Abstract
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.
Highlights
Ventricular tachycardia (VT) is a lifethreatening arrhythmia and major clinical problem
There are differences in the electrophysiology of canine versus clinical myocardial substrate when re-entrant VT is inducible, there are many similarities. These include the presence of an infarct border zone (IBZ), which is typically subepicardial in canine and subendocardial in clinical cases, the presence of a nonconducting infarct region at depth, the possibility of induction of a re-entrant circuit via programmed electrical stimulation from the IBZ, formation of a unidirectional block line, and activation wavefront bifurcation around the line followed by coalescence and re-entry into the previously excited region, typically resulting in the formation of a double-loop re-entrant circuit that drives VT, with functional block bounding the lateral borders of the isthmus
Activation mapping in the postinfarction IBZ was reviewed to show the predictive capability of the source-sink mismatch model for localizing functional conduction block leading to the onset and maintenance of re-entrant VT
Summary
ABBREVIATIONS electrical conduction there and thereby to AND ACRONYMS stop re-entrant VT from recurring. It travels through the isthmus region, exits, bifurcates, and propagates as 2 wavefronts in the opposite direction along the outer pathway. Functional conduction block resulting from source-sink mismatch can occur as the wavefront propagates outwardly when the isthmus thickness T # 500 mm [5,32,33], DT per unit space step c is large, and with the time between oncoming activation wavefronts in the range of VT cycle length intervals, approximately 175 to 300 ms [34].
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