderick Tung, Center for Arrhythmia Care, The University of Chicago Medicine, 5841 South Maryland Avenue, MC 6080, Chicago, Illinois 60637.
- magnetic navigation
- premature ventricular contraction
- ventricular septal defect
- ventricular tachycardia
A 35-year-old man with congenital mitral atresia, a double outlet right ventricle with a hypoplastic left ventricle (HLV), and post-bidirectional Glenn and Fontan status was referred for ablation of symptomatic premature ventricular contractions (PVCs) and nonsustained ventricular tachycardia. He had a history of cardiac arrest with subsequent implantation of an epicardial defibrillator. The most frequent clinical PVC noted was right bundle branch block morphology, rightward directed, and isoelectric in the inferior leads, with late precordial lead V6 transition.
The earliest site of activation in the systemic ventricle via retrograde approach was on the most leftward aspect of the septum. Access to the HLV was restricted by both mitral atresia for the transseptal approach and by the aorta to morphologic right ventricular communication for the retrograde aortic approach. Intraprocedural transthoracic echocardiographic (2- and 3-dimensional) guidance facilitated access across the ventricular septal defect (VSD) into the HLV (Figure 1). Remote magnetic navigation (Stereotaxis, St Louis, Missouri) was used to facilitate mapping within the HLV due to the circuitous retrograde route required to cross the small membranous VSD.
An electroanatomic voltage map (CARTO, Biosense Webster. Diamond Bar, California) identified a diffuse region of scar (<1.5 mV) with a multiple fractionated split and late potentials throughout the lateral wall of the HLV. The site of earliest activation (−30 ms) was identified within the scar substrate and ablated, which resulted in suppression of ectopy. Scar homogenization was then performed by targeting abnormal electrograms in the hypoplastic substrate.
Although HLV has more frequently been associated with atrial arrhythmias, reports of ventricular arrhythmias are rare (1,2). Although the HLV had no contribution to the circulation, the abnormal fibrosis in the hypoplastic heart served as the nidus for arrhythmia. To our knowledge, this is the first report of a retrograde transaortic, transmembranous ventricular septal defect route to map and ablate the left ventricle.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- Received April 25, 2017.
- Revision received May 22, 2017.
- Accepted June 12, 2017.
- 2017 American College of Cardiology Foundation