Author + information
- David F. Briceño, MD1,
- Andres Enriquez, MD2,
- Jackson J. Liang, DO1,
- Yasuhiro Shirai, MD1,
- Pasquale Santangeli, MD, PhD1,
- Gustavo Gundalini, MD1,
- Gregory E. Supple, MD1,
- Robert Schaller, DO1,
- Jeffrey Arkles, MD1,
- David S. Frankel, MD1,
- Carlos Tapias, MD3,
- Diego Rodriguez, MD3,
- Luis C. Saenz, MD3,
- David J. Callans, MD1,
- Francis Marchlinski, MD1 and
- Fermin C. Garcia, MD1,3,† ()
- 1Electrophysiology Section, Cardiovascular Division, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PAElectrophysiology Section, Cardiovascular Division, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA
- 2Heart Rhythm Service, Queen's University, Kingston, Ontario, CanadaHeart Rhythm Service, Queen's University, Kingston, Ontario, Canada
- 3Fundación Cardioinfantil, Instituto de Cardiología, Centro Internacional de Arritmias Andrea Natale, Bogotá, ColombiaFundacion Cardioinfantil, Instituto de Cardiologia, Centro Internacional de Arritmias Andrea Natale, Bogota, Colombia
- ↵†Corresponding author Fermin C. Garcia, MD Assistant Professor of Medicine Section of Cardiac Electrophysiology Hospital of the University of Pennsylvania 9 Founders Pavilion 3400 Spruce St. Philadelphia, PA 19104
Background Intramural septal ventricular arrhythmias (VAs) represent a challenge for substrate definition and catheter ablation.
Objective To describe the use of septal coronary venous mapping to facilitate substrate characterization and ablation of intramural septal VAs.
Methods Between 2015 and 2018, 12 patients with structural heart disease, recurrent VAs and suspected intramural septal substrate underwent septal coronary venous mapping by advancing a wire into the septal perforator branches of the anterior interventricular vein. Five patients with idiopathic VAs were also included as control to compare substrate characteristics.
Results Mean age of patients was 63 ± 14 years and 11 (92%) were men. Most patients with structural heart disease had non-ischemic cardiomyopathy (83%). Six patients underwent ablation for PVCs and 6 for VT. All patients had larger septal unipolar than bipolar voltage abnormalities (mean area 35.3 ± 16.8 cm2 vs. 10.7 ± 8.4 cm2, p=0.01), while idiopathic patients had normal voltage. Septal coronary venous mapping revealed low voltage, fractionated and multicomponent electrograms in sinus rhythm in all patients with substrate compared to patients with idiopathic VAs (amplitude 0.9 ± 0.9 mV vs. 4.4 ± 3.7 mV, p=0.007; and duration 147 ± 48 ms vs. 92 ± 10 ms, p=0.03). Ablation targeted early activation, pacemap match and/or good entrainment sites from intraseptal recording. Over a mean follow-up of 339 ± 240 days, the PVC and ICD therapies burden were significantly reduced (mean 22 ± 11% to 4 ± 8%, p=0.005; mean 5 ± 2 to 1 ± 1, p=0.001, respectively). Most patients (80%) with idiopathic VAs remain arrhythmia free.
Conclusion In patients with suspected intramural septal VAs, mapping of the septal coronary veins may be helpful to characterize the arrhythmia substrate, identify ablation targets and guide endocardial ablation.
Funding: This research was supported in part by the Winkelman Family Fund in Cardiovascular Innovation
Disclosures: No disclosures relevant to the contents of this paper.
- Received April 12, 2019.
- Revision received April 29, 2019.
- Accepted April 29, 2019.
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