Author + information
- Received June 8, 2017
- Revision received August 14, 2017
- Accepted August 31, 2017
- Published online January 15, 2018.
- Edward J. Ciaccio, PhDa,b,∗ (, )
- James Coromilas, MDc,
- Andrew L. Wit, PhDd,
- Nicholas S. Peters, MD, PhDb and
- Hasan Garan, MDa
- aDepartment of Medicine, Division of Cardiology, Columbia University College of Physicians and Surgeons, New York, New York
- bElectroCardioMaths Programme, Imperial Centre for Cardiac Engineering, Imperial College London, London, United Kingdom
- cDepartment of Medicine, Division of Cardiovascular Disease and Hypertension, Rutgers University, New Brunswick, New Jersey
- dDepartment of Pharmacology, Columbia University College of Physicians and Surgeons, New York, New York
- ↵∗Address for correspondence:
Dr. Edward J. Ciaccio, Department of Medicine, Division of Cardiology, Columbia University, P&S 7-445, 630 West 168th Street, New York, New York 10032.
Ventricular tachycardia (VT) caused by a re-entrant circuit is a life-threatening arrhythmia that at present cannot always be treated adequately. A realistic model of re-entry would be helpful to accurately guide catheter ablation for interruption of the circuit. In this review, models of electrical activation wavefront propagation during onset and maintenance of re-entrant VT are discussed. In particular, the relationship between activation mapping and maps of transition in infarct border zone thickness, which results in source-sink mismatch, is considered in detail and supplemented with additional data. Based on source-sink mismatch, the re-entry isthmus can be modeled from its boundary properties. Isthmus boundary segments with large transitions in infarct border zone thickness have large source-sink mismatch, and functional block forms there during VT. These alternate with segments having lesser thickness change and therefore lesser source-sink mismatch, which act as gaps, or entrance and exit points, to the isthmus during VT. Besides post-infarction substrates, the source-sink model is likely applicable to other types of volumetric changes in the myocardial conducting medium, such as when there is presence of fibrosis or dissociation of muscle fibers.
Dr. Peters has received funding from the British Heart Foundation (RG/16/3/32175 and Centre of Research Excellence), Rosetrees Trust, and the National Institute for Health Research (UK) Biomedical Research Centre. All 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 June 8, 2017.
- Revision received August 14, 2017.
- Accepted August 31, 2017.
- 2018 The Authors
This article requires a subscription or purchase to view the full text. If you are a subscriber or member, click Login or the Subscribe link (top menu above) to access this article.