Author + information
- Received March 9, 2018
- Revision received April 19, 2018
- Accepted April 26, 2018
- Published online June 27, 2018.
- Elad Anter, MD∗ (, )
- Andre G. Kleber, MD,
- Markus Rottmann, PhD,
- Eran Leshem, MD, MHA,
- Michael Barkagan, MD,
- Cory M. Tschabrunn, PhD,
- Fernando M. Contreras-Valdes, MD and
- Alfred E. Buxton, MD
- Harvard-Thorndike Electrophysiology Institute, Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts
- ↵∗Address for correspondence:
Dr. Elad Anter, Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Medical Center, 185 Pilgrim Road, Baker 4, Boston, Massachusetts 02215.
Objective In this study, the scientific objective was to characterize the electrophysiological substrate of the ventricular tachycardia (VT) isthmus during sinus rhythm.
Background The authors have recently described the electrophysiological characteristics of the VT isthmus using a novel in vivo high-resolution mapping technology.
Methods Sixteen swine with healed infarction were studied using high-resolution mapping technology (Rhythmia, Boston Scientific, Cambridge, Massachusetts) in a closed-chest model. The left ventricle was mapped during sinus rhythm and analyzed for activation, conduction velocity, electrogram shape, and amplitude. Twenty-four VTs allowed detailed mapping of the common-channel “isthmus,” including the “critical zone.” This was defined as the zone of maximal conduction velocity slowing in the circuit, often occurring at entrance and exit from the isthmus caused by rapid angular change in activation vectors.
Results The VT isthmus corresponded to sites displaying steep activation gradient (SAG) during sinus rhythm with conduction velocity slowing of 58.5 ± 22.4% (positive predictive value [PPV] 60%). The VT critical zone displayed SAG with greater conduction velocity slowing of 68.6 ± 18.2% (PPV 70%). Critical-zone sites were consistently localized in areas with bipolar voltage ≤0.55 mV, whereas isthmus sites were localized in areas with variable voltage amplitude (1.05 ± 0.80 mV [0.03 to 2.88 mV]). Importantly, critical zones served as common-site “anchors” for multiple VT configurations and cycle lengths. Isthmus and critical-zone sites occupied only 18.0 ± 7.0% of the low-voltage area (≤1.50 mV). Isolated late potentials were present in both isthmus and nonisthmus sites, including dead-end pathways (PPV 36%; 95% confidence interval: 34.2% to 39.6%).
Conclusions The VT critical zone corresponds to a location characterized by SAG and very low voltage amplitude during sinus rhythm. Thus, it allows identification of a re-entry anchor with high sensitivity and specificity. By contrast, voltage and electrogram characteristics during sinus rhythm have limited specificity for identifying the VT isthmus.
This study was supported by research grants from Boston Scientific and the National Institutes of Health (1R21HL127650-01 and 1R01HL129185).
Dr. Anter has received research grants from Boston Scientific and speaking honoraria at the di minis threshold of Harvard Medical School. Dr. Buxton has received research grants from Biosense Webster and Medtronic, Inc. All other 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 March 9, 2018.
- Revision received April 19, 2018.
- Accepted April 26, 2018.
- 2018 American College of Cardiology Foundation
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